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. 2008 Jun;19(4):237-42.
doi: 10.1097/MCA.0b013e32830042a8.

Association of statin therapy with reduced coronary plaque rupture: an optical coherence tomography study

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Association of statin therapy with reduced coronary plaque rupture: an optical coherence tomography study

Stanley Chia et al. Coron Artery Dis. 2008 Jun.

Abstract

Objective: Statin therapy induces plaque regression and may stabilize atheromatous plaques. Optical coherence tomography (OCT) is a high-resolution in-vivo imaging modality that allows characterization of atherosclerotic plaques. We aimed to demonstrate the potential utility of OCT in evaluating coronary plaques in patients with or without statin therapy.

Methods: Patients undergoing cardiac catheterization were enrolled. We identified culprit lesions and performed intracoronary OCT imaging. Plaque lipid pool, fibrous cap thickness, and frequency of thin-cap fibroatheroma were evaluated using previously validated criteria. Macrophage density was determined from optical signals within fibrous caps. Presence of calcification, thrombosis, and rupture was assessed.

Results: Forty-eight patients were included (26 on statins, 22 without statins). Baseline characteristics were similar apart from lipid profile. Patients on statin therapy had lower total and low-density lipoprotein cholesterol concentrations (4.45+/-1.35 vs. 5.26+/-0.83 mmol/l, P=0.02; 2.23+/-0.78 vs. 3.26+/-0.62 mmol/l, P<0.001, respectively). Frequencies of lipid-rich plaque (69 vs. 82%), thin-cap fibroatheroma (31 vs. 50%), plaque calcification (15 vs. 5%) and thrombosis (15 vs. 32%), and fibrous cap macrophage density were comparable between statin and nonstatin groups (5.9 vs. 6.3%; all P=NS). Ruptured plaques were, however, significantly less frequent in patients on established statin therapy (8 vs. 36%; P=0.03) with a trend toward increased minimum fibrous cap thickness (78 vs. 49 microm; P=0.07).

Conclusion: We demonstrated the use of OCT in plaque characterization and found that patients on prior statin therapy have reduced incidence of ruptured plaques and a trend toward thicker fibrous caps. This suggests that statins may stabilize coronary plaques.

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Figures

Fig. 1
Fig. 1
In-vivo optical coherence tomography image of a ruptured coronary plaque. Ruptured plaque (RP) is seen in this patient with severe disruption of plaque fibrous cap at the 6 o’clock position. Adherent thrombus (Thr) is also observed at 1 o’clock position. Guidewire artifact is represented by GW.
Fig. 2
Fig. 2
Minimum fibrous cap thickness in (a) patients with or without statin therapy; and (b) ruptured and nonruptured coronary plaques. A trend was observed toward increased fibrous cap thickness in patients with established statin therapy (*P = 0.07) that was also detected in nonruptured plaques (**P = 0.06). Fibrous cap thickness was measured at the thinnest part for all images with an optical coherence tomography-determined lipid pool. Median ± interquartile range.

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