Daniel S Ong1, Jay S Lee1, Tsunenari Soeda1, Takumi Higuma1, Yoshiyasu Minami1, Zhao Wang1, Hang Lee1, Hiroaki Yokoyama1, Takashi Yokota1, Ken Okumura1, Ik-Kyung Jang2. 1. 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.). 2. 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.). ijang@mgh.harvard.edu.
Abstract
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.
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.
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