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Angina pectoris, the primary symptom of ischemic heart disease, is caused by transient episodes of myocardial ischemia that are due to an imbalance in the myocardial oxygen supply–demand relationship that may be caused by an increase in myocardial oxygen demand or by a decrease in myocardial oxygen supply or sometimes by both (Figure 27–1). Typical angina is experienced as a heavy, pressing substernal discomfort (rarely described as a "pain"), often radiating to the left shoulder, flexor aspect of the left arm, jaw, or epigastrium. However, a significant minority of patients note discomfort in a different location or of a different character. Myocardial ischemia also may be silent, with electrocardiographic, echocardiographic, or radionuclide evidence of ischemia appearing in the absence of symptoms.

Figure 27–1

Pharmacological modification of the major determinants of myocardial O2 supply. When myocardial O2 requirements exceed O2 supply, an ischemic episode results. This figure shows the primary hemodynamic sites of actions of pharmacological agents that can reduce O2 demand (left side) or enhance O2 supply (right side). Some classes of agents have multiple effects. Stents, angioplasty, and coronary bypass surgery are mechanical interventions that increase O2 supply. Both pharmacotherapy and mechanotherapy attempt to restore a dynamic balance between O2 demand and O2 supply.

This section describes the principal pharmacological agents used in the treatment of angina: nitrovasodilators, β adrenergic receptor antagonists, and Ca2+ channel antagonists. These anti-anginal agents improve the balance of myocardial O2 supply and O2 demand, increasing supply by dilating the coronary vasculature and/or decreasing demand by reducing cardiac work (see Figure 27–1).

Drugs used in typical angina function principally by reducing myocardial O2 demand by decreasing heart rate, myocardial contractility, and/or ventricular wall stress. By contrast, the principal therapeutic goal in unstable angina is to increase myocardial blood flow; strategies include the use of antiplatelet agents and heparin to reduce intracoronary thrombosis, often accompanied by efforts to restore flow by mechanical means, including percutaneous coronary interventions using coronary stents, or (less commonly) emergency coronary bypass surgery. The principal therapeutic aim in variant or Prinzmetal angina is to prevent coronary vasospasm.


These agents are prodrugs that are sources of nitric oxide (NO) (Table 27–1).

Table 27–1Organic Nitrates

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