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The name angina pectoris refers to a strangling or pressure-like pain caused by cardiac ischemia. Angina is the most common condition involving tissue ischemia in which vasodilatordrugs or cardiac depressants are used. The pain may be located substernally, radiating to the neck, in the left upper extremity, occasionally in the right upper extremity, or in the epigastrium. However, not all cardiac ischemia is associated with pain. Clinical conditions exist, such as silent myocardial infarction, in which myocardial ischemia or necrosis may occur without pain. Anginal pain is often atypical in women.

This chapter reviews the pathophysiology of angina and the therapeutic strategies for its treatment. Pharmacologic treatments are divided into vasodilators and cardiac depressants (Figure 8–1). In addition to the drugs discussed in this chapter, patients with angina are often treated with lipid-lowering drugs to minimize additional lipid plaque formation and antithrombotics or anticoagulants to control thrombosis at the site of these plaques. These drugs are discussed in Chapters 11 and 26.

Figure 8–1.

Pharmacologic classes used in the treatment of angina pectoris.

The pharmacologic treatment of coronary insufficiency is based on physiologic factors that control the myocardial oxygen requirement. A major determinant of oxygen requirement is myocardial fiber tension. The higher the tension, the greater the oxygen requirement. Several variables contribute to fiber tension (Figure 8–2).

Figure 8–2.

Determinants of the volume of oxygen required by the heart. Both diastolic and systolic factors contribute to the oxygen requirement; most of these factors are directly influenced by sympathetic discharge.

Among the diastolic factors, venous tone determines the capacity of the venous circulation and controls the amount of blood sequestered there versus the amount returned to the heart. Venous tone is maintained by sympathetic activity and increases when sympathetic activity increases. Venous tone and blood volume together determine preload, and preload is the major diastolic determinant of myocardial oxygen requirement.

The systolic factors include afterload, heart rate, contractility, and ejection time. Afterload is the pressure that the ventricle must overcome to eject blood into the arterial system. Afterload is determined by arterial blood pressure and large artery stiffness. Heart rate contributes to time-integrated fiber tension because at fast heart rates, fibers spend more time contracted at systolic tension levels. Because coronary perfusion is maximal during diastole, faster heart rates lead to decreased myocardial perfusion; that is, faster rates abbreviate the time spent in diastole and decrease myocardial perfusion. Systolic blood pressure and heart rate may be multiplied to yield the double product, a measure of cardiac work and, therefore, of oxygen requirement. In patients with atherosclerotic angina, effective drugs reduce the double product. Force of cardiac contraction is another systolic factor controlled mainly by sympathetic activity to the heart. ...

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