Influence of hypertension on systolic and diastolic left ventricular function including segmental strain and strain

Mikhail Kornev1,2, Hatice Akay Caglayan1,2, Alexander V Kudryavtsev3,4

  • 1Department of Cardiology, Division of Cardiothoracic and Respiratory Medicine, University Hospital of North Norway, Tromso, Norway.

Insights

Hypertension impairs left ventricular (LV) systolic and diastolic functions, reducing strain and strain rate parameters. Impaired relaxation (SR E) is key in diastolic dysfunction, while SR A is less affected by hypertension.

Area of Science:

  • Cardiology
  • Cardiovascular Imaging
  • Hypertension Research

Background:

  • Left ventricular (LV) systolic and diastolic functions are crucial cardiovascular risk predictors.
  • Limited data exists on segmental, layer-specific strain, and diastolic strain rates in hypertensive patients.

Purpose of the Study:

  • To investigate segmental two-dimensional strain rate imaging (SRI)-derived parameters.
  • To characterize LV systolic and diastolic function in hypertensive individuals compared to normotensive individuals.

Main Methods:

  • Utilized data from 1194 participants in Russia and 1013 in Norway.
  • Divided participants into four blood pressure (BP) subgroups (normal, treated normal BP, moderate hypertension, severe hypertension).
  • Analyzed global and segmental layer-specific strains and strain rates (SR E, SR A) using strain and SR (S/SR) analysis.

Main Results:

  • Systolic and diastolic global and segmental S/SR decreased with increasing BP.
  • SR E, indicating impaired relaxation, showed the most significant differences between groups.
  • Apico-basal gradients in S/SR were observed, with SR A increasing with BP, while end-systolic strain showed epicardial-to-endocardial gradients.

Conclusions:

  • Arterial hypertension negatively impacts global and segmental LV systolic and diastolic S/SR parameters.
  • Impaired relaxation (SR E) is the primary driver of diastolic dysfunction in hypertension.
  • Segmental strain, SR E, and SR A offer novel insights into LV mechanics in hypertensive hearts.
Abstract

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