Baseline left ventricular diastolic dysfunction affects midterm mortality after transcatheter aortic valve implantation

Abstract

Objectives To determine whether preprocedural left ventricular (LV) diastolic dysfunction impairs midterm mortality after transcatheter aortic valve implantation (TAVI) for patients with severe aortic stenosis (AS), we performed a meta‐analysis of currently available evidence. Methods We identified all studies investigating impact of preprocedural severity of LV diastolic dysfunction on midterm (≥1‐year) all‐cause mortality after TAVI for patients with AS through a search of databases (MEDLINE and EMBASE) until September 2019. From each study, we extracted an adjusted (if unavailable, unadjusted) hazard ratio (HR) of midterm mortality. We pooled study‐specific estimates in the random‐effects model. Results Ten eligible studies with a total of 2380 patients with AS undergoing TAVI were identified. In accordance with pooled analyses, higher‐grade preprocedural LV diastolic dysfunction was associated with significantly worse midterm all‐cause mortality after TAVI compared to lower‐grade dysfunction (HR for grade II vs I, 1.15; P = .002; HR for grade III vs I, 1.35; P = .001; HR for grade III vs II; 1.16, P = .002; HR for grade II‐III vs I, II‐III vs 0‐I, or III vs I‐II, 1.34; P < .00001 [primary meta‐analysis]; HR per grade, 1.16; P = .003). No funnel plot asymmetry for the primary meta‐analysis (for grade II‐III vs I, II‐III vs 0‐I, or III vs I‐II) was identified, which probably indicated no publication bias (P = .381 by the linear‐regression test). Conclusion Higher‐grade preprocedural LV diastolic dysfunction was associated with worse midterm all‐cause mortality after TAVI for patients with AS compared to lower‐grade dysfunction.

Low Circulating Musclin is Associated With Adverse Prognosis in Patients Undergoing Transcatheter Aortic Valve Implantation at Low‐Intermediate Risk

“…In addition, diabetes, insulin therapy, and body mass index were included in a second multiple Cox regression analysis (model 2 with an effect size of 0.109), as musclin has been implicated as a putative target for obesity and associated diseases. 14 , 24 To assess the predictive capacity of musclin in terms of 1‐year cumulative survival, the following variables were included as possible confounders: previous percutaneous coronary intervention, 25 , 26 EuroSCORE II, 8 left ventricular dysfunction, 27 frailty, 28 , 29 atrial fibrillation, 30 NTproBNP, 31 high‐sensitivity troponin T, 32 absence of preexisting AR, 33 , 34 chronic obstructive pulmonary disease, 35 arterial hypertension, peripheral artery disease, 36 albumin level, 37 age, sex, 38 , 39 body mass index, 40 , 41 diabetes, 24 , 42 and insulin therapy 43 . For exploratory purposes, we further estimated improved risk stratification by log‐rank test for linear trend to compare survival curves based on dichotomized circulating musclin and clinical risk: (1) higher musclin level (≥2.862 ng/mL) and low clinical risk (EuroSCORE II <4%); (2) higher musclin level (≥2.862 ng/mL) and intermediate EuroSCORE II; (3) lower musclin level (<2.862 ng/mL) and low EuroSCORE II; and (4) lower musclin level (<2.862 ng/mL) and intermediate EuroSCORE II.…”