Angina pectoris is a symptom of myocardial ischemia, oc-curring when the requirement for oxygen by either ventricle exceeds its supply. The most common underlying disease is atherosclerotic coronary artery disease, although occasionally angina occurs secondary to other entities, such as hypertrophic cardiomyopathy, aortic stenosis, and coronary arteritis.

The major determinants of myocardial oxygen demand in-elude heart rate, contractility, and ventricular wall tension, a function of ventricular volume and intraventricular pressure. An increase in one or more of these determinants--as might occur with exercise, emotional stress, or other states of heightened adrenergic activity--triggers an increase in myocar-dial oxygen demand, and myocardial ischemia results unless myocardial oxygen supply rises proportionately.

Myocardial oxygen supply is governed by coronary blood flow and the ability of the myocardium to extract oxygen from the blood delivered to it. Unlike other organs, the heart al-ways extracts oxygen with near maximal efficiency from the blood, even under situations of minimal demand, so there is little potential for enhanced oxygen extraction to counter in-creased oxygen demands. Coronary blood flow, on the other hand, can increase several-fold in normal subjects as a result of coronary arterial vasodilation, most importantly at the arterio-lar level, triggered by the local build-up of lactate, adenosine, and other vasoactive substances as myocardial oxygen demands increase.

In the presence of obstructive coronary artery disease, myocardial ischemia may result when the coronary arterial stenosis prevents autoregulatory vasodilation so that coronary blood flow can no longer increase proportional to rising oxygen demands. In other situations, myocardial ischemia may occur when oxygen demands are constant but there is a primary de-crease in coronary blood flow mediated via 1.coronary artery spasm, 2. rapid evolution of the underlying atherosclerotic plaque (plaque disruption) leading to a reduced coronary arte-rial lumen caliber, and/or 3.intermittent microvascular plug-ging by platelet aggregates.

In some patients with exertional angina, ischemia is pri-marily a manifestation of increased oxygen demands in the face of fixed coronary blood flow, whereas in patients with primary vasospastic angina, ischemia results when coronary artery spasm causes blood flow to diminish in the face of stable oxy-gen demands. However, many, if not most, patients fall be-tween these two extremes, experiencing angina as a result of both heightened oxygen demands and diminished supply, and are said to have mixed angina.

Angina is but one manifestation of myocardial ischemia. Ischemia typically begins in the subendocardium, where wall tension is high and compressive forces limit coronary microvas-cular flow, and then spreads like a wavefront toward the epi-cardium. The electrocardiogram often depicts ST-segment de-pression or T-wave inversion as manifestations of subendocar-dial ischemia but may show ST-segment elevation (injury cur-rent) if ischemia is prolonged and extends transmurally. These electrocardiographic changes may occur without typical anginal symptoms, a condition termed silent ischemia.

Segmental left ventricular contraction abnormalities occur in the region of the myocardium served by the coronary arterial branches distal to the stenosis responsible for the ischemia (the culpirt lesion), and, if about 10 per cent or more of the my-0cardium is rendered ischemic, a reduction in global function of the left ventricle may be detectable. In addition to abnormal systolic function during ischemia, increased diastolic stiffness of the left ventricle manifests by a rising left ventricular end-diastolic pressure and rising pulmonary venous pressure. Con-sequently, transient clinical evidence of left ventricular failure may occur during episodic ischemia and may explain why many patients describe their angina not as pain but as a feeling of "breathlessness" or "chest tightness".

It is prognostically and clinically useful to classify anginal syndromes into stable and unstable categories. Unstable angina refers to angina of recent onset (within 2 months) or angina that has begun to intensify or to occur at rest or with a lower level of exertion within the previous 2 months. Stable angina, as the name implies, describes a relatively constant pattern of pain with regard to its severity and precipitating factors within the recent months. Some authorities classify angina of recent onset as "stable angina" if it is precipitated by moderate or se-vere levels of exertion and maintains a constant threshold over time, because "stable angina" has to begin at some point in time.

Of patients with unstable angina, up to 20 per cent progress to acute myocardial infarction within the next 3 months. Coronary angiography and angioscopy reveal that more than 50 per cent of patients with unstable angina have multivessel disease with eccentric, irregular, or ulcerated atherosclerotic lesions associated with endothelial disruption and adherent thrombus. Left main coronary artery disease oc-curs in about 10 per cent of patients with unstable angina; It is likely that unstable angina represents a point on a continuum between stable exertional angina and acute myocardial infarc-tion.

Variant angina, originally described by Printzmetal, is characterized by rest pain accompanied by transient ST-seg-ment changes (often ST elevation resembling acute myocardial infarction, although ST depression can also occur) and ventric-ular arrhythmias. Variant angina is a form of unstable angina caused by coronary arterial spasm, usually within a coronary artery narrowed by plaque, but occasionally within an angio-graphically normal appearing artery.

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