4.7 Article

Relationship of clinical presentation and calcification of culprit coronary artery stenoses

Journal

ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
Volume 21, Issue 10, Pages 1618-1622

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/hq0901.095554

Keywords

calcinosis; calcium; coronary vessels; ultrasonography, interventional; myocardial infarction

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Coronary artery calcification is increased in the presence of atherosclerosis. However, there is great variability in the calcification of individual coronary stenoses, and the clinical significance of this finding remains unknown. We tested the hypothesis that culprit lesions associated with myocardial infarction or unstable angina are less calcified than are stenoses associated with stable angina. The study consisted of 78 patients who underwent intravascular ultrasound imaging of culprit stenoses after the placement of a stent. Seventeen patients presented with stable angina; 43, with unstable angina; and 18, with myocardial infarction. The extent of coronary calcification was measured by the angle of its are and was quantified with a computer-based protractor. The are of calcium was measured in the stented area at the point of maximal calcification and also as an average of the calcification found at proximal, middle, and distal stent segments. The maximal arc of calcium decreased progressively from patients with stable angina (91 +/- 10 degrees) to those with unstable angina (59 +/-8 degrees) and to those with myocardial infarction (49 +/- 11 degrees, P=0.014). Similarly, the average arc of calcium was greatest (32 +/-7 degrees) in patients with stable angina, less (15 +/-4 degrees) in patients with unstable angina, and least (10 +/-5 degrees) in patients with acute myocardial infarction (P=0.014). These associations remained significant after adjustment for other factors that potentially affect arterial calcification. Acute coronary syndromes are associated with a relative lack of calcium in the culprit stenoses compared with stenoses of patients with stable angina. These findings have implications for the understanding of the biology of acute coronary syndromes as well as for the identification of coronary stenoses by methods that rely solely on the presence of calcium.

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