Heart failure (HF) is a clinical syndrome that occurs in patients who, because of an inherited or acquired abnormality of cardiac structure and/or function, develop a constellation of clinical symptoms (dyspnea and fatigue) and signs (edema and rales) that lead to frequent hospitalizations, a poor quality of life, and a shortened life expectancy.
HF is a burgeoning problem worldwide, with more than 20 million people affected. The overall prevalence of HF in the adult population in developed countries is 2%. HF prevalence follows an exponential pattern, rising with age, and affects 6–10% of people over age 65. Although the relative incidence of HF is lower in women than in men, women constitute at least one-half the cases of HF because of their longer life expectancy. In North America and Europe, the lifetime risk of developing HF is approximately one in five for a 40-year-old. The overall prevalence of HF is thought to be increasing, in part because current therapies for cardiac disorders, such as myocardial infarction (MI), valvular heart disease, and arrhythmias, are allowing patients to survive longer. Very little is known about the prevalence or risk of developing HF in emerging nations because of the lack of population-based studies in those countries. Although HF once was thought to arise primarily in the setting of a depressed left ventricular (LV) ejection fraction (EF), epidemiologic studies have shown that approximately one-half of patients who develop HF have a normal or preserved EF (EF ≥40–50%). Accordingly, HF patients are now broadly categorized into one of two groups: (1) HF with a depressed EF (commonly referred to as systolic failure) or (2) HF with a preserved EF (commonly referred to as diastolic failure).
As shown in Table 234-1, any condition that leads to an alteration in LV structure or function can predispose a patient to developing HF. Although the etiology of HF in patients with a preserved EF differs from that of patients with depressed EF, there is considerable overlap between the etiologies of these two conditions. In industrialized countries, coronary artery disease (CAD) has become the predominant cause in men and women and is responsible for 60–75% of cases of HF. Hypertension contributes to the development of HF in 75% of patients, including most patients with CAD. Both CAD and hypertension interact to augment the risk of HF, as does diabetes mellitus.
Table 234-1 Etiologies of Heart Failure
| Save Table
Table 234-1 Etiologies of Heart Failure
|Depressed Ejection Fraction (<40%)|
|Coronary artery disease||Nonischemic dilated cardiomyopathy|
|Myocardial infarctiona||Familial/genetic disorders|
|Myocardial ischemiaa||Infiltrative disordersa|
|Chronic pressure overload||Toxic/drug-induced damage|
|Obstructive valvular diseasea||Viral|
|Chronic volume overload||Chagas' disease|
|Regurgitant valvular disease||Disorders of rate and rhythm|
|Intracardiac (left-to-right) shunting||Chronic bradyarrhythmias|
|Extracardiac shunting||Chronic tachyarrhythmias|
|Preserved Ejection Fraction (>40–50%)|
|Pathologic hypertrophy||Restrictive cardiomyopathy|
|Primary (hypertrophic cardiomyopathies)||Infiltrative disorders (amyloidosis, sarcoidosis)|
|Secondary (hypertension)||Storage diseases (hemochromatosis)|
|Pulmonary Heart Disease|
|Pulmonary vascular disorders|
|Metabolic disorders||Excessive blood-flow requirements|
|Thyrotoxicosis||Systemic arteriovenous shunting|
|Nutritional disorders (beriberi)||Chronic anemia|
In 20–30% of the cases of HF with a depressed EF, the exact etiologic basis is not known. These patients are referred to as having nonischemic, dilated, or idiopathic cardiomyopathy if the cause is unknown (Chap. 238). Prior viral infection or toxin exposure (e.g., alcoholic or chemotherapeutic) also may lead to a dilated cardiomyopathy. Moreover, it is becoming increasingly clear that a large number of cases of dilated cardiomyopathy are secondary to specific genetic defects, most notably those in the cytoskeleton. Most forms of familial dilated cardiomyopathy are inherited in an autosomal dominant fashion. Mutations of genes that encode cytoskeletal proteins (desmin, cardiac myosin, vinculin) and nuclear membrane proteins (laminin) have been identified thus far. Dilated cardiomyopathy also is associated with Duchenne's, Becker's, and limb-girdle muscular dystrophies. Conditions that lead to a high cardiac output (e.g., arteriovenous fistula, anemia) are seldom responsible for the development of HF in a normal heart; however, in the presence of underlying structural heart disease, these conditions can lead to overt HF.
Rheumatic heart disease remains a major cause of HF in Africa and Asia, especially in the young. Hypertension is an important cause of HF in the African and African-American populations. Chagas' disease is still a major cause of HF in South America. Not surprisingly, anemia is a frequent concomitant factor in HF in many developing nations. As developing nations undergo socioeconomic development, the epidemiology of HF is becoming similar to that of Western Europe and North America, with CAD emerging as the single most common cause of HF. Although the contribution of diabetes mellitus to HF is not well understood, diabetes accelerates atherosclerosis and often is associated with hypertension.
Despite many recent advances in the evaluation and management of HF, the development of symptomatic HF still carries a poor prognosis. Community-based studies indicate that 30–40% of patients die within 1 year of diagnosis and 60–70% die within 5 years, mainly from worsening HF or as a sudden event (probably because of a ventricular arrhythmia). Although it is difficult to predict prognosis in an individual, patients with symptoms at rest [New York Heart Association (NYHA) class IV] have a 30–70% annual mortality rate, whereas patients with symptoms with moderate activity (NYHA class II) have an annual mortality rate of 5–10%. Thus, functional status is an important predictor of patient outcome (Table 234-2).
Table 234-2 New York Heart Association Classification
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