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Circ J. 2013;77(10):2573-7. Epub 2013 Jun 19.

Regression of luminal stenosis at the site of silent plaque disruption in the era of optimal medical therapy. Low high-density lipoprotein cholesterol level isa potential risk of stenosis progression.

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Cardiovascular Division, Osaka Police Hospital.



Plaque disruption and its healing is thought to be the major mechanism of atherosclerosis, but the contribution of silent plaque disruption to luminal stenosis progression has not been fully clarified. The aim of this study was therefore to examine the change in luminal stenosis at the site of silent plaque disruption.


Consecutive patients (n=36) who received coronary angiography and angioscopy that identified silent plaque disruption (baseline) and had repeated coronary angiography later (follow-up) were included for analysis. Silent plaque disruption was defined as plaque with thrombus detected in non-culprit segments. Diameter stenosis of the site was angiographically measured at baseline and at follow-up, and their difference was defined as stenosis change. Statin was used in 89% of study patients, and serum low-density lipoprotein cholesterol level was 91 ± 21 mg/dl. The diameter stenosis decreased significantly from baseline to follow-up at 12 ± 4 months (32 ± 14% vs. 27 ± 14%, P<0.001), and the stenosis change was -5.6 ± 7.9%. High-density lipoprotein cholesterol (HDL-C) was significantly associated with stenosis change (r=-0.51, P=0.001) and was the only factor significantly associated with stenosis change.


In the era of optimal medical therapy with statin, the site of silent plaque disruption showed significant regression of luminal stenosis. Nevertheless, serum HDL-C was inversely associated with stenosis change, and its low level remained as a potential risk of luminal stenosis progression at the site of silent plaque disruption. 

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