Antiatherosclerotic Effects of Long-Term Maximally Intensive Statin Therapy After Acute Coronary Syndrome

Abstract

Objectives— 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. Approach and Results— 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 exhibited lower high-density lipoprotein cholesterol (43.5±11 versus 45.8±11 mg/dL; P =0.002), a higher apolipoprotein B: apolipoprotein A-1 ratio (0.90±0.24 versus 0.83±0.24; P <0.001) and greater percent atheroma volume (37.3±8.5% versus 35.9±8.1%; P =0.01) when compared with non-ACS patients. Despite similar achieved levels of lipid and inflammatory markers after high-intensity statin therapy, patients with ACS demonstrated greater percent atheroma volume regression than non-ACS patients (−1.46±0.14 versus −0.89±0.13; P =0.003). After propensity-weighted multivariable adjustment, baseline percent atheroma volume ( P <0.001) and an ACS clinical presentation ( P =0.02) independently associated with plaque regression. The 24-month major adverse cardiovascular events–free survival was similar between patients with ACS and non-ACS (90.6 versus 92.9%; P =0.25). Conclusions— Long-term high-intensity statin therapy caused greater plaque regression and comparable major adverse cardiovascular events rates in ACS when compared with non-ACS patients. Despite a higher clinical risk profile, patients with ACS harbor a more modifiable disease substrate and seem to benefit the most from potent statin therapy.

Cigarette smoking and cardio-renal events in patients with atherosclerotic renal artery stenosis

“…Even though smokers were 9.1 years younger at enrollment, they did not differ from non-smokers in renal artery stenosis severity. This is consistent with the known effect of smoking to accelerate atherosclerosis onset and progression [24][25][26], and that smoking increases risk for renal artery stenosis [17]. The effect of active smoking on renal function was less clear in the current study.…”

Atherosclerosis

“…5,12-14 In contrast, plasma HDL cholesterol concentrations are negatively associated with atherosclerosis. 5,15 Although the major clinical use of statins is to reduce plasma LDL cholesterol concentrations, this class of drug may also increase plasma HDL cholesterol concentrations.…”

Effects of 4 Statins on Regression of Coronary Plaque in Acute Coronary Syndrome

“…5,22-25 Previous studies also showed that coronary plaque regression induced by statin therapy appeared to be more predominant in ACS patients than in non-ACS patients. [26][27][28] This may be related to the underlying differences in coronary plaque composition in patients with ACS compared with those with stable angina pectoris. In pathology and imaging studies, ACS patients have a larger percentage of lipid-laden plaque with inflammatory cells, 29 compared with a higher percentage of fibrocalcific plaque in patients with chronic stable lesions.…”

“…In pathology and imaging studies, ACS patients have a larger percentage of lipid-laden plaque with inflammatory cells, 29 compared with a higher percentage of fibrocalcific plaque in patients with chronic stable lesions. 26 Statin therapy has been reported to reduce the plaque lipid component, which may translate into entire plaque regression. 25 Therefore, it can be argued that coronary plaque in ACS patients is more susceptible to plaque regression.…”