Prognostic role of diastolic dysfunction in patients undergoing transcatheter aortic valve replacement. Academic Article uri icon

Overview

abstract

  • OBJECTIVES: Prior studies have shown that left ventricular diastolic dysfunction (DD) is associated with increased mortality after surgical aortic valve replacement but studies on transcatheter aortic valve replacement (TAVR) are limited and have not taken into account mitral annular calcification (MAC), which limits the use of mitral valve annular tissue Doppler imaging. We performed a single-center retrospective analysis to better evaluate the role of baseline DD on outcomes after TAVR. METHODS: After excluding patients with atrial fibrillation, mitral valve prostheses and significant mitral stenosis, 359 consecutive TAVR patients were included in the study. Moderate-to-severe MAC was present in 58% of the patients. We classified patients into severe versus nonsevere DD based on the evaluation of elevated left ventricular filling pressure. The outcome measure was all-cause mortality or heart failure hospitalization. RESULTS: Over a mean follow-up time of 13 months, severe DD was associated with an increased risk for the outcome measure (HR 2.02 [1.23-3.30], p = .005). However, this association was lost in a propensity-matched cohort. In multivariate analysis, STS score was the only independent predictor of all cause mortality of heart failure hospitalization (HR 1.1 [1.05-1.15], p < .001). CONCLUSIONS: We evaluated the role of baseline DD on outcomes after TAVR by taking into account the presence of MAC. Severe DD was associated with increased all-cause mortality or heart failure hospitalization but not independently of other structural parameters and known predictors of the outcome measure.

publication date

  • August 9, 2019

Research

keywords

  • Aortic Valve
  • Aortic Valve Stenosis
  • Transcatheter Aortic Valve Replacement
  • Ventricular Dysfunction, Left
  • Ventricular Function, Left

Identity

Scopus Document Identifier

  • 85070466616

Digital Object Identifier (DOI)

  • 10.1002/ccd.28426

PubMed ID

  • 31397970

Additional Document Info

volume

  • 95

issue

  • 5