Abstract 13344: Beneficial Effects of Long-acting Nifedipine on Coronary Vasomotion Abnormalities After Drug-Eluting Stent Implantation -The NOVEL Study

Abstract

Introduction: It is widely known that drug-eluting stents (DES) induce coronary vasomotion abnormalities. We have previously demonstrated that chronic treatment with long-acting nifedipine, which exerts cardiovascular protective effects through inhibition of vascular inflammation, suppresses DES-induced abnormal coronary vasoconstriction in pigs. In order to test whether this is also the case in humans, we performed a prospective, randomized, multicenter trial, termed as the NOVEL Study. Methods and Results: We enrolled 146 patients with stable angina pectoris who underwent elective implantation of everolimus-eluting stents (EES) in the left coronary arteries. They were randomly assigned to receive either conventional treatments alone (aspirin, clopidogrel, renin-angiotensin system inhibitor and statin) or additionally long-acting nifedipine (10-60 mg/day) (n=73 each). After 8-10 months, 53 patients in the control and 57 in the nifedipine group were finally examined for coronary reactivity to intracoronary acetylcholine (ACh) by quantitative coronary angiography after 48-hour withdrawal of nifedipine. Baseline patient characteristics and procedural profiles were comparable between the two groups. Coronary vasoconstricting responses to ACh were significantly enhanced at the distal segment adjacent to EES as compared with non-stented vessel (P<0.001) and were significantly inhibited in the nifedipine group (P<0.01) (Figure). Furthermore, the inflammatory profiles, including serum levels of high-sensitivity CRP and adiponectin, were improved only in the nifedipine group (P<0.05) (Figure). Conclusions: These results indicate that DES-induced coronary vasomotion abnormalities still remain an important clinical issue even with the second-generation of DES, for which long-acting nifedipine exerts beneficial effects associated with its anti-inflammatory effects.