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Heart failure occurs when the cardiac output is inadequate to provide the oxygen needed by the body. Heart failure is a highly lethal condition, with a 5-year mortality rate conventionally said to be about 50%. In systolic failure, cardiac contractility and the ejection fraction of the heart are reduced. In diastolic failure, stiffening and loss of adequate relaxation plays a major role in reducing cardiac output, although the ejection fraction may be normal. Because other cardiovascular conditions such as myocardial infarction are now being treated more effectively, more patients are surviving long enough to develop heart failure. Thus, heart failure is increasing in prevalence. Although research suggests that the primary defect in early heart failure resides in the excitation-contraction coupling machinery of the heart, the clinical condition also involves many other processes and organs, including the baroreceptor reflex, the sympathetic nervous system, the kidneys, angiotensin II and other peptides, and death of cardiac cells. The most common cause of heart failure in the United States is coronary artery disease.

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This chapter reviews normal cardiac contractility and the pathophysiology and major clinical manifestations of heart failure. Drugs used to treat heart failure include positive inotropic agents, vasodilators, diuretics, and several miscellaneous drug classes (Figure 9–1). The positive inotropic agents increase the contractility of the heart, whereas the vasodilators and miscellaneous drugs have effects at both cardiac and noncardiac sites. Several drugs acting at noncardiac sites, such as the vasculature, kidneys, and central nervous system, have been discussed in Chapters 6, 7, and 8.

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Figure 9–1.
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Drugs used in the treatment of heart failure. Several pharmacologic classes have a combination of physiologic effects and do not fall into a single category. ACE = angiotensin-converting enzyme inhibitors; PDE = phosphodiesterase. Spironolactone is a potassium-sparing diuretic that inhibits the aldosteronereceptor in the collecting tubules of the kidney and nonrenal tissue sites.

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The force of contraction of heart muscle is determined by several processes that lead to the movement of actin and myosin filaments in the cardiac sarcomere (Figure 9–2). During systole, contraction results from the interaction of calcium with the actin-troponin-tropomyosin system, thereby releasing the actin-myosin interaction from inhibition. The calcium involved in this interaction is released from the sarcoplasmic reticulum (SR). The amount released depends on the amount stored in the SR and on the amount of trigger calcium that enters the cell during the action potential.

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Figure 9–2.
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Schematic diagram of a cardiac muscle sarcomere, with the sites of action of several drug classes that alter contractility (numbered structures). Site 1 is Na+/K+–ATPase, the sodium pump. Site 2 is the Na-Ca2+ exchanger. Site 3 is the voltage-gated calcium channel. Site 4 is a calcium transporter that pumps ...

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