Department School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine Position Assistant Professor
|Title||HIJ-PROPER - LDL cholesterol targeting with pitavastatin + ezetimibe for patients with acute coronary syndrome and dyslipidemia|
|Conference||ESC Congress 2016|
|Promoters||European Society of Cardiology|
|Conference Type||International society and overseas society|
|Publisher and common publisher||◎HAGIWARA Nobuhisa, WATANABE Erisa, KOYANAGI Ryo, ARASHI Hiroyuki, YAMAGUCHI Junichi, NAKAO Koichi, TOBARU Tetsuya, TANAKA Hiroyuki, Matsui Kunihiko, OGAWA Hiroshi|
(city and name of the country)
|Summary||This study included 1734 patients(aged ≥ 20 years) with ACS and dyslipidemia who were hospitalized for STEMI, NSTEMI, or unstable angina (UA) within the 10 days prior to randomization. Patients randomized to combination therapy received 2 mg of pitavastatin and 10 mg of ezetimibe as a starting dose, targeting an LDL-C level of < 70mg/dL while the monotherapy group targeted a LDL-C level of 90-100 mg/dL with 2 mg of pitavastatin (patients already receiving a statin discontinued their current medication and were switched to 2 mg of pitavastatin (patients already receiving a statin discontinued their current medication and were switched to 2 mg of pitavastatin as a starting dose). In both groups, the pitavastatin dose was adjusted daily to produce the appropriate LDL-C target level.
The composite primary endpoint consisted of all-cause death, nonfatal myocardial infarction (MI), nonfatal stroke, UA, or revascularization with either percutaneous coronary intervention (PCI) or coronary-artery bypass grafting (CABG). Secondary endpoints included CV events (nonfatal MI, nonfatal stroke, UA, ischemia-driven revas-cularization with either PCI or CABG), all-cause death, heart failure, inflammatory markers, and adverse events (including new occurrence of malignant tumor). Patients were followed for a minimum of 3 years.
At baseline, participants were a mean age of 65.6 years and had a mean body mass index of 24.3 kg/ m2; 75.5% were men and 83.3 % were statin naïve. Index ACS events were STEMI (51.0%), NSTEMI (10.5%), and UA (38.5%). Hypertension was present in 68% of patients and diabetes in 30%. The mean LDL-C at study entry was 135 mg/dL (SD ± 30) and mean sitosterol (a cholesterol absorption marker) was 2.50 μg/mL. The index revascularization for ACS was PCI in 94.5 % of individuals.
Patients treated with pitavastatin and ezetimibe had significantly lower LDL-C (67.5 mg/dL vs 87.2 mg/dL; P < .001), total cholesterol (142.7 mg/dL vs 165.3 mng/dL; P < .001), and triglyceride values (125.2 mg/dL vs 144.2 mg/dL; P < .001) after 1 year compared with those receiving pitavastatin monotherapy. However, the reduction in the composite primary endpoint events among patients receiving intensive LDL-C lowering with the combination of pitavastatin and ezetimibe was not significantly differently from the reductions achieved with pitavastatin alone in patients with ACS and dyslip-idemia at 3 years (32.8% vs 36.9; HR, 0.89; 95% CI, 0.76 to 1.04; P=.152).
There were no significant differences between groups for the secondary outcomes (CV death, nonfatal MI, or nonfatal stroke) and safety outcomes were similar between the 2 arms.
There were no differences between the 2 therapeutic approaches for the major pre-specified subgroups of age, diabetes status, prior lipid-lowering therapy, or median LDL-C mg/dL.