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Impact of baseline lipoprotein and C-reactive protein levels on coronary atheroma regression following high-intensity statin therapy.
Am J Cardiol. 2014 Nov 15; 114(10):1465-72.AJ

Abstract

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 mm(3) (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.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Puri R
Cleveland Clinic Coordinating Center for Clinical Research, Cleveland, Ohio; Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
Nissen SE
Cleveland Clinic Coordinating Center for Clinical Research, Cleveland, Ohio; Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
Shao M
Cleveland Clinic Coordinating Center for Clinical Research, Cleveland, Ohio.
Uno K
Cleveland Clinic Coordinating Center for Clinical Research, Cleveland, Ohio.
Kataoka Y
South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia.
Kapadia SR
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
Tuzcu EM
Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, Ohio.
Nicholls SJ
South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia. Electronic address: stephen.nicholls@sahmri.com.

MeSH

BiomarkersC-Reactive ProteinCoronary AngiographyCoronary Artery DiseaseDisease ProgressionDose-Response Relationship, DrugFemaleFollow-Up StudiesHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteinsMaleMiddle AgedPlaque, AtheroscleroticProspective StudiesTreatment OutcomeUltrasonography, Interventional

Pub Type(s)

Journal Article
Multicenter Study
Randomized Controlled Trial

Language

eng

PubMed ID

25282317

Citation

Puri, Rishi, et al. "Impact of Baseline Lipoprotein and C-reactive Protein Levels On Coronary Atheroma Regression Following High-intensity Statin Therapy." The American Journal of Cardiology, vol. 114, no. 10, 2014, pp. 1465-72.
Puri R, Nissen SE, Shao M, et al. Impact of baseline lipoprotein and C-reactive protein levels on coronary atheroma regression following high-intensity statin therapy. Am J Cardiol. 2014;114(10):1465-72.
Puri, R., Nissen, S. E., Shao, M., Uno, K., Kataoka, Y., Kapadia, S. R., Tuzcu, E. M., & Nicholls, S. J. (2014). Impact of baseline lipoprotein and C-reactive protein levels on coronary atheroma regression following high-intensity statin therapy. The American Journal of Cardiology, 114(10), 1465-72. https://doi.org/10.1016/j.amjcard.2014.08.009
Puri R, et al. Impact of Baseline Lipoprotein and C-reactive Protein Levels On Coronary Atheroma Regression Following High-intensity Statin Therapy. Am J Cardiol. 2014 Nov 15;114(10):1465-72. PubMed PMID: 25282317.
* Article titles in AMA citation format should be in sentence-case
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, Y1 - 2014/08/27/ PY - 2014/05/15/received PY - 2014/08/12/revised PY - 2014/08/12/accepted PY - 2014/10/6/entrez PY - 2014/10/6/pubmed PY - 2015/3/4/medline SP - 1465 EP - 72 JF - The American journal of cardiology JO - Am J Cardiol VL - 114 IS - 10 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 mm(3) (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. SN - 1879-1913 UR - https://www.unboundmedicine.com/medline/citation/25282317/Impact_of_baseline_lipoprotein_and_C_reactive_protein_levels_on_coronary_atheroma_regression_following_high_intensity_statin_therapy_ DB - PRIME DP - Unbound Medicine ER -