ObjectivePrevious studies have indicated that statin therapy may promote plaque regression. However, the impact of statin therapy on plaque composition has not been clearly elucidated. We performed a meta-analysis to investigate the effect of statin therapy on coronary plaque composition as assessed by virtual histology intravascular ultrasound (VH-IVUS).MethodsOnline databases were searched from inception to March 1, 2015. Studies providing VH-IVUS volumetric analyses of coronary plaque composition at baseline and follow-up in patients receiving statin therapy were included. Weighted mean difference (WMD) using a random-effects model was used.ResultsTen studies involving 682 patients were included. There was a substantial reduction in fibrous volume between baseline and follow-up (WMD: -2.37 mm3, 95% confidence interval (CI) -4.01 to -0.74 mm3, P=0.004), and a significant increase in dense calcium (DC) volume (WMD: 0.89 mm3, 95% CI 0.70 to 1.08 mm3, P<0.00001). No significant change was seen in fibro-fatty and necrotic core (NC) volumes. In stratified analyses, the fibrous volume was decreased significantly (WMD: -3.39 mm3, 95% CI -6.56 to -0.21 mm3, P=0.04) and the absolute DC volume (WMD: 0.99 mm3, 95% CI 0.23 to 1.76 mm3, P=0.01) was increased in the subgroup with ≥12 months follow-up, whereas no significant change was observed in the subgroup with < 12 months follow-up. Similarly, a substantial decrease in fibrous volume (WMD: -2.01 mm3, 95% CI -3.05 to -0.96 mm3, P< 0.0002) and an increase in DC volume (WMD: 0.90 mm3, 95% CI 0.70 to 1.10 mm3, P< 0.00001) were observed in the subgroup with high-intensive statin therapy, while the change in fibrous and DC volumes approached statistical significance (P=0.05 and P=0.05, respectively) in the subgroup with low-intensive statin therapy.ConclusionsStatin treatment, particularly of high-intensity and long-term duration, induced a marked modification in coronary plaque composition including a decrease in fibrous tissue and an increase in DC.
Statin therapy induced a significant increase in coronary FCT evaluated by OCT. This increase in FCT was independent of traditional coronary risk factors including the lipid profile.
ObjectiveAlthough the plaque characteristics have been recognized in patients with acute myocardial infarction (AMI), the plaque spatial distribution is not well clarified. Using color-mapping intravascular ultrasound (iMAP-IVUS), we examined culprit lesions to clarify plaque morphology, composition and spatial distribution of the sites of potential vulnerability.MethodsSixty-eight culprit lesions in 64 consecutive AMI patients who underwent angiography and IVUS examinations before intervention were analyzed. Plaque morphology and composition were quantified with iMAP-IVUS. The spatial distribution of the sites of potential vulnerability was assessed with longitudinal reconstruction of the consecutive IVUS images. The plaque characteristics were also compared between ruptured and non-ruptured lesions, and between totally occlusive (TO) and non-TO lesions.ResultsThe sites with maximum necrotic area (maxNA), maximum plaque burden (maxPB) and most severely narrowed (minimal luminal area, MLA) were recognized vulnerability. In the majority of cases, maxNA sites were proximal to the maxPB sites, and MLA sites were distal to the maxNA and maxPB sites. Ruptures usually occurred close to maxNA sites and proximal to maxPB and MLA sites. The average distance from the site of rupture to the maxNA site was 0.33 ± 4.04 mm. Ruptured lesions showed significant vessel remodeling, greater plaque volume, and greater lipidic volume compared to those of non-ruptured lesions. Both the length and plaque burden (PB) of TO lesions were greater than those of non-TO lesions.ConclusionsInstead of overlapping on maxPB sites, most maxNA sites are proximal to the maxPB sites and are the sites most likely to rupture. Plaque morphology and composition play critical roles in plaque rupture and coronary occlusion.
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