Effect of sacubitril/valsartan on cardiac remodeling compared with other renin–angiotensin system inhibitors: a difference-in-difference analysis of propensity-score matched samples

Abstract

Background In patients with heart failure with reduced ejection fraction (HFrEF), treatment with sacubitril–valsartan (S/V) may reverse left ventricular remodeling (rLVR). Whether this effect is superior to that induced by other renin–angiotensin system (RAS) inhibitors is not well known. Methods HFrEF patients treated with S/V (n = 795) were compared, by propensity score matching, with a historical cohort of 831 HFrEF patients (non-S/V group) treated with angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (RAS inhibitors). All patients were also treated with beta-blockers and shared the same protocol with repeat echocardiogram 8–12 months after starting therapy. The difference-in-difference (DiD) analysis was used to evaluate the impact of S/V on CR indices between the two groups. Results After propensity score matching, compared to non-S/V group (n = 354), S/V group (n = 354) showed a relative greater reduction in end-diastolic and end-systolic volume index (ESVI), and greater increase in ejection fraction (DiD estimator = + 5.42 mL/m2, P = 0.0005; + 4.68 mL/m2, P = 0.0009, and + 1.76%, P = 0.002, respectively). Reverse LVR (reduction in ESVI ≥ 15% from baseline) was more prevalent in S/V than in non-S/V group (34% vs 26%, P = 0.017), while adverse LVR (aLVR, increase in ESVI at follow-up ≥ 15%) was more frequent in non-S/V than in S/V (16% vs 7%, P < 0.001). The beneficial effect of S/V on CR over other RAS inhibitors was appreciable across a wide range of patient’s age and baseline end-diastolic volume index, but it tended to attenuate in more dilated left ventricles (P for interaction = NS for both). Conclusion In HFrEF patients treated with beta-blockers, sacubitril/valsartan is associated with a relative greater benefit in LV reverse remodeling indices than other RAS inhibitors. Graphical abstract

Mechanisms of vibration-induced structural myocardial remodeling

“…Не изучены изменения адреномедуллина, системы предсердного натрийуретического пептида, регулирующего патологическую активизацию ренин-ангиотензин-альдостероновой системы и симпатического отдела вегетативной нервной системы. Углубление фундаментальных знаний о вибрационно-опосредованной патологии определяет не только развитие и внедрение новых методов исследования в клинику профессиональной патологии, но и точки-мишени для фармакологического воздействия лекарственных препаратов, способных тормозить и вызывать регресс структурного ремоделирования миокарда и сосудов, как то ингибиторы ангиотензинпревращающего фермента, блокаторы ангиотензиновых рецепторов в комбинации с ингибитором неприлизина [67][68][69][70][71], блокаторы кальциевых каналов [72], а также пероральные сахароснижающие лекарственные средства [73,74].…”