Angina pectoris is pain that occurs in the chest region during ischemic heart disease. Attacks of angina pectoris begin suddenly and are often described as a sensation of intense compression and tightness in the retrosternal region, with pain sometimes radiating to the jaw or left arm. In many patients, episodes of angina pectoris are precipitated by physical exertion often called “stable angina.” Some forms of angina may occur spontaneously even when the patient is at rest or asleep called “variant angina” or “unstable angina.” Variant angina, also called Prinzmetal angina, is a result of coronary artery vasospasm. Unstable angina is a result of ischemia due to sudden rupture of atherosclerotic plaque in coronary arteries and is a precursor to a myocardial infarction. This latter type of angina is considered urgent, requiring medical intervention.
The problem in angina pectoris is that the supply of oxygen to the heart is insufficient to meet myocardial demands at a given point in time, which results in an imbalance between myocardial oxygen supply and demand (Fig. 22-1).1,2 This imbalance leads to myocardial ischemia, which results in several metabolic, electrophysiological, and contractile changes in the heart. The painful symptoms inherent to angina pectoris seem to result from the accumulation of metabolic by-products such as lactic acid. Presumably, these metabolic by-products act as nociceptive substances and trigger the painful compressive sensations characteristic of angina pectoris.
Myocardial ischemia equation. (Adapted from: Miller AB. Mixed ischemic subsets. Comparison of the mechanism of silent ischemia and mixed angina. Am J Med. 1985;79 [suppl 3a]:25, with permission.)
Although angina pectoris is believed to be caused by the buildup of lactic acid and other metabolites, the exact mechanisms responsible for mediating anginal pain remain unknown. Also, the patient’s emotional state and other factors that influence central pain perception play a role in angina pectoris.3 In fact, the majority of anginal attacks may be silent in many patients, and myocardial ischemia may frequently occur without producing any symptoms.3,4 Certain patients may also exhibit symptoms of angina even though their coronary arteries appear to be normal and there is no obvious obstruction to coronary blood flow.2 Clearly, there is much information regarding the nature of angina pectoris still remaining to be clarified.
Considering the prevalence of ischemic heart disease in the United States, many patients receiving physical therapy and occupational therapy may suffer from angina pectoris. These patients may be undergoing rehabilitation for a variety of clinical disorders, including (but not limited to) coronary artery disease. This chapter describes the primary drug groups used to treat angina pectoris, as well as the pharmacological management of specific forms of angina. You should be aware of the manner in which these drugs work and the ways in which antianginal drugs can influence patient performance in rehabilitation sessions.