Angina pectoris is an episodic pain or crushing and/or squeezing sensation in the chest caused by reversible myocardial ischaemia. The discomfort may radiate into the neck, jaw and arms (particularly the left) and, more rarely, into the back. Other common symptoms include shortness of breath, abdominal pain and dizziness. Syncope (unconsciousness) occurs infrequently. Ischaemia can produce classic angina or may be totally silent without any symptoms. The clinical outlook from silent ischaemia is similar to symptomatic angina.

Three forms of angina are recognized. Stable and variant angina are discussed below, and unstable angina is described in Chapter 42.

Pathophysiology

Figure 40 shows the factors that determine myocardial O₂ supply and demand. O₂ demand is determined by heart rate, left ventricular contractility and systolic wall stress, and therefore increases with exercise, hypertension and left ventricular dilatation (e.g. during chronic heart failure). Myocardial O₂ supply is primarily determined by coronary blood flow and coronary vascular resistance, which mostly occurs at the level of the intramyocardial arterioles. With exercise the coronary blood flow can increase to four to six times baseline, which is the normal coronary flow reserve (see Chapter 23).

Stable or exertional (typical) angina arises when the flow reserve of one or more coronary arteries is limited by a significant structural stenosis (>70%) resulting from atherosclerotic coronary heart disease. Stenoses typically develop in the epicardial region of arteries, within 6 cm of the aorta. Under resting conditions, cardiac O₂ demand is low enough to be satisfied even by a diminished coronary flow. However, when exertion or emotional stress increases myocardial O₂ demand, dilatation of the non-diseased areas of the artery cannot increase the supply of blood to the heart because the stenosis presents a fixed non-dilating obstruction. The resulting imbalance between myocardial O₂ demand and supply causes myocardial ischaemia. Ischaemia develops mainly in the subendocardium, the inner part of the myocardial wall. This is because the blood flow to the left ventricular wall occurs mainly during diastole as a result of arteriolar compression during systole. The arterioles of the subendocardium are compressed more than those of the mid- or subepicardial layers, so that the subendocardium is most vulnerable to a relative lack of O₂.

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