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The key to understanding the mechanisms by which antianginal medications relieve anginal symptoms requires the understanding of the (1) hemodynamic determinants of coronary perfusion and the myocardial oxygen supply/demand relationship; (2) pathophysiologic processes that lead to angina, an established symptom of myocardial ischemia; and (3) the subtypes of angina and their individual and distinct underlying etiologies.

The term “angina pectoris” refers to a clinical symptom characterized by substernal chest pain resulting from inadequate perfusion of the myocardium, leading to myocardial ischemia. Anginal symptoms can therefore be caused by anatomical or functional abnormalities that compromise coronary blood flow within the intravascular space (ie, atherosclerosis), as well as by extravascular factors that disrupt the normal physiologic regulation of coronary circulation and microvascular networks.

Patients with obstructive epicardial coronary artery disease (CAD), the most common cause of angina pectoris, may be further categorized into stable or unstable disease. Stable or chronic angina is defined by predictable and reproducible chest discomfort that arises at a certain level of exertion and is relieved with rest. In contrast, those with unstable or acute angina experience increasing chest discomfort that is more frequent and/or longer in duration compared to prior episodes or have discomfort that occurs even at rest. A sizeable subset of patients with non-occlusive CAD may have anginal symptoms and evidence of myocardial ischemia but angiographically normal or near-normal coronary arteries. In most of these individuals, angina is caused by dysfunction of the coronary microcirculation, termed microvascular angina. Patients with vasospastic angina may similarly present with a benign coronary angiogram, however experience transient angina due to abnormal reactivity and vasospasm of the coronary arteries.

Fundamentals of Antianginal Pharmacotherapy

The current clinical guidelines recommend pharmacologic therapy for control of symptoms prior to intervention for revascularization. Generally, antianginal medications are classified into two groups: (1) first-line agents, consisting of calcium channel blockers, beta-blockers, and short-acting nitrates, and (2) second-line agents, which include ivabradine, ranolazine, and trimetazidine (Figure 175-1). Despite the hierarchical classification of these medications, there is limited scientific evidence that supports the use of first-line agents preferentially over second-line agents. Choice of therapy rests largely on the existence of contraindications to medications within the first tier, poor patient tolerance of first-line agents, or clinician preference.

FIGURE 175-1

Anti-anginal medications categorized into their respective lines of therapy by traditional clinical guidelines.

Pharmacologic medications used in the treatment of stable CAD should serve two broad purposes: (1) prevention of disease progression to myocardial infarction or death and (2) relief of anginal symptoms through mechanisms that address the underlying pathophysiological processes of angina. The paradox of antianginal pharmacotherapy is that antianginal medications recommended by standard clinical guidelines do not retard disease progression or alter prognosis, and medications that are shown to reduce cardiovascular events with demonstrated prognostic benefits ...

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