CORONARY ARTERY SPASM

Abstract

INTRODUCTIONIt is now well over 100 years since Latham1 postulated coronary artery spasm as a mechanism for angina pectoris. In 1889, Huchard2 suggested that coronary spasm, superimposed on organic lesions, might explain some aspects of ischaemic heart disease. However, in the 1930s and 40s demonstration of coronary atherosclerosis in pathological specimens led to the concept of obstructive atheroma as the basis for anginal syndromes. In the late 1950s Prinzmetal repopularised Huchard's concept of spasm superimposed on an organic lesion as a basis for angina in some clinical settings (Prinzmetal's variant angina).3 He reported that pain only came on with the subject at rest, or during routine daily activity, rather than with effort. This form of angina is associated with ST segment elevation on the electrocardiogram, rather than with the more usually noted ST depression. Three decades after Prinzmetal described this variant form of angina, there are still doubts about its causation and prevalence.