Abstract: Statin therapy after transcatheter aortic valve replacement (TAVI) is associated with better short-term and long-term outcomes. It is of interest to identify specific patient populations that may profit from… Click to show full abstract
Abstract: Statin therapy after transcatheter aortic valve replacement (TAVI) is associated with better short-term and long-term outcomes. It is of interest to identify specific patient populations that may profit from statin therapy. In this retrospective, observational analysis of 2862 patients with symptomatic aortic stenosis after successful transfemoral TAVI, survival during a three-year observation period was characterized by Kaplan–Meier analyses according to statin therapy. Hazard ratios and potential interactions for specific subgroups of patients were determined by Cox regression analyses. At hospital discharge 1761 patients were on low-intensity or moderate-intensity statins, 246 patients were on high-intensity statins, and 855 patients did not take statins. Statin therapy adherence during the first 3 months post-TAVI was 91%. Mortality rates were 18.5%, 12.9%, and 6.9% for patients with no statin, low-intensity or moderate-intensity statins, and high-intensity statins (P < 0.001). Any statin therapy proved to be effective in patients in different classes of age, risk, and manifest cardiovascular disease and was independent of background medication. Statins were of particular benefit in high-risk patients with coronary artery disease [hazard ratio (HR) = 0.57], ejection fraction <40% (HR = 0.64), or low-flow low-gradient aortic stenosis (HR = 0.58) and showed additional benefit even in patients taking renin–angiotensin system blockers (HR = 0.74). Statins also reduced mortality in patients with malignant disease (HR = 0.47). Our analysis confirmed the beneficial effect of statins on survival after TAVI and documented this phenomenon in key patient subsets. The protective effect of statins in our study is consistent with the cardioprotective mechanisms but must be explained by other, yet undetermined pleiotropic effects of statins.
               
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