Myocardial dysfunction in patients with aortic stenosis and hypertensive heart disease assessed by MR tissue phase

Florian von Knobelsdorff-Brenkenhoff1, Pierre Hennig1, Marius Menza2

  • 1Working Group Cardiovascular Magnetic Resonance, Experimental and Clinical Research Center, a joint cooperation between the Charité Medical Faculty and the Max-Delbrueck Center for Molecular Medicine; and HELIOS Klinikum Berlin Buch, Department of Cardiology and Nephrology, Berlin, Germany.

Insights

Left ventricular pressure overload from aortic stenosis and hypertensive heart disease reduces myocardial velocities, even with preserved ejection fraction. This indicates early functional impairment in these conditions.

Area of Science:

  • Cardiovascular Imaging
  • Cardiac MRI
  • Myocardial Mechanics

Background:

  • Left ventricular pressure overload, caused by conditions like aortic stenosis and hypertensive heart disease, can lead to subtle myocardial dysfunction.
  • Early detection of functional impairment is crucial for timely intervention and improved patient outcomes.

Purpose of the Study:

  • To investigate abnormalities in myocardial velocities in patients with left ventricular pressure overload using magnetic resonance tissue phase mapping (TPM).
  • To assess the impact of aortic stenosis (AS) and hypertensive heart disease (HYP) on left ventricular (LV) myocardial motion.

Main Methods:

  • Utilized three-directional velocity-encoded phase-contrast MRI at 3T to acquire basal, midventricular, and apical slices in 33 patients (9 HYP, 24 AS) and 41 controls.
  • Measured peak longitudinal (Vz) and radial (Vr) velocities during systole and diastole (Peaksys, Peakdias) in myocardial segments.
  • Assessed changes during handgrip exercise in a subgroup of patients and controls.

Main Results:

  • Patients with AS showed significantly reduced Vz-Peaksys and Vr-Peaksys compared to controls.
  • Both AS and HYP groups exhibited lower diastolic velocities (Vz-Peakdias, Vr-Peakdias) in multiple LV segments.
  • AS patients with fibrosis had reduced velocities even in non-fibrotic segments; velocities remained unchanged during exercise in AS/HYP but decreased in controls.

Conclusions:

  • Reduced peak longitudinal and radial velocities in the LV are present in AS and HYP, even with preserved ejection fraction.
  • These velocity reductions signify early functional impairment in the left ventricle due to pressure overload.
  • TPM is a valuable tool for detecting subtle myocardial functional changes in cardiovascular diseases.
Abstract

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