Treatment of Chronic Heart Failure

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Abstract

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Citation
US Cardiology, 2006;3(1):1-5

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Chronic heart failure (CHF) is a major public health problem in industrialized societies, with an incidence approaching 10 per 1,000 population after age 65 and an age-dependent prevalence of less than 1% between ages 45 and 55, 2-5% between ages 65 and 75, and approximately 10% for patients aged 80 years or more.1-3 Thus, HF is primarily a condition of the elderly, and approximately 80% of patients hospitalized with HF are more than 65 years old. Underlying causes are numerous and include cardiac brady- or tachyarrhythmias, systolic dysfunction due to coronary artery disease, dilated cardiomyopathy, or myocarditis, as well as diastolic dysfunction due to hypertension, pericardial disease, or restrictive cardiomyopathy, and finally volume or pressure overload due to valvular heart disease, cardiac defects, hypertrophic obstructive cardiomyopathy, and arterial or pulmonary hypertension.

HF is a complex clinical syndrome characterized by the inability of the heart to provide the cardiac output needed by the organism at normal end-diastolic ventricular pressures. Ventricular dysfunction limits exercise tolerance and may impair the quality of life of affected individuals. Clinically, forward failure of the heart leads to low blood pressure and fatigue, while backward failure results in dyspnea and fluid retention, which may lead to pulmonary congestion, pleural effusions, and peripheral edema, as well as impairment of hepatic, gastric, and renal function. Complications of HF include thromboembolic events, arrhythmias, pulmonary edema, cardiogenic shock, and death. Diagnosis of HF is based on history, physical examination, and echocardiography, while additional tests such as 12-lead electrocardiogram, chest radiography, cardiac magnetic resonance imaging, cardiac catheterization, and laboratory testing including brain natriuretic peptide (BNP) levels can provide useful information about the etiology, severity, and prognosis.

In general, HF is a progressive process in which predisposing conditions eventually lead to structural heart damage and asymptomatic ventricular dysfunction before the development of overt HF with clinical symptoms. The hallmark of this progression is cardiac remodeling with changes in left-ventricular geometry and structure that decrease mechanical performance, increase wall stress, and augment atrioventricular regurgitation. Pathophysiologically, major contribution to cardiac remodeling and thereby to the progression of HF stems from the activation of endogenous neurohormonal systems with elevated plasma and/or tissue levels of norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and various cytokines.

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