TY - JOUR
T1 - Impact of baseline lipoprotein and C-reactive protein levels on coronary atheroma regression following high-intensity statin therapy
AU - Puri, Rishi
AU - Nissen, Steven E.
AU - Shao, Mingyuan
AU - Uno, Kiyoko
AU - Kataoka, Yu
AU - Kapadia, Samir R.
AU - Tuzcu, E. Murat
AU - Nicholls, Stephen J.
N1 - Funding Information:
SEN has received research support to perform clinical trials through the Cleveland Clinic Coordinating Center for Clinical Research from Pfizer , AstraZeneca , Novartis , Roche , Daiichi-Sankyo , Takeda , Sanofi-Aventis , Resverlogix , and Eli Lilly ; and is a consultant/advisor for many pharmaceutical companies but requires them to donate all honoraria or consulting fees directly to charity so that he receives neither income nor a tax deduction. SJN has received speaking honoraria from AstraZeneca, Pfizer, Merck Schering-Plough and Takeda, consulting fees from AstraZeneca, Pfizer, CSL Behring, Boehringer Ingelheim, Merck Schering-Plough, Takeda, Roche, NovoNordisk, Omthera, LipoScience and Anthera and research support from AstraZeneca, Anthera, Eli Lilly, Cerenis, Novartis, Resverlogix, Atheronova and Lipid Sciences. All other authors have reported that they have no relationships to disclose.
Publisher Copyright:
© 2014 Elsevier Inc. All rights reserved.
PY - 2014/11/15
Y1 - 2014/11/15
N2 - Guidelines now recommend high-intensity statin therapy in all patients with proven atherosclerotic disease. Yet the impact of baseline lipoprotein and C-reactive protein (CRP) levels on measures of disease regression to this therapy are unknown. The aim of this study was to test the hypothesis that high-intensity statin therapy causes equivalent degrees of coronary atheroma regression irrespective of baseline lipoprotein and CRP levels. In 8 prospective randomized trials using serial coronary intravascular ultrasound, 1,881 patients who maintained or switched to 18- to 24 months of high-intensity statin therapy (rosuvastatin 40 mg or atorvastatin 80 mg) were stratified according to baseline lipoprotein and CRP levels. Changes in coronary percentage atheroma volume (PAV) and total atheroma volume (TAV) were evaluated. High-intensity statin therapy produced significant reductions from baseline in low-density lipoprotein cholesterol by 38.4%, non-high-density lipoprotein (HDL) cholesterol by 33.6%, triglycerides by 13.1%, and CRP by 33.3%, while increasing HDL cholesterol by 11.7% (p <0.001 for all). This was associated with regression of PAV by 0.7% and of TAV by 8.2 mm3 (p <0.001 for both). No significant differences of changes in PAV and TAV were observed across baseline quintiles of low-density lipoprotein cholesterol, HDL cholesterol, non-HDL cholesterol, triglycerides, or CRP. Moreover, across all measured lipoproteins and CRP, most patients demonstrated plaque regression (defined as any change from baseline in PAV or TAV <0). In conclusion, high-intensity statin therapy attenuated the natural progression of coronary atherosclerosis in all strata of patients with coronary artery disease irrespective of baseline lipoprotein or CRP levels. These findings provide support for the latest United States guideline recommendations for the broad use of high-intensity statin therapy in all patients with atherosclerosis, regardless of baseline lipid status.
AB - Guidelines now recommend high-intensity statin therapy in all patients with proven atherosclerotic disease. Yet the impact of baseline lipoprotein and C-reactive protein (CRP) levels on measures of disease regression to this therapy are unknown. The aim of this study was to test the hypothesis that high-intensity statin therapy causes equivalent degrees of coronary atheroma regression irrespective of baseline lipoprotein and CRP levels. In 8 prospective randomized trials using serial coronary intravascular ultrasound, 1,881 patients who maintained or switched to 18- to 24 months of high-intensity statin therapy (rosuvastatin 40 mg or atorvastatin 80 mg) were stratified according to baseline lipoprotein and CRP levels. Changes in coronary percentage atheroma volume (PAV) and total atheroma volume (TAV) were evaluated. High-intensity statin therapy produced significant reductions from baseline in low-density lipoprotein cholesterol by 38.4%, non-high-density lipoprotein (HDL) cholesterol by 33.6%, triglycerides by 13.1%, and CRP by 33.3%, while increasing HDL cholesterol by 11.7% (p <0.001 for all). This was associated with regression of PAV by 0.7% and of TAV by 8.2 mm3 (p <0.001 for both). No significant differences of changes in PAV and TAV were observed across baseline quintiles of low-density lipoprotein cholesterol, HDL cholesterol, non-HDL cholesterol, triglycerides, or CRP. Moreover, across all measured lipoproteins and CRP, most patients demonstrated plaque regression (defined as any change from baseline in PAV or TAV <0). In conclusion, high-intensity statin therapy attenuated the natural progression of coronary atherosclerosis in all strata of patients with coronary artery disease irrespective of baseline lipoprotein or CRP levels. These findings provide support for the latest United States guideline recommendations for the broad use of high-intensity statin therapy in all patients with atherosclerosis, regardless of baseline lipid status.
UR - http://www.scopus.com/inward/record.url?scp=84908318230&partnerID=8YFLogxK
U2 - 10.1016/j.amjcard.2014.08.009
DO - 10.1016/j.amjcard.2014.08.009
M3 - Article
C2 - 25282317
AN - SCOPUS:84908318230
VL - 114
SP - 1465
EP - 1472
JO - American Journal of Cardiology
JF - American Journal of Cardiology
SN - 0002-9149
IS - 10
ER -