Abstract

The term ‘angina pectoris’, proposed over 200 years ago, is generally considered synonymous with obstructive coronary artery disease (CAD). In recent years, however, it has become apparent that abnormalities of the coronary microcirculation (coronary microvascular dysfunction, CMD) play an additional pathogenic role in the pathogenesis of myocardial ischaemia and angina. Functional and structural mechanisms can affect the physiological function of the coronary microvasculature and lead to myocardial ischaemia in people without CAD. Abnormal dilatory responses of the coronary microvessels, coronary microvascular spasm, and increased extravascular compressive forces have been identified as pathogenic mechanisms.1 The condition characterized by anginal symptoms and evidence of myocardial ischaemia triggered by CMD, in the absence of obstructive CAD, is known as ‘microvascular angina’ (MVA).

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