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Congestive heart failure (CHF) is responsible for more than half a million deaths annually in the U.S., carries a 1-year mortality rate of more than 50% in patients with advanced forms of the condition. Substantive advances in CHF pharmacotherapy have altered clinical practice by shifting the paradigm of its management from exclusively symptom palliation to modification of disease progression and prolonged survival.

DEFINING CONGESTIVE HEART FAILURE. The onset and progression of clinically evident CHF from left ventricular (LV) systolic dysfunction follows a pathophysiologic sequence in response to an initial insult to myocardial dysfunction. A reduction in forward cardiac output leads to expanded activation of the sympathetic nervous system and the renin–angiotensin–aldosterone axis that, together, maintain perfusion of vital organs by increasing LV preload, stimulating myocardial contractility, and increasing arterial tone. Acutely, these mechanisms sustain cardiac output by allowing the heart to operate at elevated end-diastolic volumes, while peripheral vasoconstriction promotes regional redistribution of the cardiac output to the CNS, coronary, and renal vascular beds.

Unfortunately, these compensatory mechanisms over time propagate disease progression. Intravascular volume expansion increases diastolic and systolic wall stress that disrupts myocardial energetics and causes pathologic LV hypertrophy. By increasing LV afterload, peripheral arterial vasoconstriction also adversely affects diastolic ventricular wall stress, thereby increasing myocardial O2 demand. Finally, neurohumoral effectors such as NE and AngII are associated with myocyte apoptosis, abnormal myocyte gene expression, and pathologic changes in the extracellular matrix that increase LV stiffness.

Clinically, the term CHF describes a final common pathway for the expression of myocardial dysfunction. While some emphasize the clinical distinction between systolic versus diastolic heart failure, many patients demonstrate dysfunction in both contractile performance and ventricular relaxation/filling. Indeed, these physiologic processes are interrelated; for example, the rate and duration of LV diastolic filling are directly influenced by impairment in systolic contractile performance. The following definitions are useful for establishing a conceptual framework to describe this clinical syndrome:

Congestive heart failure is the pathophysiologic state in which the heart is unable to pump blood at a rate commensurate with the requirements of metabolizing tissues, or can do so only from an elevated filling pressure.

Heart failure is a complex of symptoms—fatigue, shortness of breath, and congestion—that are related to the inadequate perfusion of tissue during exertion and often to the retention of fluid. Its primary cause is an impairment of the heart's ability to fill or empty the left ventricle properly.

One may consider CHF as a condition in which failure of the heart to provide adequate forward output at normal end-diastolic filling pressures results in a clinical syndrome of decreased exercise tolerance with pulmonary and systemic venous congestion. Numerous cardiovascular comorbidities are associated with CHF, including coronary artery disease, MI, and sudden cardiac death.


The abnormalities of myocardial structure and ...

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