Early Statin Treatment in Patients With Acute Coronary Syndrome (original) (raw)
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Acute Effects of Statin Therapy on Coronary Atherosclerosis Following an Acute Coronary Syndrome
The American Journal of Cardiology, 2009
No data exist on the acute effects of statin therapy on human coronary atherosclerotic plaques. The objective of our study was to evaluate the early (<2 months) effects of newly initiated statin therapy on coronary atherosclerosis as evaluated by intravascular ultrasonography. The study population consisted of 74 patients (mean age 58 ؎ 8 years) who had been included in the ERASE trial (evaluating the effects of reconstituted high-density lipoprotein infusions). All patients underwent serial intravascular ultrasonographic (IVUS) evaluation at baseline (3 ؎ 2 days after an acute coronary syndrome [ACS]) and after 6 ؎ 1 weeks of follow-up. Statin therapy was initiated after ACS in 36 patients who received <1 dose of statins before baseline IVUS examination (newly initiated statin therapy group), and 38 patients were already on a stable statin dose before the ACS (long-term statin therapy group). Atorvastatin at a dose of 40 mg/day was the most common regimen in the 2 groups. Percent changes in atheroma volume (prespecified primary efficacy parameter) were ؊4.71 ؎ 0.96% in the newly initiated statin therapy group (p <0.0001) and ؊0.54 ؎ 0.89% in the long-term statin therapy group (p ؍ 0.546; p ؍ 0.002 for comparison between groups). Median nominal changes in atheroma volume were ؊9.10 mm 3 (interquartile range ؊12.56 to ؊3.73, p <0.0001 vs baseline) and 1.21 mm 3 (interquartile range ؊6.41 to 3.76, p ؍ 0.429 vs baseline) in the newly initiated and long-term statin therapy groups, respectively (p ؍ 0.003 for comparison between groups). Greater decreases in total cholesterol (r ؍ 0.25, p ؍ 0.035), ratio of total to high-density lipoprotein cholesterol (r ؍ 0.28, p ؍ 0.018), and high-sensitivity C-reactive protein (r ؍ 0.31, p ؍ 0.046, for patients with high-sensitivity C-reactive protein measurements within 7 days after IVUS examination) were associated with larger percent changes in atheroma volume. In conclusion, newly initiated statin therapy is associated with rapid regression of coronary atherosclerosis within 2 months. This effect was in part associated with decreases in atherogenic lipid and inflammatory parameters. These results provide insight into the rapid clinical benefits of statin therapy after an ACS.
Update on the efficacy of statin treatment in acute coronary syndromes
European Journal of Clinical Investigation, 2014
Background The natural history of atherosclerosis might involve coronary plaque rupture/erosion, thrombus formation and vessel lumen occlusion, clinically recognized as acute coronary syndrome (ACS). International guidelines strongly recommend early statin administration in patients admitted for ACS. In addition to lowering circulating levels of low-density lipoprotein cholesterol (LDL-c), statin treatment was shown to promote plaque stabilization or regression in several ways, including reduction in necrotic lipid core, anti-inflammatory effects and improvement in endothelial function. The aim of this review is to summarize clinical evidence on the role of statins in secondary prevention of ACS.
EUROPEAN JOURNAL OF CARDIOVASCULAR MEDICINE, 2011
Statins exert beneficial effects on the endothelium, inflammation and the coagulation cascade that are independent of cholesterol lowering. The main mechanism underlying these effects is inhibition of isoprenoid synthesis, modulating the inflammatory cascade and the endothelial activation reliable of atherosclerosis. Different studies demonstrated that statins improve endothelial function in patients with stable atherosclerotic plaque and that this effect is dose-dependent. Statins may modulate endothelial expression of adhesion molecules, as demonstrated in the ARMYDA-CAMS, and may enhance mobilisation of endothelial progenitor cells. Elevated C-reactive protein levels, an inflammatory marker that also plays a direct pathogenetic role in the atherosclerotic process, have been correlated with worse outcome in patients with cardiovascular disease. Multiple studies demonstrated that statin attenuates the rise of inflammatory markers and improves clinical outcome in patients with stable angina, unstable angina and non-Q wave acute myocardial infarction. During percutaneous coronary intervention randomised trials showed a benefical effect of statin pre-treatment in reducing peri-procedural myocardial damage probably by plaque stabilisation and inhibition of microembolisation phenomena during stent implantation. The ARMYDA study and the NAPLES II trial demonstrated this beneficial effect in patients undergoing coronary revascularisation for stable angina. Also in patients with ACS, receiving invasive strategy, the role of statins in preventing peri-procedural damage was demonstrated in the ARMYDA-ACS study by the administration of an acute high loading-dose with atorvastatin. In patients already on chronic statin therapy at the time of the procedure, an acute drug reload before stenting would have cardioprotective effects, like demonstrated in the ARMYDA RECAPTURE study.
Atherosclerosis, 2011
Aim: To clarify whether the effects of statin treatment on plaque regression vary according to the presence or absence of polyvascular disease (PVD) in patients with acute coronary syndrome (ACS). Methods: 307 patients with ACS who underwent percutaneous coronary intervention for the culprit lesion at 33 centers were treated with atorvastatin or pitavastatin. Noncoronary atherosclerosis was defined as coexistent, clinically recognized arterial disease other than coronary artery disease (CAD) (cerebral, aortic, or lower extremity). Intravascular ultrasound (IVUS) was performed to assess non-culprit coronary atherosclerosis at baseline and at 8-12 months follow-up. Serial IVUS examinations were obtained in 252 patients. Atheroma volume and percent change in atheroma volume of the target plaque was assessed. Results: Patients of the CAD + PVD (n = 19) were older (68 vs. 62 years, p = 0.02), had lower low-density lipoprotein cholesterol (LDL-C) levels at baseline (116 vs. 134 mg/dL, p = 0.03) than those of the CAD-only group (n = 233), whereas LDL-C levels at follow-up were similar (81 vs. 83 mg/dL). Although the baseline plaque volume was similar in the two groups (59 vs. 57 mm 3), patients of the CAD + PVD group showed milder regression of atherosclerosis than those of the CAD-only group (−8.9% vs. −18.2%, p = 0.005). This difference remained significant even after adjustment for coronary risk factors including age and serum LDL-C (p = 0.047). Conclusions: Statin treatment results in milder regression of coronary atherosclerosis in CAD patients with polyvascular disease compared to those with CAD only.
European heart journal, 2015
The effect of long-term high-intensity statin therapy on coronary atherosclerosis among patients with acute ST-segment elevation myocardial infarction (STEMI) is unknown. The aim of this study was to quantify the impact of high-intensity statin therapy on plaque burden, composition, and phenotype in non-infarct-related arteries of STEMI patients undergoing primary percutaneous coronary intervention (PCI). Between September 2009 and January 2011, 103 STEMI patients underwent intravascular ultrasonography (IVUS) and radiofrequency ultrasonography (RF-IVUS) of the two non-infarct-related epicardial coronary arteries (non-IRA) after successful primary PCI. Patients were treated with high-intensity rosuvastatin (40 mg/day) throughout 13 months and serial intracoronary imaging with the analysis of matched segments was available for 82 patients with 146 non-IRA. The primary IVUS end-point was the change in per cent atheroma volume (PAV). After 13 months, low-density lipoprotein cholesterol...
Journal of Atherosclerosis and Thrombosis, 2011
Some randomized studies have shown a delay of up to a few years in the statin-related survival advantage, whereas others have demonstrated an early survival benefit for some patients. We examined the short-term effects of statins in patients with acute coronary syndrome (ACS), stratified according to baseline LDL-C. Methods: Patients with ACS (n 180) were randomized to receive 6 months of atorvastatin (20 mg) in the Extended-ESTABLISH trial. Six months after ACS onset, all patients were treated with statins to achieve an LDL-C value of 100 mg/dL. Patient outcomes were analyzed with respect to LDL-C at the time of ACS onset: high baseline (≥ 100 mg/dL, n 124) or low baseline (100 mg/dL, n 56) LDL-C. Results: The cumulative incidence rates of major adverse cardiac and cerebrovascular events (MACCE) did not significantly differ between the early-statin and control groups in the high baseline groups at 6 months (p 0.158), whereas a significant benefit of early intensive statins appeared 1 year (p 0.034) later. In contrast, we found no significant short-term benefits of statins after either 6 months or 1 year in the low baseline group. Multivariate analysis showed that early intensive atorvastatin therapy was associated with a lower risk of MACCE at 1 year in the high baseline group (OR, 0.25; 95% CI, 0.05 to 0.83; p 0.035). Conclusions: The effects of 6 months of intensive lipid-lowering therapy appear after 1 year in patients with ACS and baseline LDL-C ≥ 100 mg/dL.
Effects of statin therapy on non-calcified coronary plaque assessed by 64-slice computed tomography
International Journal of Cardiology, 2011
Computed tomography angiography (CTA) enables characterization of non-calcified coronary atherosclerotic lesions (NCALs) and assessment of plaque vulnerability. We investigated whether the characteristics of NCALs detected by 64-slice CTA were influenced by preceding statin therapy and serum lipid profiles. Methods: Among 493 consecutive patients who underwent coronary CTA, we enrolled 114 patients with NCALs. We divided the patients into three groups according to preceding statin therapy: intensive statins (IS, n = 24), moderate statins (MS, n = 26), and no statin (NS, n = 64). The vulnerability of each NCAL was evaluated by density (low-density plaque defined as CT density ≤ 38 HU), positive remodeling (remodeling index N 1.05), and the presence of adjacent spotty calcification. Results: Percentages of patients in the IS, MS, and NS groups with low-density NCALs were 46%, 58%, and 80%, respectively (p = 0.009) and positive remodeling NCALs were 54%, 58%, and 75%, respectively (p = 0.10). We also found an inverse correlation between serum LDL-C level and the minimum plaque CT density. According to the regression equation, a CT density of 38 HU corresponded with LDL-C of 100 mg/dl. The number of lowdensity plaques was positively correlated with low-density to high-density lipoprotein cholesterol ratio (LDL-C/HDL-C). An LDL-C/HDL-C N 2.5 independently predicted multiple low-density plaques (OR 2.39 [95% CI: 1.28-4.86], p b 0.001). Conclusions: Our CTA findings demonstrate that low-density NCALs occur less frequently in patients with intensive statin pre-treatment. A high LDL-C/HDL-C ratio is also associated with larger numbers of lowdensity NCALs.