Dataset Information

Effect of statin therapy on the progression of coronary atherosclerosis.

ABSTRACT:

Background

An increasing number of authors employing intravascular ultrasound (IVUS) and virtual histology (VH-IVUS) have investigated the effect of statin use on plaque volume (PV) and plaque composition. However, inconsistent results have been reported. Therefore, we conducted a meta-analysis to determine the appropriate regimen of statins to effectively stabilize vulnerable coronary plaques.

Methods

Online electronic databases were carefully searched for all relevant studies. We compared mean values of PV and plaque composition between baseline and follow-up in patients receiving statin therapy. We pooled treatment effects and calculated mean differences (MD) with the 95% confidence interval (CI) using a random-effects model. By stratified analyses, we explored the influence of clinical presentation, dose and duration of statin treatment, and low-density lipoprotein-cholesterol (LDL-C) levels on the effects of statins.

Results

Seventeen studies involving 2,171 patients were analyzed. Statin therapy significantly decreased PV (-5.3 mm(3); 95% CI: -3.3 mm(3) to -7.2 mm(3) P < 0.001), without heterogeneity. When considering the dose and duration of statins used, only subgroups employing a high dose and long duration demonstrated a significant reduction in PV (p < 0.001). A significant decrease in PV was noted if achieved LDL-C levels were <100 mg/dL (p < 0.001). Statin treatment could induce a twofold decrease in PV in patients with acute coronary syndrome (ACS) compared with that observed in patients with stable angina pectoris (SAP). A regressive trend was seen for necrotic core volume (MD: -2.1 mm(3); 95% CI: -4.7 mm(3) to 0.5 mm(3), P = 0.11). However, statin use did not induce a significant change for fibrotic, fibro-fatty, or dense calcium compositions.

Conclusions

Our meta-analysis demonstrated that statin therapy (especially that involving a high dose and long duration and achieving <100 mg/dL LDL-C levels) can significantly decrease PV in patients with SAP or ACS. These data suggested that statins can be used to reduce the atheroma burden for secondary prevention by appropriately selecting the statin regimen. No significant change in plaque composition was seen after statin therapy.

SUBMITTER: Tian J

PROVIDER: S-EPMC3468364 | biostudies-literature | 2012 Sep

REPOSITORIES: biostudies-literature

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Publications

Effect of statin therapy on the progression of coronary atherosclerosis.

Tian Jinwei J Gu Xia X Sun Yanli Y Ban Xiang X Xiao Yun Y Hu Sining S Yu Bo B

BMC cardiovascular disorders 20120901

<h4>Background</h4>An increasing number of authors employing intravascular ultrasound (IVUS) and virtual histology (VH-IVUS) have investigated the effect of statin use on plaque volume (PV) and plaque composition. However, inconsistent results have been reported. Therefore, we conducted a meta-analysis to determine the appropriate regimen of statins to effectively stabilize vulnerable coronary plaques.<h4>Methods</h4>Online electronic databases were carefully searched for all relevant studies. W ...[more]

PMID: 22938176

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Project description:ImportanceCoronary plaques that are prone to rupture and cause adverse cardiac events are characterized by large plaque burden, large lipid content, and thin fibrous caps. Statins can halt the progression of coronary atherosclerosis; however, the effect of the proprotein convertase subtilisin kexin type 9 inhibitor alirocumab added to statin therapy on plaque burden and composition remains largely unknown.ObjectiveTo determine the effects of alirocumab on coronary atherosclerosis using serial multimodality intracoronary imaging in patients with acute myocardial infarction.Design, setting, and participantsThe PACMAN-AMI double-blind, placebo-controlled, randomized clinical trial (enrollment: May 9, 2017, through October 7, 2020; final follow-up: October 13, 2021) enrolled 300 patients undergoing percutaneous coronary intervention for acute myocardial infarction at 9 academic European hospitals.InterventionsPatients were randomized to receive biweekly subcutaneous alirocumab (150 mg; n = 148) or placebo (n = 152), initiated less than 24 hours after urgent percutaneous coronary intervention of the culprit lesion, for 52 weeks in addition to high-intensity statin therapy (rosuvastatin, 20 mg).Main outcomes and measuresIntravascular ultrasonography (IVUS), near-infrared spectroscopy, and optical coherence tomography were serially performed in the 2 non-infarct-related coronary arteries at baseline and after 52 weeks. The primary efficacy end point was the change in IVUS-derived percent atheroma volume from baseline to week 52. Two powered secondary end points were changes in near-infrared spectroscopy-derived maximum lipid core burden index within 4 mm (higher values indicating greater lipid content) and optical coherence tomography-derived minimal fibrous cap thickness (smaller values indicating thin-capped, vulnerable plaques) from baseline to week 52.ResultsAmong 300 randomized patients (mean [SD] age, 58.5 [9.7] years; 56 [18.7%] women; mean [SD] low-density lipoprotein cholesterol level, 152.4 [33.8] mg/dL), 265 (88.3%) underwent serial IVUS imaging in 537 arteries. At 52 weeks, mean change in percent atheroma volume was -2.13% with alirocumab vs -0.92% with placebo (difference, -1.21% [95% CI, -1.78% to -0.65%], P < .001). Mean change in maximum lipid core burden index within 4 mm was -79.42 with alirocumab vs -37.60 with placebo (difference, -41.24 [95% CI, -70.71 to -11.77]; P = .006). Mean change in minimal fibrous cap thickness was 62.67 μm with alirocumab vs 33.19 μm with placebo (difference, 29.65 μm [95% CI, 11.75-47.55]; P = .001). Adverse events occurred in 70.7% of patients treated with alirocumab vs 72.8% of patients receiving placebo.Conclusions and relevanceAmong patients with acute myocardial infarction, the addition of subcutaneous biweekly alirocumab, compared with placebo, to high-intensity statin therapy resulted in significantly greater coronary plaque regression in non-infarct-related arteries after 52 weeks. Further research is needed to understand whether alirocumab improves clinical outcomes in this population.Trial registrationClinicalTrials.gov Identifier: NCT03067844.

Project description:BACKGROUND:Worldwide clinical practice guidelines for dyslipidemia emphasize allocating statin therapy to those at the highest absolute atherosclerotic cardiovascular disease (CVD) risk. METHODS AND RESULTS:We examined 5534 Multi-Ethnic Study of Atherosclerosis (MESA) participants who were not on baseline medications for dyslipidemia. Participants were classified by baseline coronary artery calcium (CAC) score (>0, ? 100) and the common clinical scheme of counting lipid abnormalities (LA), including low-density lipoprotein cholesterol ? 3.36 mmol/L (130 mg/dL), high-density lipoprotein cholesterol <1.03 mmol/L (40 mg/dL) for men or <1.29 mmol/L (50 mg/dL) for women, and triglycerides ? 1.69 mmol/L (150 mg/dL). Our main outcome measure was incident CVD (myocardial infarction, angina resulting in revascularization, resuscitated cardiac arrest, stroke, cardiovascular death). Over a median follow-up of 7.6 years, more than half of events (55%) occurred in the 21% of participants with CAC ? 100. Conversely, 65% of events occurred in participants with 0 or 1 LA. In those with CAC ? 100, CVD rates ranged from 22.7 to 29.5 per 1000 person-years across LA categories. In contrast, with CAC=0, CVD rates ranged from 2.7 to 5.9 per 1000 person-years across LA categories. Individuals with 0 LA and CAC ? 100 had a higher event rate compared with individuals with 3 LA but CAC=0 (22.7 versus 5.9 per 1000 person-years). Similar results were obtained when we classified LA using data set quartiles of total cholesterol/high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, or low-density lipoprotein particle concentration and guideline categories of low-density lipoprotein cholesterol or non-high-density lipoprotein cholesterol. CONCLUSIONS:CAC may have the potential to help match statin therapy to absolute CVD risk. Across the spectrum of dyslipidemia, event rates similar to secondary prevention populations were observed for patients with CAC ? 100.

Project description: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.

Project description:ImportanceThe 2018 American Heart Association/American College of Cardiology Guideline on the Management of Blood Cholesterol recommends the use of risk-enhancing factor assessment and the selective use of coronary artery calcium (CAC) scoring to guide the allocation of statin therapy among individuals with an intermediate risk of atherosclerotic cardiovascular disease (ASCVD).ObjectiveTo examine the association between risk-enhancing factors and incident ASCVD by CAC burden among those at intermediate risk of ASCVD.Design, setting, and participantsThe Multi-Ethnic Study of Atherosclerosis is a multicenter population-based prospective cross-sectional study conducted in the US. Baseline data for the present study were collected between July 15, 2000, and July 14, 2002, and follow-up for incident ASCVD events was ascertained through August 20, 2015. Participants were aged 45 to 75 years with no clinical ASCVD or diabetes at baseline, were at intermediate risk of ASCVD (≥7.5% to <20.0%), and had a low-density lipoprotein cholesterol level of 70 to 189 mg/dL.ExposuresFamily history of premature ASCVD, premature menopause, metabolic syndrome, chronic kidney disease, lipid and inflammatory biomarkers, and low ankle-brachial index.Main outcomes and measuresIncident ASCVD over a median follow-up of 12.0 years.ResultsA total of 1688 participants (mean [SD] age, 65 [6] years; 976 men [57.8%]). Of those, 648 individuals (38.4%) were White, 562 (33.3%) were Black, 305 (18.1%) were Hispanic, and 173 (10.2%) were Chinese American. A total of 722 participants (42.8%) had a CAC score of 0. Among those with 1 to 2 risk-enhancing factors vs those with 3 or more risk-enhancing factors, the prevalence of a CAC score of 0 was 45.7% vs 40.3%, respectively. Over a median follow-up of 12.0 years (interquartile range [IQR], 11.5-12.6 years), the unadjusted incidence rate of ASCVD among those with a CAC score of 0 was less than 7.5 events per 1000 person-years for all individual risk-enhancing factors (with the exception of ankle-brachial index, for which the incidence rate was 10.4 events per 1000 person-years [95% CI, 1.5-73.5]) and combinations of risk-enhancing factors, including participants with 3 or more risk-enhancing factors. Although the individual and composite addition of risk-enhancing factors to the traditional risk factors was associated with improvement in the area under the receiver operating curve, the use of CAC scoring was associated with the greatest improvement in the C statistic (0.633 vs 0.678) for ASCVD events. For incident ASCVD, the net reclassification improvement for CAC was 0.067.Conclusions and relevanceIn this cross-sectional study, among participants with CAC scores of 0, the presence of risk-enhancing factors was generally not associated with an overall ASCVD risk that was higher than the recommended treatment threshold for the initiation of statin therapy. The use of CAC scoring was associated with significant improvements in the reclassification and discrimination of incident ASCVD. The results of this study support the utility of CAC scoring as an adjunct to risk-enhancing factor assessment to more accurately classify individuals with an intermediate risk of ASCVD who might benefit from statin therapy.

Dataset Information

Effect of statin therapy on the progression of coronary atherosclerosis.

Background

Methods

Results

Conclusions

Publications

Effect of statin therapy on the progression of coronary atherosclerosis.

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