The role and clinical implications of diastolic dysfunction in aortic stenosis Review uri icon

Overview

MeSH Major

  • Aortic Valve Stenosis
  • Heart Ventricles
  • Hypertrophy, Left Ventricular
  • Ventricular Dysfunction, Left
  • Ventricular Function, Left
  • Ventricular Remodeling

abstract

  • Diastolic dysfunction in aortic stenosis results primarily from left ventricular hypertrophy and myocardial fibrosis due to chronically elevated left ventricular systolic pressure. Currently, diastolic dysfunction does not have an explicit clinical role in management of patients with aortic stenosis. Studies have shown that improvement in diastolic dysfunction follows left ventricular remodelling after aortic valve replacement and that it occurs gradually or incompletely. Retrospective studies suggest that advanced grades of diastolic dysfunction at baseline are associated with increased mortality and adverse events even after aortic valve replacement. Recent studies have also associated myocardial fibrosis, a hallmark of diastolic dysfunction, with worse outcomes. In addition, these results were independent of the degree of aortic stenosis or valve replacement. Indirect evidence of the role of diastolic dysfunction in aortic stenosis also comes from paradoxical low-flow, low-gradient aortic stenosis, where disproportionate left ventricular hypertrophy leads to underfilling of the left ventricle, low-flow state and is associated with worse prognosis. Lastly, a limited number of studies suggest that worse diastolic dysfunction at baseline is detrimental in patients who develop aortic regurgitation after transcatheteraortic valve replacement, due to superimposition of volume overload on a stiff left ventricle. Current major limitations in our understanding of the prognostic role of diastolic dysfunction are the lack of universally accepted classification schemes, its dependence on dynamic loading conditions and the lack of larger prospective studies.

publication date

  • October 2017

Research

keywords

  • Review

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1136/heartjnl-2017-311506

PubMed ID

  • 28684437

Additional Document Info

start page

  • 1481

end page

  • 1487

volume

  • 103

number

  • 19