Statins, high-density lipoprotein cholesterol, and regression of coronary atherosclerosis (original) (raw)
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Factors underlying regression of coronary atheroma with potent statin therapy
European Heart Journal, 2013
Statins can inhibit the progression of coronary atherosclerosis. We aimed to characterize clinical factors that associate with differing measures of coronary atheroma volume following potent statin therapy. SATURN employed serial intravascular ultrasound (IVUS) to monitor changes in measures of coronary atheroma burden [total atheroma volume (TAV) and per cent atheroma volume (PAV)] in 1039 patients with coronary artery disease, treated with rosuvastatin (40 mg) or atorvastatin (80 mg) daily for 24 months. Rosuvastatin-treated patients demonstrated greater reductions in low-density lipoprotein cholesterol (LDL-C, 47 vs. 40%, P < 0.001) and greater increases in high-density lipoprotein cholesterol (HDL-C, 13 vs. 10%, P = 0.02). These alterations in the lipid profile associated with greater TAV (-6.4 vs. -4.4 mm(3), P = 0.01), but not PAV (-1.22 vs. -0.99%, P = 0.17) regression. Greater TAV reductions with rosuvastatin vs. atorvastatin occurred in patients with diabetes (P = 0.01, treatment by diabetic status interaction P-value 0.05). Greater PAV reductions with rosuvastatin were evident in females (P = 0.01, treatment by sex interaction P-value 0.03) and in those with greater than or equal to median baseline LDL-C (P = 0.02, treatment by LDL-C group interaction P-value 0.03) or HDL-C levels (P = 0.02, treatment by HDL-C group interaction P-value 0.04). On multivariable analysis assessing change in TAV and PAV, both higher baseline TAV and PAV independently associated with TAV and PAV regression, respectively (standardized estimates: TAV -0.25, P < 0.001; PAV -0.23, P < 0.001). Higher-risk patients, particularly those with greater baseline coronary atheroma volume, are more likely to experience less disease progression with potent statin therapy.
Arteriosclerosis, thrombosis, and vascular biology, 2014
Patients with acute coronary syndromes (ACS) display diffuse coronary atheroma instability and heightened risk of early and late recurrent coronary events. We compared the long-term antiatherosclerotic efficacy of high-intensity statins in patients with ACS when compared with stable disease. Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) used serial intravascular ultrasound measures of coronary atheroma volume in patients treated with rosuvastatin 40 mg or atorvastatin 80 mg for 24 months. The overall effect of high-intensity statins on the change in coronary percent atheroma volume and major adverse cardiovascular events (death/nonfatal myocardial infarction/coronary revascularization) were evaluated in this post hoc analysis. When compared with non-ACS patients (n=678), patients with ACS (n=361) were younger, actively smoking, and have had a previous myocardial infarction (all P<0.001). At baseline, patients with ACS ...
Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease
… England Journal of …, 2005
Recent trials have demonstrated better outcomes with intensive than with moderate statin treatment. Intensive treatment produced greater reductions in both low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP), suggesting a relationship between these two biomarkers and disease progression.
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.
Lipids in Health and Disease, 2020
Background Several studies have investigated the association between non-statin lipid-lowering therapy and regression of atherosclerosis. However, these studies were mostly small and their results were not always robust. The objectives were: (1) to define if a dual lipid-lowering therapy (statin + non-statin drugs) is associated with coronary atherosclerosis regression, estimated by intravascular ultrasound (IVUS); (2) to assess the association between dual lipid-lowering-induced changes in low density lipoprotein cholesterol (LDL-C) and non-high-density-lipoprotein cholesterol (non-HDL-C) levels and atherosclerosis regression. Methods A meta-analysis including trials of non-statin lipid-lowering therapy, reporting LDL-C, non-HDL-C and total atheroma volume (TAV) with a minimum of 6 months of follow-up was performed. The primary endpoint was defined as the change in TAV measured from baseline to follow-up, comparing groups of subjects on statins alone versus combination of statin an...
JACC. Cardiovascular imaging, 2018
This study sought to describe the impact of statins on individual coronary atherosclerotic plaques. Although statins reduce the risk of major adverse cardiovascular events, their long-term effects on coronary atherosclerosis remain unclear. We performed a prospective, multinational study consisting of a registry of consecutive patients without history of coronary artery disease who underwent serial coronary computed tomography angiography at an interscan interval of ≥2 years. Atherosclerotic plaques were quantitatively analyzed for percent diameter stenosis (%DS), percent atheroma volume (PAV), plaque composition, and presence of high-risk plaque (HRP), defined by the presence of ≥2 features of low-attenuation plaque, positive arterial remodeling, or spotty calcifications. Among 1,255 patients (60 ± 9 years of age; 57% men), 1,079 coronary artery lesions were evaluated in statin-naive patients (n = 474), and 2,496 coronary artery lesions were evaluated in statin-taking patients (n =...
Statins and cardiovascular diseases: the multiple effects of lipid-lowering therapy by statins
Atherosclerosis, 2000
Cholesterol lowering involving different therapies improves the clinical outcome of patients. To define the underlying pathomechanism, we studied whether treatment with statins was associated with changes in blood thrombogenicity, endothelial dysfunction and soluble adhesion molecule levels. Fifty hypercholesterolemic patients were treated with pravastatin (40 mg/day, n= 24) or simvastatin (20 mg/day, n=26). Lipid profile and blood thrombogenicity were assessed in all patients before and after 3 months of cholesterol reducing therapy. Blood thrombogenicity was assessed as thrombus formation, perfusing non-anticoagulated blood directly from the patients' vein through the Badimon perfusion chamber (shear rate 1690/s). Endothelial-dependent vasomotor response was tested by laser-Doppler flowmeter. Soluble adhesion molecule level were measured by ELISA. Total and LDL cholesterol were reduced in the two treatment groups by statin therapy. Statin therapy was associated with a significant reduction in blood thrombogenicity and endothelium-dependent vasoresponse. No differences were observed between simvastatin or pravastatin treatment. Lipid lowering by statins had no effect on plasma levels of fibrinogen, sL-selectin, sP-selectin and sICAM-1 antigen. Cholesterol lowering by both statins reduced the increased blood reactivity and endothelial dysfunction present under hypercholesterolemia. The multiple effects of lipid lowering therapy by statins may explain the benefits observed in recent epidemiological trials.