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  • Title: [Calcification in culprit lesions of coronary artery disease].
    Author: Wada A, Yamanaka O, Yamagami S, Hayashi Y, Nakayama R, Kanoh T.
    Journal: J Cardiol; 2000 Jan; 35(1):27-32. PubMed ID: 10654247.
    Abstract:
    Coronary calcification, a type of coronary atherosclerosis, has recently been closely examined in clinical cardiology because its presence may influence the selection of interventional therapy. In addition, plaque instability is one of the most important factors in the mechanism of acute coronary syndrome, and calcium deposit is frequently detected in advanced lesions. However, little is known about the clinical significance of coronary calcification. The incidence of calcium deposits was investigated in the culprit lesions (culprit coronary calcification) of patients with serious coronary artery disease to discover any cardioprotective effect. Initial coronary angiography was performed in 179 consecutive patients with acute myocardial infarction with Q wave on electrocardiography (AMI group; male 139, female 40, mean age 60.2 +/- 10 yr) and in 119 consecutive patients with stable effort angina pectoris (SAP group; male 78, female 41, mean age 63.8 +/- 8 yr) for which balloon plasty or bypass surgery was necessary from 1990 to 1997. Culprit coronary calcification was defined positive if the calcification deposit was present cinefluoroscopically within 5 mm from the culprit point. The culprit point was defined as the narrowest point after successful intracoronary thrombolytic therapy or the latest point to be dilated during a balloon inflation in direct or rescue percutaneous transluminal coronary angioplasty in the AMI group, and the narrowest point of the culprit lesion in the SAP group. There was no statistical difference in clinical background between the 2 groups other than male dominance in the AMI group and high incidence of family history of ischemic heart disease in the SAP group (p < 0.05). Culprit coronary calcification in patients over 50 years old was less frequently positive in the AMI group than the SAP group (26% vs 66%, p < 0.005, respectively). In younger patients under 50 years old, the incidence of culprit coronary calcification was low (14-15%) in both groups. Culprit coronary calcification was frequently positive in the right or the left anterior descending coronary artery in the SAP group (p < 0.005). There was no incidental sex difference of culprit coronary calcification. This comparison suggests that if a plaque contains cinefluoroscopically visible calcification, it may be regarded as less vulnerable or having a history of chronic process of atherosclerosis which results in protecting plaque rupture.
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