Management of Heart Failure

Heart failure is a complex syndrome physiologically characterized as low cardiac output leading to inadequate blood supply of tissues and vital organs. No matter the etiology, damage to the cardiocytes starts a complicated neurohormonal cascade that causes poor renal perfusion, leading to stimulation of the renin–angiotensin–aldosterone system and elevated levels of circulating catecholamines. These compensatory mechanisms lead to sodium and water retention and tachycardia that may cause pulmonary, hepatic, and splenic congestion, as well as peripheral and splanchnic bed constriction. The patient may experience symptoms such as dyspnea on exertion, lower extremity edema, early satiety, paroxysmal nocturnal dyspnea, fatigue, dizziness, and/or syncope. Heart failure is a serious public health concern in the United States and other industrialized countries. It continues to increase in incidence and prevalence, with a prevalence of 5 million Americans having the syndrome in 2003 and with an incidence 550,000 new persons diagnosed annually (1). These derangements lead to frequent hospitalizations, totaling 1,093,000 hospital discharges (2) and 3.4 million visits to physicians, emergency departments, and hospital outpatient departments annually (3). The mortality rate remains high despite complex and expensive medical regimens, with selfassessment of the patient’s quality of life rated as poor. The Framingham Heart Study now has 44 years of follow-up and, based upon these data, heart failure incidence approaches 10 per 1,000 population after age 65 (1). The lifetime risk for development of symptomatic heart failure is one in five for both men and women (4). The lifetime risk for heart failure is doubled for both sexes with blood pressure greater than or equal to 160/100 mm Hg compared to those without hypertension. Thus, given current demographics, cases of heart failure are predicted to continue to rise. Risk factors for heart failure continue to include hypertension, with 75% of heart failure cases having antecedent hypertension (1). About 22% of male and 46% of female victims of myocardial infarction (MI) will become disabled with heart failure within 6 years of the MI (1). Diabetes mellitus is another significant risk factor for heart failure. In women with coronary heart disease, diabetes mellitus was found to be the strongest risk factor for the development of heart failure. Additionally, in this study, those with an elevated body mass index or depressed creatinine (Cr) clearance in diabetic women were noted to be at highest risk, with annual incidence rates of 7% and 13%, respectively (5). In another study of patients with heart failure, African American women with elevated body mass index and pre-existing hypertension were the cohort with the highest risk for the development of heart failure (6). With regard to mortality, deaths from heart failure based on the International Classification of Disease (Code 428) increased 20.5% from 1993 to 2003. In 2003, the overall death rate for heart failure was 19.1%. Examined by race and gender, death rates were 20.3% for Caucasian males, 22.9% for African American males, 18.3% for Caucasian females, and 19.0% for African American females. Heart failure discharges from hospitals were 1,093,000 in 2003. Heart failure is a syndrome with diverse etiologies, anatomies, and physiologic presentations. The World Health Organization developed classification nomenclature for the cardiomyopathies. This nomenclature is based on anatomic and physiologic findings: restrictive, hypertrophic, and dilated. This chapter focuses on the dilated cardiomyopathies. The myocardial muscle disease causing dilated cardiomyopathy may be either a primary cardiocyte disorder or secondary to another disease process. Whether primary or secondary, the hallmark findings of dilated cardiomyopathy are a dilated left ventricle and a low left ventricular ejection fraction. The most common etiology of dilated cardiomyopathy (DCM) is secondary to ischemic heart disease. Ischemic cardiomyopathy accounts for nearly half of all cases of DCM in the United States. All the remaining dilated cardiomyopathies are considered primary muscle diseases. Although 75% of patients diagnosed with heart failure have antecedent hypertension, only about 22% of patients with DCM have hypertension as the only identifiable etiology (1). Nearly 25% of patients with dilated cardiomyopathy have no pre-existing risk factors for DCM and are given the diagnosis of idiopathic dilated cardiomyopathy. Nearly 25% of patients with idiopathic dilated cardiomyopathy have a familial component, likely related to abnormalities in cardiac βadrenergic receptors (7). Once the common etiologies are excluded, a small but important number of other causes remains, including DCM secondary to toxins such as alcohol, anthracyclines, and cocaine. Endocrine diseases such as diabetes mellitus and thyroid disease may also cause heart failure. Other possible etiologies include human immunodeficiency virus (HIV) and Lyme disease infections, sarcoidosis, thiamine deficiency, peripartum cardiomyopathy, hemochromatosis, and underlying collagen vascular diseases.