TY - JOUR
T1 - Coronary atheroma volume and cardiovascular events during maximally intensive statin therapy
AU - Puri, Rishi
AU - Nissen, Steven E.
AU - Shao, Mingyuan
AU - Ballantyne, Christie M.
AU - Barter, Phillip J.
AU - Chapman, M. John
AU - Erbel, Raimund
AU - Libby, Peter
AU - Raichlen, Joel S.
AU - Uno, Kiyoko
AU - Kataoka, Yu
AU - Nicholls, Stephen J.
N1 - Funding Information:
Conflict of interest: S.E.N. has received research support to perform clinical trials through the Cleveland Clinic Coordinating Centre 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. S.J.N. has received speaking honoraria from AstraZeneca, Pfizer, Merck Schering-Plough, and Takeda; consulting fees from AstraZeneca, Pfizer,Merck Schering-Plough, Takeda, Roche, NovoNordisk, LipoScience, and Anthera; research support from AstraZeneca and Lipid Sciences. C.M.B. has received grant support from Abbott, Astra-Zeneca, Bristol-Myers Squibb, Genentech, GlaxoSmithKline, Kowa, Merck, Novartis, Roche, Sanofi-Synthelabo, and Takeda; consulting fees and honoraria from Abbott, Adnexus, Amarin, Amylin, AstraZeneca, Bristol-Myers Squibb, Esperion, Genentech, GlaxoSmithKline, Idera, Kowa, Merck, Novartis, Omthera, Resverlogix, Roche, Sanofi-Synthelabo, and Takeda; lecture fees from Abbott, AstraZeneca, GlaxoSmithKline, and Merck. Dr. P.J.B. holds an advisory board position in AstraZeneca, Merck, Roche, CSL. Behring, and Pfizer; receives grant support from Merck; consulting fees from CSL Behring; lecture fees from AstraZeneca, Kowa, Merck, Pfizer, and Roche. M.J.C. receives grant support from Merck and Kowa; consulting fees from Merck and Pfizer; lectures fees from Merck and Kowa. Dr. Erbel receives grant and travel support from the Heinz Nixdorf Foundation, German Research Foundation; accommodations/meeting expenses from Biotronik, Sanofi, and Novartis. P.L serves as an unpaid consultant for Novartis, Johnson & Johnson, Amgen, and Roche; serves in unpaid leadership roles for clinical trials sponsored by AstraZeneca, GlaxoSmithKline, Novartis, Pfizer, Pronova, and Sigma Tau and previously received royalties from Roche for the patent on CD40L in cardiovascular risk stratification. J.S.R. is an employee and owns stock in AstraZeneca. All other authors have no disclosures.
PY - 2013/11/1
Y1 - 2013/11/1
N2 - Aims The impact of baseline coronary plaque burden on the clinical outcome in patients receiving aggressive low-density lipoprotein cholesterol (LDL-C) lowering therapy to levels,70 mg/dL is unknown.We assessed the prognostic significance of baseline coronary plaque burden following high-intensity statin therapy. Methods and results SATURNused serial intravascular ultrasound (IVUS) to measure coronary atheroma volume in 1039 patients before and after 24 months of treatment with rosuvastatin 40 mg or atorvastatin 80 mg. This post hoc analysis compared the relationship between baseline percent atheroma volume (PAV) and major adverse cardiovascular events(MACE: Death, myocardial infarction, stroke, coronary revascularization, hospitalization for unstable angina) in patients with baseline PAV less than (n = 519) or greater than (n = 520) the median. Patients with a higher baseline PAV had a similar LDL-C compared with those with a lower baseline PAV at baseline (119.0±29 vs. 121.0±27 mg/dL, P = 0.09) and at follow-up (65.3±23 vs. 65.8±22 mg/dL, P = 0.47). In multivariable analysis, each standard deviation increase in baseline PAV was associated with a 28% increase in MACE [HR 1.28 (1.05, 1.57), P = 0.01]. Those with the highest quartile of baseline PAV(>41.8%) had a 2-year cumulativeMACErate of 12%, whichwas significantly higher (log-rank P = 0.001) thanMACE rates of all lower PAV quartiles (MACE: Quartile 3, 2, and 1were 5.7, 7.9, and 5.1%, respectively). LDL-C levels at baseline [HR 0.96 (0.79, 1.18), P = 0.73] and on-treatment [HR 1.19 (0.83, 1.73), P = 0.35] were not associated with MACE. Conclusion Following 2 years of high-intensity statin therapy, a baseline coronary atheroma volume predicted MACE, despite the achievement of very low on-treatment LDL-C levels.
AB - Aims The impact of baseline coronary plaque burden on the clinical outcome in patients receiving aggressive low-density lipoprotein cholesterol (LDL-C) lowering therapy to levels,70 mg/dL is unknown.We assessed the prognostic significance of baseline coronary plaque burden following high-intensity statin therapy. Methods and results SATURNused serial intravascular ultrasound (IVUS) to measure coronary atheroma volume in 1039 patients before and after 24 months of treatment with rosuvastatin 40 mg or atorvastatin 80 mg. This post hoc analysis compared the relationship between baseline percent atheroma volume (PAV) and major adverse cardiovascular events(MACE: Death, myocardial infarction, stroke, coronary revascularization, hospitalization for unstable angina) in patients with baseline PAV less than (n = 519) or greater than (n = 520) the median. Patients with a higher baseline PAV had a similar LDL-C compared with those with a lower baseline PAV at baseline (119.0±29 vs. 121.0±27 mg/dL, P = 0.09) and at follow-up (65.3±23 vs. 65.8±22 mg/dL, P = 0.47). In multivariable analysis, each standard deviation increase in baseline PAV was associated with a 28% increase in MACE [HR 1.28 (1.05, 1.57), P = 0.01]. Those with the highest quartile of baseline PAV(>41.8%) had a 2-year cumulativeMACErate of 12%, whichwas significantly higher (log-rank P = 0.001) thanMACE rates of all lower PAV quartiles (MACE: Quartile 3, 2, and 1were 5.7, 7.9, and 5.1%, respectively). LDL-C levels at baseline [HR 0.96 (0.79, 1.18), P = 0.73] and on-treatment [HR 1.19 (0.83, 1.73), P = 0.35] were not associated with MACE. Conclusion Following 2 years of high-intensity statin therapy, a baseline coronary atheroma volume predicted MACE, despite the achievement of very low on-treatment LDL-C levels.
KW - Atherosclerosis
KW - Intravascular ultrasound
KW - Statins
UR - http://www.scopus.com/inward/record.url?scp=84890059009&partnerID=8YFLogxK
U2 - 10.1093/eurheartj/eht260
DO - 10.1093/eurheartj/eht260
M3 - Article
C2 - 23886915
AN - SCOPUS:84890059009
VL - 34
SP - 3182
EP - 3190
JO - European Heart Journal
JF - European Heart Journal
SN - 0195-668X
IS - 41
ER -