From the Division of Cardiology (D.S.O., J.S.L., T.S., Y.M., Z.W., I.-K.J.) and Biostatistics Center (H.L.), Massachusetts General Hospital, Harvard Medical School, Boston; Department of Cardiology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan (T.H., H.Y., T.Y, K.O.); and Division of Cardiology, Kyung Hee University, Seoul, South Korea (I.-K.J.).
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Background—Spotty superficial calcium deposits have been implicated in plaque vulnerability based on previous intravascular imaging studies. Biomechanical models suggest that microcalcifications between 5 and 65 µm in diameter can intensify fibrous cap stress, promoting plaque rupture. However, the 100- to 200-µm resolution of intravascular ultrasound limits its ability to discriminate single calcium deposits from clusters of smaller deposits, and a previous optical coherence tomographic investigation evaluated calcifications within a long segment of artery, which may not truly reflect the mechanics involved in potentiating focal plaque rupture.Methods and Results—Detailed optical coherence tomographic assessment of coronary calcification at the culprit plaque (10-mm length) was performed in 53 patients with acute ST-segment–elevation myocardial infarction mediated by plaque rupture and 55 patients with stable angina pectoris. The number and longitudinal length of individual calcium deposits were recorded. Cross-sectional images were analyzed every 1 mm for calcium arc and depth, and these quantitative parameters were used to define individual deposits as spotty, large, and superficial. There was no significant difference between ST-segment–elevation myocardial infarction mediated by plaque rupture and stable angina pectoris groups in the number of total (P=0.58), spotty (P=0.87), or large calcium deposits (P=0.27). Minimum calcium depth was similar between groups (P=0.27), as was the number of superficial deposits (P=0.35 using a 65-µm depth threshold and P=0.84 using a 100-µm depth threshold).Conclusions—The number and pattern of culprit plaque calcifications did not differ between patients presenting with ST-segment–elevation myocardial infarction mediated by plaque rupture versus stable angina pectoris. The optical coherence tomographic assessment of coronary calcification may not be a useful marker of local plaque vulnerability as previously suspected.Registration Information—URL: http://www.clinicaltrials.gov. Unique identifier: NCT01110538.