Angina pectoris

Angina pectoris is intermittent chest pain caused by transient, reversible myocardial ischaemia. It is typically experienced as a crushing central chest pain radiating to the left arm or jaw, although the pain can be perceived in many different ways.

In typical angina, there is fixed narrowing of the coronary arteries and oxygen supply to the heart is inadequate when the work of the heart increases (e.g. during exercise). Pain occurs on exertion and disappears on resting.

Unstable angina (or crescendo angina) refers to pain occurring with progressively less exertion. The attacks are more severe and last longer. It is thought that it is usually caused by a gradually enlarging thrombus growing on a ruptured plaque. Unstable angina may herald irreversible ischaemic injury (i.e. an infarct).

Prinzmetal angina is caused by a coronary spasm and can occur at rest or during sleep. The aetiology is unclear, but it seems to be linked to atherosclerotic disease, at least in some instances.

Sudden cardiac death

Myocardial hypoxia predisposes to the development of arrhythmias, ventricular fibrillation in particular. The consequence can be sudden collapse and death.

Myocardial infarction

Myocardial infarction is usually caused by complete occlusion of a coronary artery by a thrombus overlying a ruptured plaque. The myocardium exhibits coagulative necrosis, but it takes 8 to 12 hours for this to become visible. In experimental animals, electron microscopy demonstrates ultrastructural changes earlier than this, but these changes are of no use in the practical investigation of a sudden death in clinical circumstances. If death occurs within 8 hours of an infarct, the pathologist will probably find no abnormality of the myocardium at autopsy.

Coronary arteries are end-arteries. The ventricular wall is supplied by perforating branches arising from the epicardial coronary arteries. The subendocardial zone is furthest from the blood supply and it is here that critical ischaemia tends to occur first. As the infarct enlarges, it extends further towards the epicardial surface (Figs 3.35.1 and 3.35.2). The exception is a very narrow band of myocardium immediately adjacent to the endocardium that receives enough oxygen to survive from the blood within the ventricle. The area of infarcted muscle depends on the territory supplied by the obstructed artery. No two hearts are exactly the same, but typical regional infarcts tend to occur in the territories shown in Fig. 3.35.3.

Fig. 3.35.1 Longitudinal section of a heart showing an infarct of the left ventricle.