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Define the problem, specific population affected, cultural implications, and financial/legal/ethical implications.

Define the problem, specific population affected, cultural implications, and financial/legal/ethical implications..

Define the problem, specific population affected, cultural implications, and financial/legal/ethical implications.

Assignment 2: Analysis of an Age Related Topic: CHF
1. Conduct in-depth analysis of a pertinent topic related to aging. ( I CHOSE CHF )
2. Define the problem, specific population affected, cultural implications, and financial/legal/ethical implications.
3. What interventions can be used to improve the problem?
4. What resources are available? What are the associated costs? Is this idea sustainable?
5. Support your responses with examples.

DEAR WRITER, YOU MAY USE NURSING BOOKS, NURSING JOURNALS, ARTICLES AND THE INTERNET FOR RESOURCES. YOU MAY ALSO USE INFORMATION FOR HEALTHY PEOPLE 2020, LOOK UNDER ?OLDER ADULT?.

WHEN ASK TO DEFINE THE ?PROBLEM? THE INSTRUCTOR WANT TO KNOW WHAT CHF IS.
Submit your paper in a 3 page Microsoft Word document.
On a separate references page, cite all sources using APA format.
References must be within 3 years.

Grading Criteria Maximum Points
Defined the problem related to your aging topic. 36
Identified and described the specific population affected. 16
Identified and described the cultural implications for the identified population. 16
Identified and described the financial/legal/ethical implications for the identified population related to the problem. 16
Identified and described 2?3 interventions that can be used to improve the problem for the specific population. 16
Identified and described the resources that are available in order to improve the problem for the specific population. 16
Identified and described the associated costs related to the interventions for the identified problem. 16
Identified and described the sustainability of the interventions for the identified problem. 16
Used correct spelling, grammar, and professional vocabulary. Cited all sources using APA format. 32
Total: 180
Heart Failure Statistics
? Nearly 5 million Americans are currently living with congestive heart failure (CHF).
? Approximately 550,000 new cases are diagnosed in the U.S. each year.
? Congestive heart failure affects people of all ages, from children and young adults to the middle-aged and the elderly.
? Almost 1.4 million persons with CHF are under 60 years of age.
? CHF is present in 2 percent of persons age 40 to 59.
? More than 5 percent of persons age 60 to 69 have CHF.
? CHF annual incidence approaches 10 per 1,000 population after 65 years of age.
? The incidence of CHF is equally frequent in men and women, and African-Americans are 1.5 times more likely to develop heart failure than Caucasians.
? Heart failure is responsible for 11 million physician visits each year, and more hospitalizations than all forms of cancer combined.
? CHF is the first-listed diagnosis in 875,000 hospitalizations, and the most common diagnosis in hospital patients age 65 years and older.
? In that age group, one-fifth of all hospitalizations have a primary or secondary diagnosis of heart failure.
? More than half of those who develop CHF die within 5 years of diagnosis.
? Heart failure contributes to approximately 287,000 deaths a year.
? Sudden death is common in patients with CHF, occurring at a rate of six to nine times that of the general population.
? Deaths from heart failure have decreased on average by 12 percent per decade for women and men over the past fifty years.
http://www.emoryhealthcare.org/heart-failure/learn-about-heart-failure/statistics.html

Heart failure happens when the heart cannot pump enough blood and oxygen to support other organs in your body. Heart failure is a serious condition, but it does not mean that the heart has stopped beating.
Heart Failure in the United States
? About 5.7 million adults in the United States have heart failure.1
? One in 9 deaths in 2009 included heart failure as contributing cause.1
? About half of people who develop heart failure die within 5 years of diagnosis.1
? Heart failure costs the nation an estimated $30.7 billion each year.3 This total includes the cost of health care services, medications to treat heart failure, and missed days of work.
Deaths from Heart Failure Vary by Geography
Heart failure is more common in some areas of the United States than in others. Below is a map showing the rate of death from heart failure by county during 2011?2013.

Source: Interactive Atlas of Heart Disease and Stroke(http://www.cdc.gov/dhdsp/maps/atlas/index.htm)
Risk Factors for Heart Failure
Diseases that damage your heart also increase your risk for heart failure. Some of these diseases include
? Coronary heart disease(http://www.cdc.gov/heartdisease/coronary_ad.htm) (the most common type of heart disease) and heart attacks.
? High blood pressure(http://www.cdc.gov/bloodpressure).
? Diabetes(http://www.cdc.gov/diabetes/index.html).
Unhealthy behaviors can also increase your risk for heart failure, especially for people who have one of the diseases listed above. Unhealthy behaviors include
? Smoking tobacco.
? Eating foods high in fat, cholesterol, and sodium(http://www.cdc.gov/salt).
? Not getting enough physical activity.
? Being obese.
Signs and Symptoms of Heart Failure
Common symptoms of heart failure include:
? Shortness of breath during daily activities.
? Having trouble breathing when lying down.
? Weight gain with swelling in the feet, legs, ankles, or stomach.
? Generally feeling tired or weak.
Treating Heart Failure
Early diagnosis and treatment can improve quality and length of life for people who have heart failure. Treatment usually involves taking medications, reducing sodium in the diet, and getting daily physical activity. People with heart failure also track their symptoms each day so that they can discuss these symptoms with their health care team.
CDC’s Public Health Efforts Related to Heart Failure
? State Public Health Actions to Prevent and Control Chronic Diseases(http://www.cdc.gov/dhdsp/programs/spha/index.htm)
? Million Hearts?
Web Sites with More Information About Heart Failure
For more information about heart failure, visit the following Web sites:
? Medline Plus
? National Heart, Lung, and Blood Institute
? American Heart Association
? Heart Failure Society of America
References
1. Mozzafarian D, Benjamin EJ, Go AS, et al. on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics?2016 update: a report from the American Heart Association. Circulation. 2016;133:e38-e360.
2. Kochanek KD, Xu JQ, Murphy SL, Mini?o AM, Kung HC. Deaths: final data for 2009[PDF-3M](http://www.cdc.gov/nchs/data/nvsr/nvsr60/nvsr60_03.pdf). Natl Vital Stat Rep. 2011;60(3).
3. Heidenreich PA, Trogdon JG, Khavjou OA, Butler J, Dracup K, Ezekowitz MD, et al. Forecasting the future of cardiovascular disease in the United States: a policy statement from the American Heart Association. Circulation. 2011;123(8):933?44.

http://www.cdc.gov/DHDSP/data_statistics/fact_sheets/fs_heart_failure.htm

Treatment of Heart Failure in African Americans: A Consensus Statement

Despite advances in diagnosis and treatment of heart failure (HF), it remains a growing disease state in the United States, annually affecting millions of people that causes well over a million hospitalizations, contributing to more than 50,000 deaths, and consuming billions of dollars in health care spending. Although all segments of the population are affected, this growing burden of HF is especially evident in certain populations.1?3 This disease burden is further amplified by the fact that the beneficial impact of new treatment advances has been limited by slow penetration of evidence-based therapy into the broader community setting of clinical practice. This too is especially evident in certain special populations.4 Thus, the health and economic burden of HF continues to grow and affects certain underserved populations in a disproportionate manner.
African Americans represent a special population of great concern. The relative incidence of HF is 50% higher in African Americans, 3% of whom have HF, compared with 2% of the general population (Figure S1).5?7 Moreover, when affected by HF, African Americans experience a unique epidemiology and different natural history. The disease occurs at an earlier age, resulting in more substantial left ventricular dysfunction and more advanced disease severity as measured by functional class. The clinical consequence is a definite increase in morbidity (measured as increased hospitalizations) and an uncertain but possibly worse effect on mortality.8 As noted in recent reviews, the reasons for this apparent greater disease burden of HF in African Americans are complex and probably relate to the interplay of several factors, including the higher prevalence and severity of important risk factors such as hypertension, diabetes, and obesity; adverse socioeconomics; disparate health care; variances in physiologic responses to cardiovascular diseases; and genetics.6?8
African Americans have been consistently underrepresented in clinical trials of HF (Table S1),9?20 and data regarding the demographics, benefits, and risks of many important therapies in this group are sparse, thus compromising the ability to make definitive statements and recommendations.11,13 For example, in the Valsartan Heart Failure Trial (Val-HeFT), only 13% of the 2178 patients randomized at US centers were African American.21 In the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS), approximately l% of the study population was African American.20 The Studies on Left Ventricular Dysfunction (SOLVD) and the US Carvedilol Clinical Trials program are pivotal in supporting the routine use of angiotensin-converting enzyme (ACE) inhibitors and ?-blockers in all patients with HF. However, these studies included barely 600 African Americans combined, compared with nearly 10 times that number of all other patients.11,13 Despite this paucity of available data, current HF guidelines have recommendations to include special populations (ie, African Americans) while recognizing that extrapolation of the guidelines to all populations may include unrecognized limitations.1,2,22
Given the large burden of HF in African Americans and the worrisome natural history, more focused management of HF in this group appears warranted. In particular, existing guidelines should be emphasized and amplified where warranted to more specifically address African Americans. To that end, a national panel was convened under the sponsorship of the Association of Black Cardiologists to review available evidence and make specific recommendations for the management of HF in African Americans. This multidisciplinary panel consisted of established HF cardiologists, researchers, and members of several African American medical organizations. This consensus statement is based on a thorough survey of available pertinent literature and examination of the most recent major guidelines for HF management.1,2,22 It focuses on sections of guidelines that were judged most likely to be uniquely beneficial in the management of African Americans with HF. This statement is intended for simultaneous use with other relevant guidelines, especially those for HF, hypertension, and diabetes and is not intended to abrogate already existing HF guidelines (Table S2).
Overview of HF
The reader should refer to the major HF guidelines and published literature for a broader discussion of HF.1,2,22 In brief, HF is a clinical syndrome caused by a variety of cardiovascular diseases that produce cardiac structural changes leading to cardiac dysfunction and eventually the well-known symptoms of HF (ie, dyspnea, fatigue, exercise intolerance, and congestion). Cardiac dysfunction usually manifests as alterations in cardiac size and geometry (ie, ventricular remodeling), which is driven by neurohormonal activation. The remodeling process initiates an inexorable cycle of worsening left ventricular function, leading to progressive cardiac enlargement, increased hemodynamic and wall stresses, mitral valve dysfunction, further maladaptive neurohormonal activation, and ventricular irritability, all of which beget progressive cardiac dysfunction, sudden cardiac death and, ultimately, end-stage HF and pump failure death. This process may be associated with impaired systolic function, as evidenced by reduced left ventricular ejection fraction (LVEF); with normal to mildly impaired LVEF with or without diastolic abnormalities; or with what is considered to be essentially preserved ejection fraction, generally defined clinically as LVEF =40%, and presumably with abnormalities of relaxation (?diastolic dysfunction?).
Several approaches to classifying the patient?s stage or clinical severity of HF have been used; the most common is the New York Heart Association (NYHA) classification, which describes classes of severity based on subjective assessment of symptoms. An adjunctive and complementary approach adopted in the American College of Cardiology/American Heart Association (ACC/AHA) guidelines emphasizes disease progression from risk factors to asymptomatic cardiac abnormalities to clinical HF, classified as stages A, B, C, and D, respectively. Each of these stages has definable characteristics and recommended interventions. The goal is to prevent HF development or its progression to end-stage disease (stage D) (Figure S2).1,2 The NYHA scheme is fluid and patients may vary in functional capacity, whereas the ACC/AHA model is unidirectional and patients can only progress toward greater disease severity.
HF in African Americans
Etiology. As suggested by the clinical trials experience, HF in African Americans is much more commonly associated with a nonischemic etiology of left ventricular dysfunction. Hypertension is considered to be the putative disease process, but dilated cardiomyopathies and diabetes-related diseases are also common in African Americans. Coronary artery disease remains a cause of left ventricular dysfunction in African Americans, but, as an attributable cause of HF, it is strikingly less common in African Americans than in whites. The SOLVD registry was among the first databases to yield the observation that hypertension alone affects 30% of African Americans with HF as compared with 10% of whites with HF.23 Hypertension is an even more significant factor in HF with diastolic dysfunction, but this observation is not race-specific.24 Within the US Carvedilol Clinical Trials program, hypertension was thought to be the etiology of HF in more than half of African American participants and coronary artery disease the cause in approximately a third. These proportions were reversed in whites.25
The prevalence of hypertension in African Americans in the United States is among the highest in the world and is 3 times more likely to be severe, presenting in about 75% of African Americans aged 60 years or older.22,26,27 Among persons younger than 30 years of age, the likelihood of HF developing over the ensuing 20 years was 20 times as high among blacks as among whites.28 End-organ manifestations of hypertension are strikingly more common in African Americans, with the likelihood of end-stage renal disease being 2- to 3-fold greater. Because stroke rates are higher, rates of death resulting from stroke are also higher. Left ventricular hypertrophy occurs more frequently, affecting an estimated 30% or more of all African Americans with hypertension, compared with only 10% of hypertensive whites. Notably, left ventricular hypertrophy is 2 to 3 times more likely to develop in African Americans than in whites, even when adjusted for body composition.29 In addition, the pattern of hypertrophy (ie, concentric hypertrophy) is associated with increased morbidity and mortality. Moreover, the pathophysiology of hypertension is unique in the African American as it is more commonly associated with increased sodium sensitivity, relatively low renin activity, and possibly reduced nitric oxide (NO) production.30 Based on available evidence, hypertension is a more severe illness in African Americans than in whites, and the natural history of some African Americans affected by hypertension represents a much more malignant vascular response.
In addition to the greater prevalence of hypertension, African Americans are also 1.6 times more likely than whites to have diabetes.31 Thus, the higher prevalence of diabetes, hypertension, and hypertension-related end-organ damage among African Americans provides a plausible explanation for the apparent excess disease burden of HF in this population.6?8 These facts clearly mandate greater attention to the recognition and early and aggressive treatment of hypertension and diabetes in the African American population as per recommended guidelines.1,2,5,22,32
Pathophysiology of HF in African Americans. Neurohormonal activation remains the core pathophysiologic consideration in the genesis of HF in all populations. However, other pathologic mechanisms, especially differences in vascular function between African Americans and whites, may underlie the enhanced disease burden of HF in African Americans. Vascular reactivity of some African Americans may be more dependent on NO.33,34 Compared with whites, some African Americans have more exaggerated vasoconstrictor responses and less responsiveness to certain vasodilators and to inhibition of the renin-angiotensin system.35?37
Evidence suggests that abnormal endothelial function may contribute to abnormal blood pressure responses with more severe consequences in African Americans. This burden of endothelial dysfunction may result, in part, from insufficient NO secondary to reduced endothelial production of NO or to increased NO inactivation by reactive oxygen species.33?35 Abnormalities of NO production or metabolism also may contribute to adverse ventricular remodeling. As shown schematically in Figure S3, angiotensin II is a potent stimulator of cardiac and vascular remodeling, whereas NO is a potent inhibitor of this remodeling process.38 Hypothetically, the balance between these is the normal situation, and upsetting it leads to progressive remodeling. Available data now indicate potential racial differences between African Americans and whites in this imbalance of angiotensin II and NO in HF.33?35,37 In whites, according to this hypothesis, the imbalance in HF results mainly from a pronounced increase in angiotensin II, with modestly reduced NO. In African Americans with HF,37 NO may be reduced more and angiotensin II may be increased less than in whites.
Disturbed homeostasis of NO represents a new direction in understanding the pathophysiology of HF and is a new target for therapeutic intervention. Aside from regulating vascular tone and blood pressure, NO inhibits vascular smooth muscle cell proliferation, adhesion of leukocytes to the endothelial surface, and platelet aggregation.39 Disruption of the NO signaling pathway (ie, endothelial dysfunction) is related to increased production of reactive oxygen species (superoxide) within the vascular wall. In addition, reactive oxygen species deplete the bioavailability of NO by reacting directly with it to produce peroxynitrate: a potent oxidant that causes further oxidative injury to the endothelium. In addition to demonstrating reduced NO bioavailability, there is also evidence that African Americans have increased oxidative stress and attenuated responsiveness to the vasodilatory effects of NO.35,40 The prevalence in African Americans of genetic polymorphisms in glutathione S-transferase enzymes and endothelial NO synthase genes, which are responsible for cellular protection against reactive oxygen species and NO destruction, supports a plausible biologic hypothesis to explain these differences in NO homeostasis.41,42
Genetic Polymorphisms. The concept of race includes multiple facets and is a grouping based on a sociopolitical designation that is neither physiologic nor scientific in its construct. As such, it is an unacceptable proxy for genetics. This is especially the case for African Americans, who represent a markedly heterogeneous admixture of other races. Nevertheless, in small data sets, certain genetic markers have been identified to exist in a linkage disequilibrium (ie, higher than expected frequency) in African Americans. It is possible that genetic variations may explain some of the pathophysiologic differences in HF in African Americans.43?51 Remarkably, several of these at-risk genotypes are associated with exaggerated development of cardiovascular disease and diminished therapeutic responsiveness. Standard methodologies now permit identification of single-nucleotide polymorphisms (SNPs) that alter gene function and protein expression, resulting in either a loss or a gain of responsiveness. Prototypical SNPs relevant to HF in African Americans have been described. It has been observed that a dual-receptor polymorphism in the ?1- and a-adrenergic receptors, seen more commonly in African Americans with HF, is associated with an increased risk of HF and worse outcomes.43 This is postulated to occur as a result of an increased release of norepinephrine from the presynaptic cleft and increased sensitivity to norepinephrine. A mutation of the ?3-subunit of the Gi-type protein is also overexpressed in some African Americans, and it correlates with hypertension and renal disease as well as salt sensitivity.44,45 Other SNPs have been identified in African Americans and may be implicated in the development of left ventricular dysfunction and HF. Polymorphisms of certain genes involving ACE have been observed and might contribute to the decreased responsiveness of African Americans to ACE inhibitors.44,46,47 Other polymorphisms that affect natriuretic peptides, ?-receptors,48 and endothelin may also contribute to progressive left ventricular dysfunction in African Americans.49,50 Most recently, the Genetic Risk Assessment of Heart Failure (GRAPH) Substudy of the African American Heart Failure Trial (A-HeFT) has shown that a specific polymorphism of aldosterone synthase exists in a higher frequency in self-identified African Americans. This polymorphism at position 344 of the aldosterone synthase gene is associated with greater responsiveness to the combination of isosorbide dinitrate and hydralazine.51
These data and other preliminary findings from A-HeFT and other trials suggest that some of these genetic variants are distributed disproportionately across racial groups and that genetic screening may enable more precise targeting of patients for special management in the future. This is the promise of pharmacogenomics, but much more research is required before widespread clinical use can occur.1,2,22
Socioeconomic Factors and Quality of Care. Lower socioeconomic status and limited access to care may contribute to excess disease burden of HF in African Americans. Lower income is the usual measure of socioeconomic status, but socioeconomic status may also involve educational status, housing density, and employment status.52,53 Disparities in quality of care are a concern among health care professionals. Evidence of disparate health care is evident in the management of HF in African Americans. HF is associated with high rates of hospital readmission, especially in African Americans.53 Increased hospitalization but lower mortality rates for HF have been observed among African Americans compared with whites.54 Whereas these paradoxical results may support differences in the pathophysiology of HF in different ethnic groups, they may also relate to the quality of care following hospital discharge because of limited access to prescribed therapy or limited adequacy of follow-up care. The relationship between recurrence of hospital admission and income (as an indicator of socioeconomic status) was assessed in more than 40,000 patients with HF, and income was found to be a significant predictor of increased hospital readmission.52 In high-risk patients with HF involved in a disease management program, there were no observed differences in quality of care between African American and white participants at baseline or throughout the 90-day study, and similar results were seen in a study in the Veterans Health Administration in which the racial gap between whites and African Americans in health care utilization was small when access to health care was equal.55,56 These examples suggest that some differences in treatment outcomes indeed may be explained by disparities in health care utilization and may support a vigorous effort to eliminate health care disparities. However, as has been observed in other cardiovascular diseases, differences in clinical outcomes between African Americans and whites are not entirely explained by socioeconomic status because other factors may be involved.57,58 These other contributing factors include delay in seeking treatment for worsening symptoms, failure to recognize symptoms, limited disease awareness, inadequate access to health care services, noncompliance with follow-up appointments, and lack of adherence to recommended treatment. Strategies to improve health care standards should include attempts to provide culturally competent care, which encourages clear communication with patients, easier access to indicated medical therapies, and utilization of performance measures.1,2
Assessment of African Americans Presenting With HF
The latest major guidelines for HF management provide detailed recommendations on initial and follow-up assessments for patients with HF. The key recommendations from the ACC/AHA guidelines are summarized in Table S3. Although these apply generally to all patients with HF, we wish to focus here on assessments of particular concern for African American patients.
Initial Assessment. The initial evaluation of all patients presenting with HF or suspected HF includes establishing the diagnosis, assessing severity, and clarifying the etiology of HF. Patients may present with symptoms of HF along with other conditions, including hypertension, diabetes, dyslipidemia, or angina, and they may have associated cardiac structural or functional changes. Usually, HF can be readily diagnosed by a careful history and physical examination, which elicit a history of exercise intolerance and/or evidence of circulatory congestion or a combination of these. These tenets of good care are race-blind. For the African American patient presenting with HF, it is imperative to carefully assess blood pressure and to seek evidence for target organ involvement (eg, fundoscopic changes, third and fourth heart sounds, and abnormal peripheral pulses).
Following the diagnosis of HF in an African American, initial assessment should include standard diagnostic evaluations. Electrocardiography and chest radiography are routinely obtained and may provide evidence of prior myocardial infarction (MI), left ventricular hypertrophy, or cardiomegaly. Certain routine laboratory determinations are especially important in African Americans. If hypertension is present, these should include assessment of renal function and proteinuria. A search for secondary causes of hypertension is not inappropriate. The practitioner should not avoid such a search simply based on the higher prevalence of hypertension in African Americans (see details in appropriate guidelines for hypertension).5,32 In addition, blood sugar, serum lipids, and urinary microalbumin should be measured, given the increased prevalence of diabetes in African Americans.
Current guidelines recommend 2-dimensional echocardiography with Doppler flow studies as the best initial assessment of cardiac structure and function in patients presenting with HF or those suspected of having HF.1,2,22 This is imperative in African Americans given the prevalence of hypertension that may have already progressed to left ventricular hypertrophy. In addition, echocardiography provides information about cardiac dimensions and geometry and left ventricular function (LVEF and shortening fraction) and may provide evidence of valvular disease or myocardial ischemia. This initial assessment is essential to establishing a baseline for following changes in remodeling. Exercise testing may be of value in some patients, but that is not unique to African Americans.1,2,22
A guide to evaluating the cause of HF is shown in Table S4. Valvular heart disease can be effectively treated with surgery, and coronary artery disease might require intervention. Hypertension must be carefully assessed in African Americans along with identification of any target-organ involvement, and common comorbidities such as diabetes must be vigorously evaluated and treated.59 Dyslipidemia must not be overlooked because it is often less well treated in African Americans. Alcohol and substance abuse, both secondary causes of cardiomyopathy, are more common in African Americans.52 Human immunodeficiency virus (HIV) represents an HF etiology of emerging importance in African Americans. The incidence of HIV infection is higher among both African American men and women, most often from sexual transmission.60,61 HIV can affect the heart in a variety of ways, including endocarditis, pericarditis, cardiac malignancy, premature atherosclerosis, and dilated cardiomyopathy, and HF associated with HIV has an especially poor prognosis.62,63 The mechanism of HIV-related cardiomyopathy is probably multifactorial, because the virus can damage cardiac myocytes and the drugs used to treat HIV infection also may be cardiotoxic.64,65 These effects of HIV drugs appear to be mediated through disruption of endothelial function, which is potentially a greater problem in the cardiovascular dysfunction of African Americans with hypertension and/or HF, as noted above.65
Follow-Up Assessments. Many of the initial clinical assessments should be followed at regular intervals at a frequency dependent on HF severity and the patient?s clinical status. Special procedures (eg, echocardiography, exercise testing) and laboratory testing (B-type natriuretic peptide) should be repeated judiciously based on clinical status. However, without a change in clinical status, these procedures are neither productive nor indicated.
Functional capacity should be assessed at each visit using NYHA criteria. Exercise testing may be useful if a change in a patient?s symptoms or a discrepancy between physical findings and symptoms emerges. Assessment of volume status is particularly important in African Americans, who are more salt-sensitive and require careful volume status control for both hypertension and HF. Similarly, risk factors such as lipids and blood sugar, along with blood pressure and renal function, should be carefully and regularly monitored.
Treatment of HF in African Americans
The reader should refer to the major guidelines for full treatment recommendations of HF in the general population.1,2,22 This consensus statement follows the general organization of those guidelines while focusing on treatment recommendations of special importance to African American patients at risk for HF and to those in whom HF has already developed (Figure S2).
Management of Patients at Stage A. Current HF guidelines define patients in stage A as those at increased risk for HF but without current symptoms of HF and without evidence of structural heart disease. Stage A represents a critically important group because many of the risk factors can be effectively controlled and may prevent development of cardiac disease and ultimately HF. The risk factors of prime concern are hypertension, atherosclerotic disease, diabetes, obesity, dyslipidemia, substance abuse, and family history of cardiomyopathy. Almost all of these are amenable to treatment with lifestyle modifications and/or drugs. Hence, recognition and control of risk factors is critical to attempts at reducing the excess burden of heart disease and HF in African Americans. The key recommendations from the ACC/AHA guidelines for treatment of patients in stage A are summarized in Table S5.
Control of Risk Factors. Of these several risk factors, the most important to consider for African American patients is hypertension detection and blood pressure control. Because African Americans have a higher prevalence of hypertension leading to detrimental cardiovascular and renal outcomes, there is a specific need for recommendations in this population. Adherence to both general treatment recommendations from Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) and especially to those of the International Society on Hypertension in Blacks (Figure S4) is strongly advised in the management of hypertension.5,32 Lifestyle modifications for the prevention and management of hypertension, including weight reduction, adoption of the Dietary Approaches to Stop Hypertension (DASH) eating plan,66 restriction of dietary sodium, initiation of physical activity, and moderation of alcohol consumption, should be employed. Pharmacologic therapy should be initiated with thiazide diuretics as first-line therapy or combination agents that include thiazide diuretics if >10 mm Hg of systolic blood pressure lowering is indicated. Ultimately, a combination of several antihypertensive agents may be necessary for optimal control of blood pressure to a level <140/90 mm Hg, especially when concomitant diabetes is present. We consider African Americans with hypertension a higher-risk cohort of hypertensives and, like those with diabetes, blood pressure should be lowered to a target level of <130/80 mm Hg.5,32
Diabetes is the next most important risk factor in African Americans. The increased prevalence of diabetes in African Americans increases the risk of HF developing, especially in women.1,2 Current diabetes treatment guidelines urge precise control of hyperglycemia. It has been suggested that a reduction in hemoglobin A1c to <7% and perhaps even to <6.5% according to certain guidelines is the preferred goal, but recent data have called into question the extent to which hemoglobin A1c is reduced and the manner in which it is reduced.67,68 In addition, ACE inhibitors and angiotensin receptor blockers (ARBs) reduce the risk of renal disease and cardiovascular mortality in type II diabetics with hypertension. Even though these data were not acquired in populations representative of African Americans, we see no reason to withhold the renoprotective and cardioprotective effects of ACE inhibitors and ARBs from African American patients with diabetes.
Among other risk factors of particular concern in African Americans is dyslipidemia, which is often poorly controlled.52,59 A recent study observed that, although the prevalence of dyslipidemia varied little across ethnic groups, fewer African Americans are receiving lipid-lowering treatment. Furthermore, of African Americans treated, significantly fewer had properly controlled dyslipidemia.59 Effective treatment of hyperlipidemia may reduce the risk of HF, and it is recommended that dyslipidemia be aggressively treated to reduce lipid levels according to current guidelines.69 These latest guidelines recommend reduction of low-density lipoprotein cholesterol to <70 mg/dL in very high?risk patients or at least to =100 mg/dL in other patients. Patients should be strongly advised against smoking and against the use of other agents that can cause myocardial injury, such as excess alcohol and illicit drugs, which may be problematic in some African Americans.70,71 Finally, patients should be strongly advised to practice safe sex.
Specific Drugs Recommended for Stage A Disease in African Americans. Thiazide diuretics represent the cornerstone of hypertension therapy in all patients, especially African Americans. As adjunctive therapy, ACE inhibitors and ARBs are recommended as drugs for use in treating hypertension, with or without diabetes, because they have been shown to prevent HF in both situations and to stop progression of renal disease in diabetics. Although African Americans may be less responsive to ACE inhibitors and ARBs in terms of blood pressure control, they do respond, especially when these agents are used at higher doses and in conjunction with diuretics32; and their use in stage A disease is strongly recommended. Furthermore, there is more conclusive evidence that African Americans respond well to these same agents in the setting of established renal disease.32,72,73
Aggressive management of dyslipidemia usually involves the addition of drugs, especially statins. Patients with known atherosclerotic events such as strokes but without evidence of cardiac structural change are at increased risk for HF and should receive the usual recommended care for these conditions, especially aspirin.1,2,69,74 There is no evidence that African Americans respond less well to aspirin or statins.74,75
Detection of Cardiac Structural Abnormalities. The increased risk of HF in stage A patients suggests that early monitoring is important to detect any cardiac structural changes. Current HF guidelines do not recommend routine echocardiography to assess cardiac structure and function in stage A due to cost-effectiveness concerns; however, they do recommend its use in patients at particularly high risk.1,2 These patients include those with a family history of cardiomyopathy or those who are suspected of continued alcohol or substance abuse. Because of their increased burden of HF, it is reasonable to consider African Americans in this group of unusually high-risk stage A patients. Although not recommended by current guidelines, we believe consideration should be given to a baseline assessment of left ventricular structure and function by echocardiography in African Americans with stage A HF, particularly in those with poorly controlled hypertension, resting electrocardiographic abnormalities, diabetes, or a history of substantial substance abuse. We recognize that this recommendation is in variance with the current guidelines but also that it is consistent with the higher-risk profile of this targeted population. The use of echocardiography in stage A HF must be judged on an individual basis in terms of the potential costs and benefits.
Management of Patients at Stage B. Patients in stage B, according to current HF guidelines, are those with evidence of structural heart disease but without current or prior symptoms of HF. The number of African Americans with stage B HF in the absence of a prior history of MI (ie, hypertension and left ventricular hypertrophy/dysfunction) is uncertain. The specific cardiac structural changes (ie, left ventricular remodeling [left ventricular hypertrophy, reduced LVEF, left ventricular dilatation]) include those caused by MI, hypertension, cardiomyopathies, and valvular heart disease. The prevalence of asymptomatic left ventricular dysfunction (ASLVD) has been estimated at 8% to 16% of the population, increasing progressively with age,22 but is unknown for African Americans and other minorities. Although the mortality risk of patients with ASLVD is considerably less than that of patients with HF symptoms, mortality and hospitalizations for HF are, nevertheless, several-fold higher in these patients when compared with the normal population.11,22 It has been demonstrated that ASLVD in African Americans progresses to symptomatic HF much more aggressively.11,76 We would suggest that when ASLVD is identified in African Americans, vigorous use of ACE inhibitor/ARB therapy be instituted. The key recommendations from the ACC/AHA guidelines for treatment of patients in stage B are summarized in Table S6.
Therapy. The goal of treatment in these patients is prevention of symptomatic HF and cardiovascular events by forestalling further cardiac damage and halting or reversing the remodeling process. Stage A recommendations should also be followed for stage B patients. In addition, specific drugs are recommended for certain patients in stage B, especially ACE inhibitors and ?-blockers for all patients with a recent or remote MI, regardless of LVEF, and for all those with asymptomatic reduction of LVEF, regardless of etiology. Despite some evidence that African Americans respond less well to ACE inhibitors, one cannot conclude that African Americans do not respond at all to these agents, and indeed, in the SOLVD prevention trial, African Americans did demonstrate responsiveness to enalapril. One of the markers of quality care is the use of ?-blockers following an MI. There is no evidence that the ?-blockers approved for use in HF in the United States (carvedilol and long-acting metoprolol succinate) are less effective in African Americans; these are the ?-blockers of choice for use in stage B.1,2 Management of coronary artery disease requiring intervention or valvular heart disease is not unique for African Americans; therefore, the major guidelines are applicable.1,2,22 However, to emphasize, available data suggest that cardiac catheterization and coronary revascularization procedures are not applied equitably, and vigorous efforts should be employed to correct these disparate health care experiences.77
Management of Patients at Stage C. Stage C is defined by current HF guidelines as evidence of structural heart disease and current or prior symptoms of HF. The symptoms include exercise intolerance, dyspnea, and evidence of circulatory congestion (rales, elevated jugular venous pressure, and edema). Treatment at this stage includes all recommendations for stages A and B as well as general measures and specific drug therapy. The goals of therapy are to improve symptoms, halt or reverse remodeling, and reduce the risks of hospitalization and mortality. The key recommendations from the ACC/AHA guidelines for treatment of patients with reduced LVEF at stage C are summarized in Table S7.
General Measures. A salt-restricted diet should be maintained, weight should be monitored daily, and patients should be encouraged to be physically active. The importance of salt restriction in salt-sensitive African Americans is again emphasized. A key to successful treatment of symptomatic HF is the relationship between patients and health care providers. However, this relationship may not be easily established between African American patients and their care providers, as previously noted. Frequent contact between the patient and the patient?s family and care providers is critical for providing patient education and for monitoring and early detection of subtle changes. There is ample evidence that disease management programs for HF that incorporate these features are successful in reducing morbidity from HF.78?80 The major HF guidelines should be consulted for a detailed discussion of general measures for stage C patients.1,2,22
Specific Drug Therapy: Responsiveness. Based largely on the hypertension experience and the known salt sensitivity of African Americans, there is ample evidence that African Americans respond well to diuretics.32,72,81,82 Limited available data suggest no difference in responsiveness or toxicity to digitalis in African Americans when compared with whites with HF.82,83 The different responsiveness of African Americans to ACE inhibitors has been noted previously. A reanalysis of the SOLVD trial, in which white and African American cohorts were matched to adjust for other potential predictors of clinical outcomes, showed no differences in mortality between African Americans and whites treated with enalapril. However, the risk of hospitalization for HF in whites was reduced by 44% (P<.001) but was not affected in African Americans (P=.74), indicating a significant racial interaction.12 It was also noted that systolic blood pressure in the enalapril-treated patients was significantly reduced at 1 year from baseline in whites but not in African Americans. The experience with ?-blockers in HF in African Americans has also been variable. Retrospective analyses of the US Carvedilol Heart Failure Trials program and of the Carvedilol Prospective Randomized Cumulative Survival (COPERNICUS) trial in severe HF showed similar beneficial effects of carvedilol in reducing the risk of mortality and the rate of worsening HF in African Americans and whites.15,25 Similarly, metoprolol succinate produced similar beneficial effects on mortality and morbidity from HF in African Americans and whites, but these results cannot be extended to other metoprolol preparations that were found to be less effective than carvedilol in the Carvedilol or Metoprolol European Trial (COMET).16,84 However, in the ?-Blocker Evaluation of Survival Trial (BEST), treatment with another ?-blocker, bucindolol, was not associated with any survival benefit in the overall population, a finding that was driven by African Americans who fared significantly worse than whites (in whom a modestly beneficial effect was observed).14 An important corollary of this ?-blocker experience in HF is that one cannot assume a consistent class effect. The experience with other agents for HF, such as ARBs and spironolactone, is too sparse in African Americans to permit any conclusions about their safety and efficacy in this special population,1,2,22 but there is no reason to assume a lack of efficacy, and these agents should be used as per published guideline statements. In addition to differences in treatment outcomes with pharmacologic agents, an increased incidence of angioedema has been observed in African Americans when compared with whites taking ACE inhibitors.85,86 For African American patients who are intolerant to ACE inhibitors, an ARB is appropriate. It is important to recall that virtually all of the information regarding responsiveness in African Americans has come from retrospective analysis of clinical trials in which racial differences were not prespecified end points. Therefore, groups that were compared may not have been well matched for other characteristics, which may affect safety and efficacy, and full-dose ranges of drugs being tested were not explored. Furthermore, some retrospective comparisons did not include adequate placebo controls, but compared racial responses between active drugs. For all these reasons, one cannot reach any firm conclusions, and drugs recommended for routine use (see below) should not be abandoned in African Americans despite any signals from retrospective analyses suggesting lesser efficacy. Drugs for Routine Use. The major HF guidelines for stage C patients recommend diuretics, ACE inhibitors, and ?-blockers for most patients. Diuretics should be given to all patients with evidence of volume overload and are needed in a majority of these patients to prevent recurrence of fluid retention.1,2,22 Most African Americans will require diuretics because of salt sensitivity and the frequent coexistence of hypertension. Thiazide diuretics are preferred in patients with hypertension; however, in the presence of HF, loop diuretics are recommended. The primary effect of diuretics in HF is to increase urinary sodium excretion and decrease circulatory congestion. Although these actions often lead to prompt symptomatic improvement, there is no conclusive evidence that diuretics produce any beneficial effects on the risk of mortality and morbidity from HF.1,2,22 Regardless of how well patients may respond to diuretics, ACE inhibitors should be given to all stage C patients with reduced LVEF who tolerate them, because there is strong evidence that they reduce the risk of mortality and morbidity in HF.1,2,11,22 ARBs approved for use in HF (currently candesartan and valsartan) are considered acceptable alternatives to ACE inhibitors in patients who cannot tolerate an ACE inhibitor.18,19 Most patients who have experienced angioedema with an ACE inhibitor will tolerate an ARB, but these should be initiated with caution. There is evidence that some ARBs may produce additional beneficial effects when given together with an ACE inhibitor; however, the side effect profiles may be exaggerated when these drugs are given together.87,88 Experience with the administration of both ACE inhibitors and ARBs is limited in African Americans.18,89 There is a very large and convincing body of evidence showing that ?-blockers significantly reduce the risk of mortality and hospitalization in HF in patients with reduced LVEF; therefore, they are recommended for all stage C patients without contraindications to their use. These agents should be given to patients who are stable and not volume overloaded, usually in combination with an ACE inhibitor and diuretics. Because not all ?-blockers have been proven effective in HF, it is strongly suggested that only those agents approved for use in HF, which are currently carvedilol and metoprolol succinate in the United States and bisoprolol in many other countries, be given.13?16,25 Both carvedilol and metoprolol succinate have been shown to be safe and effective in whites and African Americans with HF, and similar outcomes have been demonstrated for African Americans and whites who received carvedilol.13,16,25?-Blockers should be initiated at low doses and titrated gradually to minimize the risk of worsening HF.1,2,22 An aldosterone antagonist such as spironolactone can be added to manage select patients with moderately severe to severe HF symptoms and reduced LVEF despite treatment with diuretics, ACE inhibitors, and ?-blockers, as long as careful monitoring of renal function and serum potassium can be performed.1,2,17,22 Unfortunately, there are no data regarding the use of aldosterone antagonists in African Americans, and this recommendation is an extrapolation of outcomes from major clinical trials that did not include a significant number of African Americans. Digitalis is no longer recommended for routine use in all patients with HF who are in sinus rhythm because there is no convincing evidence that it produces any long-term reduction of mortality. Digitalis is generally reserved for control of atrial fibrillation and as an adjunct to patients who remain symptomatic, despite optimal treatment with the other agents described above.1,2,22,90 There are no race-specific data regarding the use of digitalis, but broad clinical experience would suggest no reason for concern. Drugs for Selected Patients: African Americans. The major HF guidelines acknowledge the existence of evidence supporting the use of certain drugs in selected cohorts of patients with HF. Among these are the combination of isosorbide dinitrate and hydralazine.1,2,22 Nitrates were among the first vasodilators evaluated for long-term use in HF. It has been shown that isosorbide dinitrate alone could effectively lower ventricular filling pressures with only modest effects on cardiac output, whereas hydralazine alone could significantly raise cardiac output and lower systemic vascular resistance with only modest effects on ventricular filling pressures.91,92 Because of the potentially synergistic hemodynamic effects of isosorbide dinitrate and hydralazine, these agents were given in combination and produced a highly favorable acute and sustained hemodynamic response in patients with HF. It was also subsequently shown that hydralazine could prevent development of tolerance to isosorbide dinitrate.93?95 Although isosorbide dinitrate alone improves symptoms of HF and exercise tolerance in patients with HF, it has never been shown to conclusively produce significant beneficial effects on mortality or morbidity in clinical trials.96,97 Hydralazine alone was likewise no better than placebo in large clinical trials in HF.98,99 The combination of isosorbide dinitrate and hydralazine was tested in the Vasodilator Heart Failure Trials (V-HeFT).9,10 In V-HeFT I, the mortality rate for the total cohort (African Americans and whites) was significantly lower in the isosorbide dinitrate/hydralazine group compared with patients treated with prazosin or with placebo added to digitalis and diuretics.9 In V-HeFT II, enalapril was compared with isosorbide dinitrate/hydralazine and, although isosorbide dinitrate/hydralazine was statistically inferior to enalapril in effect on mortality, patients taking isosorbide dinitrate/hydralazine had a similar mortality experience as those taking isosorbide dinitrate/hydralazine in V-HeFT I.10 As previously noted, a reanalysis of V-HeFT I showed that isosorbide dinitrate/hydralazine significantly reduced mortality in African American patients but not in white patients. On the other hand, in V-HeFT II, the annual mortality rate for African American patients receiving isosorbide dinitrate/hydralazine was 12.9% compared with 12.8% for African Americans receiving enalapril.100 In contrast to the results in white patients, who had a survival benefit from enalapril, this difference in African Americans was not statistically significant. However, isosorbide dinitrate/hydralazine improved quality of life scores more than enalapril in African American patients. Because of differences in prevalence, etiology, and outcomes of HF in African Americans along with data from the V-HeFT experience, the African American Heart Failure Trial (A-HeFT) was designed as a prospective trial to test the responsiveness of African Americans with HF to combined vasodilator therapy. A-HeFT was a randomized, placebo-controlled, double-blind study of fixed-dose isosorbide dinitrate/hydralazine101 added to standard recommended treatment for HF, including ACE inhibitors and ?-blockers. Patients with left ventricular dysfunction (LVEF =35% or left ventricular internal diameter in diastole >2.9 cm/m2 body surface area and LVEF <45%) were included. The primary outcome of this trial was a composite score weighing death from any cause, time to first hospitalization for HF, and quality of life. A total of 1050 self-identified African American patients with NYHA class III or IV HF were randomized.98,102 The study was terminated early because of a significant 43% reduction in mortality rate observed in the fixed-dose isosorbide dinitrate/hydralazine group compared with the placebo group (6.2% vs 10.2%, respectively; P=.01). Significant benefits were also evident in the form of reduced hospitalizations and improved quality of life (Table S8).103 It should be noted that this was a well-treated group of HF patients, with 93% taking ACE inhibitors or ARBs, 87% taking ?-blockers, and 94% receiving diuretics. Furthermore, the A-HeFT population included 40% women, as well as patients with a spectrum of left ventricular systolic dysfunction. There were no differences in clinical outcomes by sex, age, LVEF, or baseline medications.104?106
The magnitude of the benefits observed with isosorbide dinitrate/hydralazine in A-HeFT are notable and support the existing data that suggest a difference in the mechanism of HF progression in African Americans. Importantly, A-HeFT confirms the definitive need for adequate representation of special populations in clinical trials. The results of A-HeFT confirm the hypotheses generated by the reanalyses of V-HeFT and provide convincing evidence that isosorbide dinitrate/hydralazine should be used routinely with diuretics, ACE inhibitors, and ?-blockers in all African Americans with cardiac dysfunction and symptomatic HF.1,2,22,103
The results of the Extended Access African American Heart Failure Trial also have been released. These findings demonstrate that in a cohort of 198 original A-HeFT patients exposed to open-label extended access to fixed-dose isosorbide dinitrate/hydralazine, tolerability of the drug was good, functional capacity continued to improve, and annualized mortality rate remained quite low at 6%. These findings replicate outcomes noted in the primary trial.107
A plausible, but as of yet still unproven, mechanism of action of isosorbide dinitrate/hydralazine is thought to derive from the NO donor function of isosorbide dinitrate plus the antioxidant activity of hydralazine, which enhances the efficacy of nitrates. Further mechanistic studies will be necessary, but the clinical efficacy in African Americans is now well demonstrated.
Other Interventions for Patients at Stage C. Patients with HF commonly have serious arrhythmias, which may aggravate HF and/or be life-threatening. Atrial fibrillation is a common occurrence and can aggravate HF. However, for reasons not yet clear, atrial fibrillation occurs less commonly in African Americans with HF.108 Ventricular arrhythmias are potentially life-threatening and often become less prominent with effective treatment and overall improvement of HF. In patients at high risk for sudden death or in those who have experienced a cardiac arrest, an implantable cardiac defibrillator with or without cardiac resynchronization therapy is recommended.1,2,22 See Table S7 for specific device therapy recommendations.
There is no convincing evidence that the indications for, responsiveness to, and outcome of these other interventions, including device therapy, are any different in African Americans with HF.1,2,22 Of greater importance is the access African Americans have to these types of interventions. A recent review of Medicare and Medicaid experience revealed that African Americans were significantly less likely than whites to receive an implantable cardiac defibrillator for the prevention of sudden death in the presence of ischemic cardiomyopathy.109 After multivariate analysis to adjust for other variables, race remained a significant predictor; African Americans were 31% less likely to receive the device than other patients.
A suggested treatment algorithm for African Americans with stage C HF is shown in Figure S5.
Management of Patients at Stage D. Patients in stage D are defined by the major HF guidelines as those with refractory HF requiring specialized interventions. These patients are typically symptomatic at rest despite maximally tolerated medical/device therapy, and they require frequent hospitalization. Therapy includes all the recommendations described above for stages A, B, and C. Specific measures depend on the decision about the appropriate level of care, which is usually a choice between compassionate end-of-life measures or, in selected patients, extraordinary measures such as cardiac transplant, chronic administration of inotropic agents, permanent mechanical support, or experimental interventions. The key recommendations from the ACC/AHA guidelines for treatment of patients at stage D are summarized in Table S9.
Available evidence suggests that the indications for, responsiveness to, and outcome of these interventions are not any different in African Americans with stage D HF.1,2,22,110 There is, however, concern about access to appropriate care for patients with severe end-stage HF. Prior experience indicates variability in access to care, quality of care, and application of indicated procedures between African Americans and other patients hospitalized with severe cardiovascular disease.57,111,112 Earlier experiences suggested that deserving African Americans may be less likely than their white counterparts to receive a cardiac transplant. However, more recent experience shows no disproportionate use of or difference in outcomes of cardiac transplantation in African Americans when compared with whites.113,114
Implementation of Guidelines
Limitations of Guidelines. The beneficial results of clinical trials in HF have not been consistently observed in the community setting, especially in populations underrepresented in clinical trials (specifically African Americans), and concern has been expressed that guideline recommendations are not being readily transferred to the community setting.1,2,4,115 Patients with HF and their care providers differ significantly from their counterparts in clinical trials in ways that could impact management and outcomes. Despite these differences, patients in the community setting should be expected to respond as well as do those in clinical trials to treatments recommended by current HF guidelines.116 Data comparing African Americans with HF in the community setting with those in clinical trials of HF are almost nonexistent. With the exception of having adequate access to medications and follow-up (which clinical trials provide), there is no reason to believe that African Americans with HF in the community setting will not respond equally as well to treatment interventions as their counterparts have in clinical trials in HF.117,118
Recommendations for Implementation of Guidelines. The major HF guidelines include a detailed discussion of ways to enhance their implementation, which we strongly endorse. The special importance of building trust and collaboration between African American patients with HF and their care providers has been noted.1,2,22,115,119,120 The techniques recommended include increasing physician awareness through more intensive academic detailing as well as educational and community outreach programs. Multidisciplinary disease management programs that involve patient education and active participation with the health care team can reduce the risks of hospitalization.1,2,22
Performance Measures. In order to optimize the implementation of practice guidelines and impact quality of care, performance standards are required.1,2,22,121 The items incorporated in performance measures are believed to have the highest likelihood of improving outcomes and can be used within health maintenance organizations and managed care organizations to compare providers and their services. With regard to HF, separate performance-measurement standards have been developed for inpatients and outpatients, and these measures should be applied irrespective of race (Table S10).
Future Directions
Health Care Delivery Models. There is hope that specialized HF centers and disease management strategies represent an idealized mode of care for patients with HF, but questions about the long-term success and costs of these programs need to be more rigorously examined.78,80,122 Available data suggest that African Americans respond equally well to disease management programs as do all others, and this may be a unique tool to improve outcomes in this population. Finally, new effective approaches targeting the elimination of disparate health care must be identified.123
Potential Role of Pharmacogenomics. It is noteworthy that the analyses of African Americans involved in clinical trials of HF have yielded considerable insight into at-risk genotypes associated with the development and progression of left ventricular dysfunction and HF. Cardiovascular medicine is on the cusp of personalized care, which needs to be personalized not by race, but rather by precise physiologic and/or genetic risk factors for disease and/or determinants of responsiveness to medical treatment regimens. More pharmacogenomic research is needed to help identify patients at risk for HF and to aid in selection of the most appropriate individualized treatments. Indeed, the Genetic Risk Assessment in Heart Failure (GRAHF) substudy of the A-HeFT experience is being conducted to test specific at-risk alleles (eg, ACE, a- and ?-adrenergic receptors, aldosterone synthase, and eNOS), and to correlate their existence with events and therapeutic responses seen in A-HeFT. Initial results of GRAHF have recently been reported and showed that differences in eNOS genotype do influence blood pressure and left ventricular remodeling in African Americans with HF, although their relationship to treatment outcomes was not clearly established.124 The clinical implications of correlating phenotypic characteristics and genetic polymorphisms, which could be substantial, have yet to be determined and require further study.
Specific Mechanistic Research Needs. Exactly how the pathophysiology of HF differs between African Americans and the white population still remains to be understood. This includes clarifying why hypertension leads to systolic ventricular dysfunction; how endothelial function may vary in African Americans; why cardiovascular disease progresses so rapidly; and the importance of novel mechanisms such as reduced NO bioavailability. Importantly, are there proven strategies to overcome disparate health care? Finally, how do we supplant race as a descriptor of disease and responsiveness to therapy with other more physiologic markers? These are important questions that ongoing and anticipated research initiatives will need to address.
Conclusions
African Americans bear a greater burden from HF than whites do, which may result from a different prevalence of risk factors, different pathophysiology/disease progression, and disparate health care. Hypertension is an especially important risk factor requiring vigorous screening and early intervention with effective antihypertensive therapy as a standard of care for African Americans at risk for cardiovascular disease. Current major guidelines for the management of symptomatic HF with reduced ejection fraction recommend diuretics, ACE inhibitors, and ?-blockers for routine use in all appropriate patients. The most recent update of the ACC/AHA guidelines has clarified and strengthened that recommendation based on the availability of stronger evidence, especially from A-HeFT1,2: ?The combination of a regimen of isosorbide dinitrate and hydralazine to a standard medical regimen for HF, including ACE inhibitors and ?-blockers, is recommended in order to improve outcomes for self-described African American patients with NYHA functional class III or IV HF. Others may benefit similarly, but this has not yet been tested.? There are no data to suggest a differential response to indicated device therapies or to advanced interventions such as heart transplant or other ventricular replacement strategies. Disease management programs may be especially beneficial for the higher-risk African American patient with HF. Ultimately, disparate health care must be removed from the clinical domain. Broad-based application of guideline-directed, evidence-based therapy and a race-blind embrace of performance measures represent readily accessible strategies to effectively address cardiovascular disease disparities in African Americans.
Disclosures: Preparation of this consensus statement was supported by an unrestricted educational grant from NitroMed, Inc., Lexington, MA, to the Association of Black Cardiologists, Inc., who provided administrative support to the writing group. John Romankiewicz, PharmD, of Scientific Therapeutics Information, Inc provided editorial assistance, supported by NitroMed, Inc. The content reflects the independent writing, editing, and deliberations of the writing group, all of whom reviewed and approved the consensus statement. There was no review of this statement by NitroMed, Inc., and it is endorsed by the Association of Black Cardiologists, Inc.
The coauthors report the following relationships: Joseph A. Franciosa, MD, is a paid consultant to NitroMed and other pharmaceutical companies who market products for use in heart failure. Peter Carson, MD, was a consultant to NitroMed from 2004 to 2007. Charles L. Curry, MD, was an investigator in A-HeFT and a paid speaker for NitroMed (the sponsor of the trial). Keith C. Ferdinand, MD, is a consultant to NitroMed, Novartis, AstraZeneca, Merck, Roche, and Daiichi Sankyo. Barry Greenberg, MD, has received grants/research support/contract from Biogen Idec, Merck, Celladon, Corventis, Cytokinetics, and Scios; he is a consultant or member of a speakers? bureau for GlaxoSmithKline, Merck & Co., Inc, Novartis, CV Therapeutics, Sanofi Aventis, Corthera, and Cytokinetics; and he has served on the editorial boards of Congestive Heart Failure and Journal of the American College of Cardiology. Barry M. Massie, MD, serves as a consultant to Merck, Novartis, Sanofi, Bristol-Myers Squibb, GlaxoSmithKline, Nile Therapeutics, Cytokinetics, Corthera, and Takeda; he serves as a speaker for Merck; he has received research grants from Bristol-Myers Squibb and Sanofi (to VA nonprofit); and he has been a consultant for NitroMed, AstraZeneca, and Scios-Johnson & Johnson. Judith Mitchell, MD, is a former member of a speakers? bureau for NitroMed; she is a current member of speakers? bureaus for GlaxoSmithKline and Astellas; and she is a member of the women?s advisory board of Medtronic. Elizabeth Olifi, MD, served on the advisory board of NitroMed; she served on the steering committee for A-HeFT; and she has served on the board of directors, and is past president, of the Association of Black Cardiologists. Ileana L. Pi?a, MD, has received grants/research support from the National Institutes of Health; she is a consultant to the US Food and Drug Administration and Sanofi Aventis; and she serves on speakers? bureaus for AstraZeneca, Merck, Solvay, and Novartis. Malcolm P. Taylor, MD, was a member of the A-HeFT steering committee. Paul L. Underwood, MD, is an employee of Boston Scientific Corporation; has served on speakers? bureaus for Eli Lilly Corporation, Esai, Forest, GlaxoSmithKline, NitroMed, Novartis, and Pfizer; and has received research grant support from Anthera, Atherogenics, Aryx, Bayer Corporation, Bristol-Myers Squibb, GlaxoSmithKline, Novartis, and Pfizer. Clyde W. Yancy, MD, was formerly a consultant for ARCADiscovery, Medtronic, Inc, and GlaxoSmithKline; he received research support from SCIOS, Inc, NitroMed, and GlaxoSmithKline/Medtronic; he serves on the data safety and monitoring boards for Texas Medical Center, Mayo Clinic, and Thoratec, Inc; he is associate editor of American Journal of Cardiology; he serves on the editorial boards of American Heart Journal, Cardiology Quarterly, Circulation, Circulation-Heart Failure, Circulation-Quality and Outcomes, Congestive Heart Failure, and the heart.org; he was a member of the US Food and Drug Administration circulatory devices panel, which he chaired from 2007 to 2008 (he is currently an ad hoc member); and he is a member of the National Institutes of Health study section, Clinical and Integrative Cardiovascular Science.
Appendix
Writing Group:
Joseph A. Franciosa, MD, Mt Sinai School of Medicine, New York, NY, and SUNY Downstate Medical Center, Brooklyn, NY; Kirkwood F. Adams, Jr, MD, University of North Carolina, Chapel Hill, NC; Peter Carson, MD, Veterans Affairs Medical Center, Washington, DC; Charles L. Curry, MD, Howard University, Washington, DC; Keith C. Ferdinand, MD, Division of Cardiology, Emory University, Atlanta, GA; Barry Greenberg, MD, University of California at San Diego Medical Center, San Diego, CA; Barry M. Massie, MD, University of California, and VA Medical Center, San Francisco, CA; Judith Mitchell, MD, SUNY Downstate Medical Center, Brooklyn, NY; Elizabeth Ofili, MD, Morehouse School of Medicine, Atlanta, GA; Ileana L. Pi?a, MD, University Hospitals of Cleveland, Cleveland, OH; Elijah Saunders, MD, University of Maryland School of Medicine, Baltimore, MD; Malcolm P. Taylor, MD, University of Mississippi, St. Dominic Hospital, Jackson, MS; Paul L. Underwood, MD, North Phoenix Heart Center, Phoenix, AZ; Clyde W. Yancy, MD, Baylor Heart and Vascular Institute, Baylor University Medical Center, Dallas, TX.

Geriatrics: Managing Congestive Heart Failure
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Managing Congestive Heart Failure (CHF)
Hone your skills at diagnosing and treating CHF in the elderly.
Congestive heart failure (CHF) in the elderly is a quiet, complicated problem. The condition, which can stem from a range of structural or functional cardiac disorders, is compounded by the effects of old age. CHF often goes undiagnosed, particularly in mild cases, and yet even with the best therapy it is associated with an annual mortality of 10%. In fact, heart failure is the most common reason for hospital admission in the group older than 65, with 900,000 admissions a year in the US alone.
Gender, Ethnic Divide
Older women tend to have diastolic dysfunction more frequently than older men because the 50+ year-old female heart tolerates a heavy afterload better than the male and is less prone to decompensation at that early age. Men typically develop CAD at an earlier age. Note that hypertension is the number one cause of CHF in the older female.
Some ethnic differences also exist. Heart failure is found more commonly in African-Americans primarily due to the high prevalence of hypertension, with the highest prevalence of CHF found in older black females.
Systolic v. Diastolic
Heart failure is categorized as systolic if the left ventricular ejection fraction (LVEF) is between 35?45% or diastolic if LVEF is normal. In the group older than 65, heart failure is typically associated with preserved LV systolic function, whereas those younger than 65 tend to have systolic LV dysfunction because of coronary artery disease and nonischemic dilated cardiomyopathy. Diastolic heart failure is described echocardiographically as a small stiff ventricle with a thickened wall. The small ventricle does not have enough blood for a normal cardiac output. Fifty percent of heart failure cases are diastolic in nature. Clinically, the signs and symptoms of diastolic and systolic heart failure are practically identical, even though jugular venous distention and an S3 heart sound may be more common in systolic failure.
Causes & Symptoms
Remember that heart failure is not a primary illness, but is the end result of other ailments. The most common causes are coronary artery disease, hypertension, cardiomyopathy and valvular heart disease. The history, if obtainable, has critical value. The clinical signs and symptoms of heart failure are common: dyspnea on exertion is the most common complaint and can worsen to dyspnea at rest. The prevalent symptoms are common to both the younger and older population afflicted with CHF. However, the elderly may complain only of fatigue, weakness, dizziness, or altered mentation. Dyspnea may be so severe that it is present with eating. In about 14% of patients, JVD may be absent. Systemic congestion may lead to varicosities that can subsequently seep fluid with resulting superficial thrombophlebitis.
The presentation of a patient dyspnea carries an extensive differential diagnosis from heart failure, MI, pulmonary embolism to pneumonia, sepsis, bronchitis, asthma, chronic obstructive pulmonary disease. Heart failure, right sided, can be a complication of long-standing COPD. Infections can precipitate the susceptible elderly to an MI and to congestion or vice versa. Iatrogenic heart failure is an entity to avoid and usually results form well-meaning but overzealous hydration of the frail elderly who may present in various hypovolemic states. Other co-morbidities may confound the clinical picture. The elderly with underlying lung cancer or pulmonary metastases may present with a clinical picture of congestive heart failure. Non-compliance, voluntary or otherwise due to dementia, polypharmacy, or abuse may contribute to the development of CHF. That is one critical reason for a clear line of communication to exist between the primary care physician and the various specialists rendering care to the elderly with various co-morbidities.
Diagnosis & Treatment
Echocardiography remains the mainstay of diagnosis and displays the LVEF, which has diagnostic and prognostic value. Two-dimensional echocardiography (2DE) and Doppler echocardiography can show LV function (systolic and diastolic), cardiac output, PA pressures, ventricular filling pressures and valvular status. Real-time echocardiography (3DE) provides even more details about the volume status of the left ventricle. The elderly with mild or severe valvular disease can be appropriately categorized and treated.
The EP has a large armamentarium as well as access to a multidisciplinary team consisting of the internist, cardiologist (non-invasive and invasive) and cardiothoracic surgeon. A useful supplement to the diagnosis of CHF is the measurement of brain natriuretic peptide (BNP), which can also gear the EP during the evaluation of dyspnea without a known history of CHF. Note that Pro-BNP level tends to be higher in older patients, females and patients with renal insufficiency (with or without CHF). The elevated BNP may be due to volume expansion from renal failure or left ventricular hypertrophy. Thus, a low BNP value is more useful to exclude CHF in the renally impaired patient than an elevated level. The BNP level in obese patients is usually lower than the non-obese patient. The BNP value does not differentiate between systolic and diastolic heart failure. Patients with an elevated BNP level with stable or unstable angina have been found to have a higher mortality than those with a lower level. Patients with more than one cause for dyspnea may still have an elevated BNP (CHF and pneumonia, for example).
Airway management is a critical first step as the elderly with HF can promptly fatigue and require emergent intubation. Diuretics such as Furosemide are the first-line therapy to decrease venous congestion. In the elderly, age-related decline in renal function and decreased circulating volume may limit their use. Be mindful that prior diuretic use may be associated with hypokalemia, hypomagnesemia, predisposing the elderly to ventricular arrhythmias and digoxin toxicity. Monitor for hyponatremia. For pulmonary edema, an extreme of CHF, morphine and IV nitrates are adjuncts. Within the first twelve hours of presentation in the ED, ACE-inhibitors can be initiated as second-line therapy. Be prepared to correct any arrhythmias and have a standby transcutaneous pacemaker available as a bridge to transvenous pacemaker. The elderly with CHF after myocardial infarction is treated similarly as the younger adult. Once stabilized, the CHF patient with CAD or valvular disease, will need an angiogram, followed by angioplasty or definitive surgery (CABG or valve replacement). The ideal treatment of CHF, like most diseases, is of course, prevention via compliance with maintenance medications for HTN, CAD, exercise, and diet.
In summary, heart failure is a serious illness extolling a heavy burden on society. Within three months of the initial ED visit, more than 60% of the elderly with CHF experienced recurrent visit, hospitalization or death. This is the disease to watch and stay abreast of as the US population ages and a potential epidemic of heart failure settles in. A meticulous eye to the history and physical exam, prompt and aggressive ED treatment in a multidisciplinary fashion can give the elderly with CHF a chance to survival to discharge from the hospital.

Geriatrics: Managing Congestive Heart Failure

Treatment of the african-american patient with congestive heart failure
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Opinion statement
African Americans have a higher burden of cardiovascular disease than white Americans, including a higher prevalence of heart failure. In addition, heart failure in African Americans conforms to a more malignant natural history. Hypertension is most often cited as the sole etiology of heart failure in African Americans. Most of the major trials of pharmacotherapy for the management of chronic heart failure have failed to include significant numbers of African-American patients. Based on the available evidence, there is no reason to withhold standard evidence-based medical therapy for heart failure. Even though there is much controversy as to the efficacy of angiotensin-converting enzyme (ACE) inhibitors and ? blockers in African Americans, in the absence of definitive data they should be used. Recently, the combination of isosorbide dinitrate and hydralazine has been demonstrated to improve survival in African Americans with New York Heart Association class III and IV heart failure, and represents an adjunctive treatment option when added to standard medical therapy consisting of ACE inhibitors, ? blockers, digoxin, diuretics, and aldosterone antagonists. Emerging evidence suggests that this therapy may be targeting a novel mechanism of heart failure progression (ie,

Cite this article as:
Kamath, S.A. & Yancy, C.W. Curr Treat Options Cardio Med (2005) 7: 307. Doi: 10.1007/s11936-005-0041-z

References and Recommended Reading
American Heart Association: African Americans and Cardiovascular Diseases Statistics Fact Sheet. Dallas, IX: American Heart Association; 2004.

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J Geriatr Cardiol. 2015 Jan; 12(1): 57?65.
doi: 10.11909/j.issn.1671-5411.2015.01.007
PMCID: PMC4308459
Dilemmas in end-stage heart failure
Carol Chen-Scarabelli,1 Louis Saravolatz,2 Benjamin Hirsh,3 Pratik Agrawal,3 and Tiziano M. Scarabelli2,3
Author information ? Article notes ? Copyright and License information ?
This article has been cited by other articles in PMC.
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Abstract
Heart failure (HF), a complex clinical syndrome due to structural or functional disorder of the heart, is a major global health issue, with a prevalence of over 5.8 million in the USA alone, and over 23 million worldwide. As a leading cause of hospitalizations among patients aged 65 years or older, HF is a major consumer of healthcare resources, creating a substantial strain on the healthcare system. This paper discusses the epidemiology of HF, financial impact, and multifaceted predicaments in end-stage HF care. A search was conducted on the U.S. National Library of Medicine website (www.pubmed.gov) using keywords such as end-stage heart failure, palliative care, ethical dilemmas. Despite the poor prognosis of HF (worse than that for many cancers), many HF patients, caregivers, and clinicians are unaware of the poor prognosis. In addition, the unpredictable clinical trajectory of HF complicates the planning of end-of-life care, such as palliative care and hospice, leading to underutilization of such resources. In conclusion, ethical dilemmas in end-stage HF are numerous, embroiling not only the patient, but also the caregiver, healthcare team, and society.
Keywords: Ethical dilemmas, Heart failure, Palliative care
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1. Introduction
Heart failure (HF) is defined as a complex clinical syndrome resulting from structural or functional disorders of the heart.[1] The current HF classification scheme emphasizes both the development and progression of the disease by identification of four stages.[2] Stage A includes those patients at risk for HF but without structural heart disease or HF symptoms (e.g., patients with diabetes mellitus, hypertension, or coronary artery disease); stage B comprises those patients who are asymptomatic but have structural heart disease (e.g., left ventricular hypertrophy or impaired left ventricular function); stage C consists of those patients with structural heart disease with current or prior heart failure symptoms (this stage accounts for the majority of HF patients); and stage D, which encompasses patients with refractory HF requiring advanced specialized treatments such as mechanical circulatory support, fluid removal procedures such as ultrafiltration, continuous inotropic infusions, heart transplant, experimental surgery or drugs, and end-of-life care or hospice.[2]
Although stage D HF patients account for 5% of the HF population,[3] and may benefit from palliative care consultation, the importance of palliative care was only acknowledged and incorporated into clinical guidelines in 2005.
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2. Epidemiology
The elderly population (65 years or older) are the primary victims of HF, and comprise 80% of patients hospitalized with HF.[1] The incidence of HF has steadily increased with the aging population, and as of 2012, 2.4% of the US population was reported to have HF.[4] It is projected that HF prevalence will increase by 23%, from 2.42% to 2.97% in 2030, affecting more than 8 million Americans.[4] Of these 8 million Americans, 2 million will be over the age of 80 years, accounting for more than 26% of all HF patients.[4]
Although HF is a progressive, incurable condition with an unpredictable clinical trajectory,[5],[6] many patients have an inaccurate perception of HF as a benign condition compared to cancer,[7] with limited understanding of their poor prognosis.[8],[9] In fact, in 2004, deaths attributed to heart failure numbered 284, 365, exceeding the combined death toll for lung cancer, breast cancer, prostate cancer, and HIV/AIDS.[10] This prevailing ignorance of patients and caregivers about their impending death is compounded by the reluctance of healthcare providers to acknowledge the terminal nature of HF,[9] with subsequent failure to assist patients and their caregivers in end-of-life planning.
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3. Prevalence
HF is a major global health issue, with a prevalence of over 5.8 million in the USA alone, and over 23 million worldwide.[11] Listed on the death certificates in 1 out of 9 Americans,[12] HF is a leading cause of hospitalizations among patients aged 65 years or older.[13] As such, HF is a major consumer of healthcare resources, creating a substantial strain on the healthcare system.
Based on the National Health & Nutrition Examination Survey (NHANES) data from 2005?2008, in the United States alone, approximately 5.7 million people ages 20 years or older were afflicted with HF, with a projected increase in HF prevalence to 6.6 million among US adults ages 18 years or older in the year 2010.[14] By the year 2030, it is predicted that an additional 3 million people will develop HF (see Figure 1).[14] Based on data from the Framingham Heart study, the lifetime risk of developing HF at age 40 years is 1 in 5, regardless of gender.[14] After age 65 years, HF incidence is estimated at 10 per 1000 population.[14]

Figure 1.
Heart failure (HF) prevalence in 2010 was estimated at 6.6 million, with projected increase to 9.6 million in year 2030.
In 2008, HF was a contributing cause in more than 280,000 deaths (approximately 1 in 9).[14] HF is the primary cause of mortality in more than 55,000 Americans each year,[15] with an estimated 50% of HF patients dying within 5 years of the diagnosis.[14]
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4. Financial burden
In addition to the lives lost, HF is a costly disease, costing the USA more than $34.4 billion dollars each year in health care services, medications, and lost productivity.[16] The total cost of HF in the USA is projected to grow from 44.6 billion dollars in 2015, to 97 billion dollars by the year 2030 (see Figure 1).[14]
Although not viewed in the same fearful context as cancer, heart failure is a progressive and incurable condition with an unpredictable clinical trajectory. That is, some cancers are curable and the clinical development is somewhat predictable in terminal cancers, thereby facilitating end-of-life planning. In contrast, the clinical course of HF is unpredictable, rendering it difficult to plan end-of-life care. In addition, many patients, their caregivers, and clinicians fail to recognize the terminal, progressive nature of HF. In Canada, although cancer accounts for 25% of deaths, 90% of cancer patients receive palliative or end-of-life care compared to patients with cardiovascular disease, which accounts for over one third of deaths, but utilize a disproportionately smaller proportion of palliative care resources.[6] Similarly, in the US, while almost 50% of patients enrolled in hospice have cancer as a primary diagnosis, only 12.2% have a primary diagnosis of cardiac disease, reflecting underutilization of hospice among HF patients.[10]
Kirkpatrick, et al.[17] reported that the prognosis of the HF patient is poor, worse than that for many cancers, yet many HF patients, caregivers, and clinicians are unaware of the poor prognosis. Acute HF is the leading medical cause of hospitalization among people aged 65 years or older in the United States, European countries, Australia, and New Zealand, with in-hospital mortality rates ranging from 2% to 20%.[18] Of those who survive to hospital discharge, 55% of hospitalized HF patients are readmitted within 6 months.[19] Furthermore, 30-day readmission rates are high, with HF being the most frequent diagnosis for hospital readmission.[20]
An analysis of 2007?2009 Medicare fee-for-service claims revealed that the median time to 30-day readmission was 12 days for those patients initially hospitalized for HF.[21] Despite a reduction in risk-adjusted 1-year mortality (decreased from 31.7% in 1999 to 29.6% in 2008; P < 0.001), 1-year mortality remained high (about 30%) for medicare beneficiaries 1998?2008, hospitalized with HF.[22] Thus, the initial hospitalization for HF should alert providers to initiate end-of-life care planning, if not already started. These HF hospitalizations and frequent readmissions with early mortality should be a harbinger to patients, caregivers, and providers about the need for end-of-life care planning. It is reported that 38% of patients will die within the first year of diagnosis of heart failure, while another 60% will die within 5 years.[5] There is a 30% mortality among heart failure patients within the year following the first hospitalization for heart failure, but mortality may be as high as 60% among those patients with multiple comorbidities.[6]
The lifetime prevalence of heart failure for all adults is 15%?20%, and increases to over 20% prevalence among octogenarians.[23] In addition, with advances in heart failure technologies (including pharmacologic agents, device therapies, mechanical assist devices, etc), and advances in coronary revascularization (drug-eluting stents and complex percutaneous coronary interventions, etc), more patients are surviving acute myocardial infarctions and living longer, but going on to develop heart failure. The primary mode of death among HF patients is variable, according to NYHA functional class. Patients with NYHA class II symptoms are at a proportionally higher risk of sudden cardiac death while those with NYHA class IV symptoms have a one-year mortality as high as 75% with a significantly higher risk of dying of progressive heart failure characterized by worsening shortness of breath, orthopnea, hypotension, and decreasing level of consciousness.[24]
Since 50% of patients died suddenly from arrhythmias and acute ischemic events,[25] implantable cardiac defibrillators (ICDs) are recommended for primary prevention of sudden cardiac death. Although many patients preferred a ?do not resuscitate? (DNR) status as death became more imminent, their perceived quality of life did not diminish significantly, with 29% to 58% of patients reporting good to excellent quality of life in all intervals before death.[26] In contrast, progressive pump failure is a more common mode of death in advanced heart failure,[25],[27] with these patients experiencing disabling symptoms such as fatigue, shortness of breath, and limited mobility, leading to restricted socialization, complicated medication regimens, and poor quality of life, as well as exerting a significant toll on the caregivers, as well as on the healthcare resources.
Compared with HF patients with reduced ejection fraction (HFREF), cardiovascular deaths, sudden death, and HF deaths are lower in patients with HF with preserved ejection fraction (HFPEF).[28] Nonetheless, mortality remains high in HFPEF patients, with non-cardiovascular deaths responsible for the majority of deaths in HFPEF.[28],[29] In addition, HFPEF is actually more common than HFREF, with an escalating incidence and prevalence in those aged 70 years or older.[30] Thus, all HF patients would benefit from early referral to palliative care but lack of awareness and understanding by both patients/caregivers and clinicians limit utilization of this much-needed resource in HF management.
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5. Palliative care, hospice and end-of-life planning
Despite being used interchangeably by many healthcare providers, palliative care, hospice, and end-of-life planning are not synonymous terms.
Palliative care, as defined by the World Health Organization (WHO), is an approach that improves the quality of life of patients, who are faced with life-threatening illnesses. This approach focuses not only on symptom alleviation, but is holistic in its approach by addressing physical, psychosocial and spiritual needs of patients. Such model is applicable early in the course of a disease and can be applied in conjunction with life-prolonging therapies.[31] Palliative care is an active process with a multidisciplinary, holistic approach which strives to address physical, emotional, psychological and spiritual aspects of care while offering a support system to both patients and their caregivers.[32]
Hospice, in contrast to palliative care, is a passive process, and focuses on symptom management in patients with a prognosis of six months or less.[32] Thus, while hospice care is based on patient prognosis, palliative care is based on patient and family/caregiver needs, independent of the prognosis which may be greater than six months. Furthermore, palliative care patients may continue life-prolonging therapies, but hospice patients must agree to forego curative or life-prolonging medical treatment.[10]
The goal of palliative care includes symptom alleviation and commonly is associated with patients with terminal cancer.[33] In contrast, end-of-life care encompasses not only symptom management, but also includes hospice care, advanced directives and advanced care planning.[34] Consequently, end-of-life care is now ?mainstream? and an integral part of the process of heart failure care.[35] End-of-life care refers to a process incorporating advance directives (i.e., living wills, healthcare power of attorney) as well as preparation for end of life, including a discussion of death. End of life planning is not defined by a specific timeframe and address numerous transitions: physical, emotional, spiritual, financial, as well as respect for choice (patient or proxy) at the end of life.[36]
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6. End-of-life care dilemmas in HF
End-of-life care dilemmas are numerous and vary according to the stakeholder (Figures 2 & 3). Patients, their caregivers, clinicians, and policymakers/society each have their own agenda and perspective on end-of-life care in HF, and these perspectives are often incongruent among the stakeholders. For example, the end stage HF patient may wish to pursue aggressive therapies to prolong life, while the clinician, in order to avoid conflict, or to avoid taking away hope, may agree to provide such therapies. At the other end, policymakers and society may view such therapies as an unnecessary financial burden to society, with cost-effectiveness of such therapies and unequal allocation of finite healthcare resources as significant considerations. Ethicists and democratic proponents may have their own perspective and view such medical therapies as distributive justice, examples of which include public programs that provide social security or medical care to all elderly and retired persons.[37]

Figure 2.
Stakeholders in end-of-life care dilemmas in heart failure, with the heart failure patient being the central stakeholder.

Figure 3.
Dilemmas of various stakeholders in the care of the heart failure patient
One of the most prominent dilemmas at end of life in HF is represented by poor or ineffective communication (for various reasons) between patients/caregivers and their clinical providers. This may be related to discomfort for both parties in addressing the terminal, progressive nature of the disease, as well as discussing end-of-life care planning. Other issues include lack of adequate training and education in the discussion of end-of-life, as well as discerning the timing of when to broach the subject of end-of-life planning.[5] The deactivation of ICDs and left ventricular assist devices (LVADs) poses another challenging quandary in care of the end stage HF patient.
Other dilemmas involve the ethical and medico-legal issues associated with deciding which patients are appropriate candidates for which therapies, provision of maximal possible care or withholding such therapies.[38] There is clinician or therapeutic inertia [failure of the clinician to titrate therapy when the treatment goals are unmet;[39] resource limitations, including limited organ availability for heart transplant, patient compliance (such as continued smoking or substance abuse), and the lack of adequate psycho-social support for the patient].[38] Another essential, though often overlooked aspect is the financial burden placed on patients and on society when dealing with a chronic condition such as organ transplantation,[38] device therapies (such as ICDs, cardiac resynchronization therapy devices-with pacemakers only/CRT-P, and cardiac resynchronization therapy devices-with defibrillators/CRT-D) and mechanical circulatory assist systems (such as LVADs as destination therapy or bridge to transplant), all of which requires continuous medical care, diagnostic assessment, and long-term care with regular interval follow-up visits.
Although the financial burden is an uncomfortable topic when discussing clinical care of patients with advanced heart failure, the cost effectiveness of technologies in heart failure is a necessary topic of discussion and consideration in many countries with a public healthcare system, as well as for countries such as the United States, with both private insurance systems and public healthcare systems, including Medicare and Medicaid.
Between 2005 and 2009, the incidence of orthotopic heart transplantation increased only marginally, whereas the annual left ventricular assist device implantation rates almost tripled. This rapid escalation in LVAD implantation rates was accompanied by a significant increase in healthcare expenditures, as the cumulative left ventricular assist device cost increased 232% within 5 years (from $143 million to $479 million). The impact of such inflation in healthcare expenses was shouldered to a great extent by taxpayers since Medicare and Medicaid were the primary payers for nearly one half of all patients (orthotopic heart transplantation, 45%; left ventricular assist device, 51%) by 2009.[40] Thus, cost-effectiveness, distributive justice, and allocation of finite resources are important factors when utilization of these technologies is considered.[41]
Based on the physician clinical model, these providers may have a treatment imperative which fosters pursuing more aggressive therapy, even when clinically inappropriate in end-stage heart failure. Clinicians often feel a sense of failure, and both clinicians and patients may fail to accept the limitations of medicine and the available treatments. The uncertain and unpredictable disease trajectory of heart failure is another obstacle in planning end-of-life care for patients in their caregivers.
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7. Dilemmas from the patient and caregiver perspective
In an interview study of 64 caregivers at 6 months after the patient’s death, there were common themes regarding end of life planning issues: (1) lack of availability of treatment options for certain patients, (2) changes in preferences at the very end of illness, (3) variability in patient and caregiver desire for and readiness to hear information about the patient’s illness, and (4) difficulties with patient?caregiver communication.[42] Patients and their caregivers may fail to raise end-of-life issues for various reasons including: lack of understanding their condition; unpredictability of the clinical trajectory of HF; discomfort and anxiety in raising end-of-life discussions; and a feeling of powerlessness while viewing clinicians as unapproachable or reluctant to give out information.[5]
In a study of patient preferences regarding end-of-life treatment in advanced HF, two distinct groups of patients were identified: one group preferred life-prolonging treatments, while the other group favoring strategies that improved quality of life despite reduced survival time. As treatment preferences were independent of functional or symptom status, this may present an important opportunity for clinicians to discuss such treatment preferences early in the course of illness and help facilitate end-of-life planning.[43]
Patients with HF often have a poor understanding of their condition and prognosis. A review of the literature identified three common themes or areas of need: education to enhance professional communication skills, communication to improve patient understanding, and communication skills to facilitate advance care planning.[44]
Patients and families are frequently unaware about the imminence of death in end-stage HF during the last few days or hours preceding their demise.[9] Bereaved family members of HF patients who succumbed to non-sudden cardiac deaths reported that they received minimal communication about what to expect, and only 1/3 reported being aware of a poor prognosis, while only 8% of patients and 44% of family members were informed about the limited remaining time, with 36% of these patients ending up dying alone.
Pain and other symptoms such as dyspnea and edema, as well as progressive and profound fatigue, may also hinder the patient’s ability to engage in end of life care discussions. HF patients report a high prevalence of pain (63%?80%), anxiety (49%) and breathlessness (60%?88%), with rates similar to those for advanced cancers and AIDS.[7]
In a qualitative and open unstructured interview of advanced HF patients, four main themes emerged: ?Living in the Shadow of Fear; Running on Empty; Living a Restricted life; and Battling the System?, with patients describing their experience as a ?fearful and tired sort of living?, characterized by growing dependence and powerlessness.[45]
Deactivation of ICDs, CRT-Ds, and LVADs may also create a conflict for patients and their caregivers. In 2010, the Heart Rhythm Society (HRS) published a consensus statement in collaboration with other professional societies, including the American Academy of Hospice and Palliative Medicine. The document, reporting that only few physicians discuss device deactivation with their heart failure patients, attempts to educate providers about paramount issues, such as legal, ethical and religious principles, withdrawal of life-sustaining therapies (including device deactivation in patients who chose this option) and importance of proactive communication with the patients nearing end of life in order to minimize fear, anxiety and suffering. In addition, such document provides the caregivers with a clinical guide to help managing the request for device deactivation.[46]
In a study of internal medicine physicians and internal medicine subspecialists at Beth Israel Deaconess Medical Center, an academic tertiary care center in Boston, Massachusetts, physicians (surveyed via an anonymous email link survey) were consistently less comfortable discussing cessation of pacemakers and ICDs compared to other life-sustaining therapies (P < 0.005), such as withdrawal or removal of mechanical ventilation, dialysis and feeding tubes.[47]
Patients with LVADs, despite improved survival and potential for improved quality of life due to symptomatic improvement, may experience not only complications, such as recurrent infections, but also reduced quality of life in terms of frequency of follow-up and monitoring. Open, honest communication regarding the impact of LVAD on daily life, as well as prognosis of HF and end-of-life planning are imperative prior to implantation.[48]
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8. Clinician/healthcare provider dilemma
Ineffective communication or lack of communication skills are recognized hindrances in raising end-of-life discussions.[44] In addition, physicians are faced with a moral and ethical dilemma of withdrawal of life-sustaining therapies in a model in which they are more accustomed to rescue and prolong life. Thus, some may incorrectly perceive device deactivation as physician-assisted suicide or euthanasia. However, the HRS consensus statement provides clarification about the differences between device deactivation and extreme measures.[46]
Although clinical guidelines now exist for recommendation for end-of-life considerations in HF,[1] they do not address the timing of when to refer end-stage HF patients for non-hospice palliative care or hospice care.[10] Since HF is characterized by unpredictable decompensations and improvements, the clinical trajectory makes timing of referrals difficult to determine, and may also lead patients and caregivers to have unrealistic expectations that, having survived and recovered from an episode of HF exacerbation, they see no reason why they should not recover again from future episodes. Thus, prognostication in HF is difficult due to the unpredictable course of the disease, which makes it even more important to discuss palliative care and end-of-life care early in the disease process.[49] Furthermore, there is a lack of research regarding the best models to implement for palliative care and end-of-life care provision in HF patients.[7]
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9. Society/policymaker dilemma
Despite the documented benefits (i.e., improved survival and symptomatic improvement) of advanced technologies, such as ventricular assist devices and cardiac resynchronization therapy for treatment of HF, the costliness of such therapies is of significant concern to policymakers. Cost-effectiveness and distributive justice will be important factors in the policy decision-making for implementation of such technologies, as many countries cannot afford the financial burden imposed by these technologies.[41]
Current medicare hospice benefit limits include, for example, a 6-month prognostication to death as a prerequisite to enrollment, a forced choice between skilled care and hospice care for Medicare patients entering nursing homes from hospitals, and limitations on the availability of therapies.[36]
Prolongation of the final stages of HF exerts a toll on patients, caregivers, medical system and society. It is reported that more than 25% of Medicare spending occurs in the last year of life. Furthermore, the costs of care during the last 6 months for a HF patient has steadily increased with a projection estimating that, by the year 2030, each US adult will pay on average $244 per year to care for the 10 million patients with HF.[4]
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10. Practical considerations
Healthcare providers who care for patients with end-stage HF need to examine their own attitudes and beliefs about terminal illness and death in order to effectively advocate for patients in the final stages of heart failure. In particular, physicians, who are at the helm in regards to continuation of care and resuscitation decisions, exert a significant impact on patients’ end of life care, even in the presence of advance directives. In a physician survey study examining the impact of external factors and perceived patients’ preferences on physicians’ decisions to honor or forgo patients’ advance directives, the majority of physicians (59%) reported that they would resuscitate a patient in ventricular fibrillation despite the known existence of an advance directive requesting no resuscitation.[50]
Likewise, a recent 2013 survey of physicians at academic medical centers exploring their personal resuscitation preferences and attitudes towards advance directives found that while the vast majority of physicians (88.3%) chose the do-not-resuscitate status for themselves if diagnosed with a terminal illness, many physicians continue to aggressively pursue futile treatments for their terminally ill patients.[51] Besides awareness of one’s own biases, the clinician should meet with the individual patient to discuss the patient’s wishes and set realistic expectations at the initial meeting or diagnosis, and revisit such wishes and goals of care at regular intervals, especially when there is a change in the patient’s clinical status. This personalized acknowledgement of the patient’s right to self-determination is important to ensure that the patient’s advance directives will be upheld.
Furthermore, a recent task force identified that early discussion between patients and their clinician was not only cost-effective (with reduced utilization of futile, non-beneficial medical care at end of life), but more importantly, with better quality of life and positive family outcomes.[52]
Early involvement of the multidisciplinary team is essential to develop trust between the patient and their team members, as well as facilitate timely interventions to assist patients and their caregivers. A thorough assessment of the patient with end-stage HF should incorporate evaluation of (a) the patient’s psychosocial support (e.g., who drives the patient to his/her appointments? Does the patient live alone? Who helps to prepare meals and assist the patient with activities of daily living and personal hygiene?); (b) financial resources (medical insurance; medication prescription coverage; hospice coverage; co-payments); (c) the patient’s emotional state and well-being; and (d) spiritual and religious needs. Holistic care is critical, and requires coordination of the entire multidisciplinary team. Consultations with the social worker (for assistance with living wills, advance directives, exploring available resources) and with palliative care team if available (to help identify the patient’s expectations, needs, pain and symptom management) are indispensable in the end of life care for the HF patient. Furthermore, these team members may ease the personal discomfort that many physicians feel when faced with the situation of ?giving up the fight?. Death is inevitable for all, but helping patients and family members have closure at the terminal stages of the disease is treating not only the body, but the soul, and allows patients to ?go gentle into that good night?.
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11. Conclusions
Prevention of HF appears to be the most logical approach to curtail costs of HF care. Control of risk factors, such as hypertension, may help reduce HF development. Lifetime risk for CHF doubled for subjects with blood pressure = 160/100 mmHg vs. < 140/90 mmHg. In those patients without an antecedent myocardial infarction (MI), at age 40 years, the lifetime risk for CHF was 11.4% (95%CI: 9.6%?13.2%) for men and 15.4% (95%CI: 13.5%?17.3%) for women. Thus, the lifetime risk for developing HF (in patients without MI) is one in nine for men and one in six for women, thereby highlighting the fact that CHF is largely attributable to hypertension.[23] Risk factor modification and prevention of HF require understanding the risk factors for the two types of HF: ischemic heart disease is the predominant risk factor for HFREF, while hypertension, atrial fibrillation and diabetes are the main risk factors for HFPEF.[53]
Through adherence to clinical guidelines (including appropriate criteria use), optimization of medical therapy, empowerment and accountability of patients/caregivers in healthcare management, as well as reduction of clinician inertia, the incidence of HF may decrease, with subsequent reduction in healthcare costs. Patient involvement and accountability, including weight loss, smoking cessation, and lifestyle modification, will be essential for a successful outcome. In the meantime, HF prevalence continues to grow and patients, their caregivers, and clinicians must become more educated and proactive in navigation of end-of-life care, in order to minimize the patient’s fears and suffering, as death becomes imminent. Life is a continuum, with death being the end of the journey. Yet, few are comfortable in accepting the inevitable. In the end, the physician’s moral and ethical imperative is primum non nocere (?first, do not harm?), which extends to the terminal patient and may entail advocating for his death.
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References
THESE ARE THE TWO REFERENCES FOR THIS INFORMATION:
? Chen-Scarabelli, C., Saravolatz, L., Hirsh, B., Agrawal, P., & Scarabelli, T. M. (2015). Dilemmas in end-stage heart failure. Journal of Geriatric Cardiology?: JGC, 12(1), 57?65. http://doi.org/10.11909/j.issn.1671-5411.2015.01.007

? Jaiswal, A., Nguyen, V. Q., Le Jemtel, T. H., & Ferdinand, K. C. (2016). Novel role of phosphodiesterase inhibitors in the management of end-stage heart failure. World Journal of Cardiology, 8(7), 401?412. http://doi.org/10.4330/wjc.v8.i7.401

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Congestive Heart Failure (CHF) In African Americans
CHF affects almost 5 million Americans, with about 500,000 new cases reported each year. The estimated yearly cost to the nation is $10 billion.
There are substantial differences between blacks and whites with heart failure regarding age, incidence, etiology, hospitalization rates, left ventricular hypertrophy, left ventricular function, clinical follow-up, and mortality. Although the data concerning black-white differences is not voluminous, there have been some studies performed which help to shed light on these disparities and their impact on patient survival. For example, one study showed that African Americans under age 65 with CHF have 2.5 times the mortality experienced by whites of the same ages. When patients older than 65 were considered, the age-adjusted death rate in 1990 for CHF was 143.9 for African American men compared to 117.8 for white men, and 113.4 for African American women compared to white females. Medicare data have also demonstrated higher rates of admission and discharge diagnoses of CHF for blacks.
It has been stated often that African Americans have a greater prevalence of hypertensive heart disease as opposed to ischemic heart disease as the underlying etiology of their CHF, and that whites have the reverse situation. These beliefs are borne out in the Study of Left Ventricular Dysfunction (SOLVD) trial, in which blacks with CHF had a higher prevalence of hypertensive heart disease and a lower prevalence of ischemic heart disease.
http://blackdoctor.org/4225/congestive-heart-failure-chf-in-african-americans/

Treatment of the African-American patient with congestive heart failure.
Kamath SA1, Yancy CW.
Author information
? 1Department of Internal Medicine/Cardiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9047, USA.
Abstract
African Americans have a higher burden of cardiovascular disease than white Americans, including a higher prevalence of heart failure. In addition, heart failure in African Americans conforms to a more malignant natural history. Hypertension is most often cited as the sole etiology of heart failure in African Americans. Most of the major trials of pharmacotherapy for the management of chronic heart failure have failed to include significant numbers of African-American patients. Based on the available evidence, there is no reason to withhold standard evidence-based medical therapy for heart failure. Even though there is much controversy as to the efficacy of angiotensin-converting enzyme (ACE) inhibitors and beta blockers in African Americans, in the absence of definitive data they should be used. Recently, the combination of isosorbide dinitrate and hydralazine has been demonstrated to improve survival in African Americans with New York Heart Association class III and IV heart failure, and represents an adjunctive treatment option when added to standard medical therapy consisting of ACE inhibitors, beta blockers, digoxin, diuretics, and aldosterone antagonists. Emerging evidence suggests that this therapy may be targeting a novel mechanism of heart failure progression (ie, nitric oxide bioavailability) found in African Americans.
http://www.ncbi.nlm.nih.gov/pubmed/16004861

Following recommendations about diet, exercise and other habits can help to alleviate symptoms, slow your disease’s progression and improve your everyday life. In fact, people with mild to moderate heart failure (HF) often can lead nearly normal lives as a result. (BELOW ARE INTERVENTIONS THAT CAN BE USED TO IMPROVE THE PROBLEMS OF CHF)
STOP SMOKING
Each puff of nicotine from tobacco smoke temporarily increases heart rate and blood pressure, even as less oxygen-rich blood circulates through the body. Smoking also leads to clumping or stickiness in the blood vessels feeding the heart. People who quit smoking are more likely to have their heart failure symptoms improve.
LOOSING OR MAINTAING YOUR WEIGHT
Sudden weight gain or weight loss can be a sign that you may be developing heart failure or that your heart failure is progressing. Weigh yourself at the same time each morning, preferably before breakfast and after urinating. Notify your healthcare professional if you gain three or more pounds in one day, five or more pounds in one week, or whatever amount you were told to report. Learn more about maintaining a healthy weight. Learn more about maintaining a healthy weight.
KEEPING A TRACK OF FLUID INTAKE
When your body is retaining fluid, as often happens with heart failure, your healthcare team may recommend limiting how much liquid you get. Many people are prescribed diuretics (water pills) to help them get rid of extra water and sodium and reduce their heart’s workload. Talk with your healthcare provider about how much liquid to drink every day.
AVOIDING FLU AND PNEUMO VAC
Flu and pneumonia pose greater dangers for people who have heart failure (or any heart condition) than for healthy people. Pneumonia is a lung infection that keeps your body from using oxygen as efficiently as it should. Your heart has to work harder to pump oxygenated blood through the body. People with heart failure should avoid putting this extra stress on their heart.

Ask a healthcare professional about getting a yearly influenza vaccine and a one-time pneumococcal vaccine (to guard against the most common form of bacterial pneumonia). Both vaccines are generally safe and seldom cause any severe reactions. It’s much riskier not to have them. You might have some pain or swelling at the site of the shot (on the arm), but this will go away after a few days.

DEVELOP SUPPORT
Join a support group for people with heart failure and other heart conditions. Contact local churches, religious congregations and volunteer centers to find out about programs that provide meals, transportation and errand services for people who need assistance.

GETTING ADEQUATE REST
To improve your sleep at night, use pillows to prop up your head. Avoid naps and big meals right before bedtime. Try napping after lunch or putting your feet up for a few minutes every couple of hours.

KEEPING TRACK OF YOUR BP
To help control high blood pressure, research has shown that monitoring blood pressure at home can be helpful in addition to regular monitoring in a healthcare provider’s office. Chart your blood pressure to provide information on what is happening with your blood pressure over time and help eliminate false readings. Find out more about how healthy eating can lower your blood pressure with the DASH eating plan.

MANAGING STRESS
Take 15 to 20 minutes a day to sit quietly, breathe deeply and think of a peaceful scene. Or try a class in yoga or meditation (check with your healthcare provider first). Count to 10 before responding when you feel angry to help reduce your stress.

BEING PHYSICALLY ACTIVE
Perhaps participating in a structured rehabilitation program. Begin an exercise program (with your healthcare provider’s permission). Schedule physical activity at the same time every day so it becomes a regular part of your lifestyle.

Eating a heart-healthy diet
Eat a healthy diet that’s low in saturated fat, trans fat, cholesterol and sodium. Consume only a moderate amount of caffeine per day, no more than a cup or two of coffee. If you drink alcohol, do so in moderation. This means no more than one to two drinks per day for men and one drink per day for women.
http://www.heart.org/HEARTORG/Conditions/HeartFailure/TreatmentOptionsForHeartFailure/Lifestyle-Changes-for-Heart-Failure_UCM_306341_Article.jsp#.V7p1i-9TGP8
http://www.heart.org/HEARTORG/Conditions/HeartFailure/LivingWithHeartFailureAndAdvancedHF/Living-with-Heart-Failure-and-Managing-Advanced-HF_UCM_477835_Article.jsp#.V7p75e9TGP8

MEDICATION INTERVENTIONS:
This information is provided at the sole discretion of the American Heart Association and the guidance of our science staff and volunteers and is not a part of the Rise Above Heart Failure initiative.

Research studies of heart failure have shown that several classes of drugs (medications) have shown to be the best for the treatment of heart failure. Heart failure patients may need multiple medications. Each one treats a different symptom or contributing factor. Each medication comes with its own instructions and rules. They can’t do their job if you don’t take them correctly. You and your caregivers should work with your healthcare team to understand the medications and how they should be taken; when, how often and in what amounts. It’s important to discuss all of the drugs you take with your doctor (or other healthcare provider) and understand their desired effects and possible side effects. Remember that your healthcare provider and pharmacist are your best sources of information. Don’t hesitate to ask them questions about your medicines.

It is critically important that persons with heart failure take their medications as directed by their healthcare provider (doctor, nurse practitioner, etc) to optimize the benefits of these drugs in the treatment of heart failure. By following prescribed directions, you have the best opportunity to benefit from heart failure treatment recommendations. The use of these drugs has been shown to save lives, prolong life and improve the heart?s function.

The following list gives you a quick look at many typical medications to treat heart failure at different stages. Your prescription may have a different name from the ones listed here. Brand names commonly available in the U.S. are shown in parentheses after the generic name for each drug.

*Some of the major types of commonly prescribed heart failure medications are summarized in this section. For your information and reference, we have included generic names as well as major trade names to help you identify what you may be taking; however, the AHA is not recommending or endorsing any specific products. If your prescription medication isn’t on this list, remember that your healthcare provider and pharmacist are your best sources of information. It’s important to discuss all of the drugs you take with your doctor and understand their desired effects and possible side effects. Never stop taking a medication and never change your dose or frequency without first consulting your doctor.

Use this list to gain a quick understanding of the common heart failure medications you may be prescribed. If you need more help understanding what medication you’re taking and why you’re taking it, talk to your doctor.
Angiotensin-Converting Enzyme (ACE) Inhibitors

Commonly prescribed include:
? Captopril (Capoten)
? Enalapril (Vasotec)
? Fosinopril (Monopril)
? Lisinopril (Prinivil, Zestril)
? Perindopril (Aceon)
? Quinapril (Accupril)
? Ramipril (Altace)
? Trandolapril (Mavik)

Angiotensin II Receptor Blockers (or Inhibitors)
(Also known as ARBs or Angiotensin-2 Receptor Antagonists)

Commonly prescribed include:
? Candesartan (Atacand)
? Losartan (Cozaar)
? Valsartan (Diovan)

Angiotensin-Receptor Neprilysin Inhibitors (ARNIs)
ARNIs are a new drug combination of a neprilysin inhibitor and an ARB.
? Sacubitril/valsartan
If Channel Blocker (or inhibitor)
This drug class reduces the heart rate, similar to another class of drugs called beta blockers.
? Ivabradine (Corlanor)
Beta Blockers
(Also known as Beta-Adrenergic Blocking Agents)

Commonly prescribed include:
? Bisoprolol (Zebeta)
? Metoprolol succinate (Toprol XL)
? Carvedilol (Coreg)
? Carvedilol CR (Coreg CR)Toprol XL

Aldosterone Antagonists

Commonly prescribed include:
? Spironolactone (Aldactone)
? Eplerenone (Inspra)
Hydralazine and isosorbide dinitrate (specifically benefits African Americans with heart failure)

Commonly prescribed:
? Hydralazine and isosorbide initrate (combination drug) – (Bidil)

Diuretics
(Also known as Water Pills)

Commonly prescribed include:
? Furosemide (Lasix)
? Bumetanide (Bumex)
? Torsemide (Demadex)
? Chlorothiazide (Diuril)
? Amiloride (Midamor Chlorthalidone (Hygroton)
? Hydro-chlorothiazide (Esidrix, Hydrodiuril)
? Indapamide (Lozol)
? Metolazone (Zaroxolyn)
? Triamterene (Dyrenium)
What this type of medication does:
Causes the body to rid itself of excess fluids and sodium through urination. Helps to relieve the heart’s workload. Also decreases the buildup of fluid in the lungs and other parts of the body, such as the ankles and legs. Different diuretics remove fluid at varied rates and through different methods.

Other possible medications that might be prescribed

Your doctor may also prescribe other less commonly used drugs depending on your additional health problems. These drugs include:
? Anticoagulants (blood thinners)
These drugs may be prescribed if you are a heart failure patient with atrial fibrillation, or have another problem with your heart where adding this drug is indicated. Anticoagulants are not used to treat heart failure without the presence of atrial fibrillation.
? Cholesterol lowering drugs (statins)
Your doctor may prescribe this class of medication if you have high cholesterol or have had a heart attack in the past. This class of drugs is not used to treat heart failure, but other conditions as indicated.
? Digoxin
There are some heart failure patients who might be prescribed this drug as the doctor feels indicated.
Additional medication information:
Find further descriptions of how these medications also affect cardiovascular diseases other than heart failure.

Medicine Management
Tools For Patients
Keeping Track / Developing a System

Keeping track of your prescribed medications can be challenging ? especially if you’re taking several different medicines. Writing things down will make managing your medications a lot easier. Use our printable medicine tracker to stay organized.

Lowering High Blood Pressure
By treating high blood pressure, you can help prevent a stroke, heart attack, heart failure, kidney failure and peripheral artery disease. Our printable blood pressure tracker will help you monitor your blood pressure and record suggestions from your doctor.

Manage Everything Online
Heart360 is a one-stop, easy-to-use set of online tracking tools for medications, blood pressure, cholesterol, blood glucose, weight and physical activity. Set goals and track your progress each time you enter your levels. Print comprehensive reports to share with your healthcare team. And manage accounts for your loved ones as well as yourself.
GET A MEDICAL CHECK -UP
Prescription and over-the-counter medicines help many people live longer, more active lives. When you take the right medicines the right way, they’re safe and effective tools for good health. But using them incorrectly can harm you. The more medicines you take, the greater your risk of problems. You can protect your health by getting a checkup on your medications. Take these simple steps as outlined by the National Council on Patient Information and Education.
? Make an appointment with your doctor or your pharmacist.

? Put all your prescription and over-the-counter drugs in a bag. Be sure to include:
Prescriptions in vials, tubes, bottles and plastic bags
Sleep and motion-sickness aids
Headache remedies
Cold remedies (liquid, capsules and tablets)
Laxatives and upset stomach aids
Other prescription or over-the-counter drugs you may be taking
Vitamins and nutritional supplements
Herbal remedies
? Remember to take all of your medications in their original containers if possible.

? Take the bag to your doctor or pharmacist and get him or her to go over all of your medicines with you.

? Ask questions about anything you don’t understand.
A checkup like this gives you the opportunity to ask your healthcare professional or pharmacist important questions about your medications. It can help you find dangerous medicine combinations you may be taking, medicines you may not need to take anymore, improper dosages of medicines, and mistakes that you may be making in taking them. Call your doctor or pharmacist today to schedule a medication checkup and take charge of your health.
SURGICAL INTERVENTION
Implantable Cardioverter-Defibrillator (ICD)
Some people who have severe heart failure or serious arrhythmias (irregular heartbeats) are candidates for implantable defibrillators. These devices are surgically placed and deliver pacing, or an electric countershock, to the heart when a life-threatening abnormal rhythm is detected. They have saved millions of lives, but may not be for everyone. This is a shared decision by the patient and physician. Learn more about implantable devices.

Cardiac Resynchronization Therapy (CRT)
Some people with heart failure develop abnormal conduction of the heart?s electrical system that changes how efficiently the heart beats. Cardiac resynchronization therapy, also known as biventricular pacing, may be needed. In this procedure, a special pacemaker is used to make the ventricles contract more like normal and in synchrony. This therapy can improve heart function, reduce hospitalization risk, and improve survival. Learn more about cardiac resynchronization therapy.

Left ventricular assist device (LVAD)
? What is a left ventricular assist device (LVAD)?
The left ventricle is the large, muscular chamber of the heart that pumps blood out to the body. A left ventricular assist device (LVAD) is a battery-operated, mechanical pump-type device that’s surgically implanted. It helps maintain the pumping ability of a heart that can’t effectively work on its own.

These devices are available in most heart transplant centers.
? When is an LVAD used?
This device is sometimes called a “bridge to transplant,” but is now used in longer-term therapy. People awaiting a heart transplant often must wait a long time before a suitable heart becomes available. During this wait, the patient’s already-weakened heart may deteriorate and become unable to pump enough blood to sustain life. An LVAD can help a weak heart and “buy time” for the patient or eliminate the need for a heart transplant. Most recently, LVADs are being used longer-term as ?destination therapy? in end-stage heart failure patients when heart transplantation is not an option.

? How does an LVAD work?
A common type of LVAD has a tube that pulls blood from the left ventricle into a pump. The pump then sends blood into the aorta (the large blood vessel leaving the left ventricle). This effectively helps the weakened ventricle. The pump is placed in the upper part of the abdomen. Another tube attached to the pump is brought out of the abdominal wall to the outside of the body and attached to the pump’s battery and control system. LVADs are now portable and are often used for weeks to months. Patients with LVADs can be discharged from the hospital and have an acceptable quality of life while waiting for a donor heart to become available.
Heart transplantation
Some people have severe, progressive heart failure that can’t be helped by medications and dietary and lifestyle changes. In such cases a heart transplant may be the only effective treatment option.

Surgeons replace the damaged heart with a healthy one taken from a donor who has been declared brain dead. It can take several months to find a donor heart that closely matches the tissues of the person receiving the transplant. But this matching process increases the likelihood that the recipient’s body will accept the heart. In some cases surgeons will implant a left ventricular assist device to help the heart function during this waiting period. This mechanical pump helps the left ventricle (lower left chamber) to pump.

During a transplant procedure, the surgeon connects the patient to a heart-lung machine, which takes over the functions of the heart and lungs. The surgeon then removes the diseased heart and replaces it with the donor heart. Finally, the major blood vessels are reconnected and the new heart is ready to work.

The outlook for people with heart transplants is good during the first few years after the transplant. In fact, about 90 percent of patients live for more than a year after their operations. However, the number of patients who receive heart transplants is still relatively low (around 2,500 each year). Read more about heart transplants.

________________________________________
Surgery isn’t frequently used to treat heart failure. However, it’s recommended when the doctor can identify a correctable problem that’s causing heart failure ? such as a defect (such as a heart valve) or a blocked coronary artery. Surgery also may be needed when the heart failure is so severe that it can’t be helped with medications or dietary and lifestyle changes. View an illustration of coronary arteries.

Percutaneous coronary intervention (PCI) (also referred to as angioplasty)
Heart failure can develop when blockages in the coronary arteries restrict the blood supply to the heart muscle. Removing these blockages can improve overall heart function, which may improve or resolve heart failure symptoms. PCI is one type of procedure to reopen blocked vessels.
The procedure is usually performed in the cardiac catheterization lab. A small tube ? a catheter ? with a tiny deflated balloon on the end is inserted through an incision in the groin (or other artery) area and pushed through to the diseased artery. Then the balloon is inflated to push open the artery. The balloon is removed once the artery has been fully opened. A stent may be placed during the procedure to keep the blood vessel open. Although there’s a slight risk of damage to the artery during this procedure, PCI usually improves the patient’s condition. Watch an animation of PCI.

Coronary artery bypass
Coronary artery bypass surgery reroutes the blood supply around a blocked section of the artery. During this procedure, surgeons remove healthy blood vessels from another part of the body, such as a leg or the chest wall. They then surgically attach the vessels to the diseased artery in such a way that the blood can flow around the blocked section.
After a bypass operation, it’s especially important for you to watch your diet and reduce the amount of fat and cholesterol you eat, since these substances cause the arteries to clog. Doctors also recommend following a routine of increased physical activity to strengthen the heart muscles. View an illustration of coronary artery bypass.

Valve replacement
Heart failure is sometimes caused by a defective or diseased heart valve. Heart valves regulate the flow of blood inside the heart. When they don’t work properly, this puts extra strain on the heart and can lead to heart failure. For some valve problems, medical management is the first step in treatment. Correcting the problem surgically can often improve or resolve the condition.

A variety of different replacement valves can be used: a mechanical valve made from metal and plastic, one made from human or animal tissue. During the surgery, the patient is connected to a heart-lung machine that supplies blood to the brain and body. The bad valve is removed and replaced.

After the operation and depending on the type of replacement heart valve used, patients may take medicines to prevent blood clots from forming around the new heart valve. This treatment is often long-term to ensure the new valve works properly. Most heart valve surgeries are a success, but the operation is only considered as an option when a defective or diseased valve threatens someone’s life.

In some patients, heart valve replacement may occur without surgery but candidacy for this kind of procedure is highly individualized. Read more about heart valve surgery.

HF


 

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Define the problem, specific population affected, cultural implications, and financial/legal/ethical implications.

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