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Evaluation of Left Ventricular Structure and Function using 3D Echocardiography
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Left ventricular geometry and function preceding neurally mediated syncope.

J E Liu1, R T Hahn, K M Stein

  • 1Department of Medicine, Division of Cardiology, The New York Hospital-Cornell Medical Center, New York, NY 10021, USA.

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|February 23, 2000
PubMed
Summary
This summary is machine-generated.

Neurally mediated syncope is not caused by increased left ventricular (LV) contractility. Reduced LV function and volume during upright tilt are linked to positive tilt-table test responses in syncope patients.

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Area of Science:

  • Cardiology
  • Physiology

Background:

  • Neurally mediated syncope is linked to increased left ventricular (LV) fractional shortening (FS) during tilt testing.
  • This suggests LV mechanoreceptor stimulation causes reflex hypotension, but FS is affected by afterload and preload, not just contractility.

Purpose of the Study:

  • To investigate the role of LV contractility in neurally mediated syncope.
  • To compare LV performance measures corrected for end-systolic stress (ESS) in patients with positive versus negative tilt-table test responses.

Main Methods:

  • Echocardiography was used to assess LV performance in 21 patients with unexplained syncope during supine and upright tilt positions.
  • LV measures, including stroke volume, FS, and stress-corrected midwall shortening, were compared between tilt-positive and tilt-negative groups.

Main Results:

  • In the supine position, both groups showed similar LV performance.
  • During upright tilt, the tilt-positive group exhibited lower stroke volume, reduced stress-corrected midwall shortening, and decreased endocardial FS.
  • The tilt-positive group also showed a greater reduction in ESS and FS early during tilt.

Conclusions:

  • Reduced end-systolic stress (ESS), LV volume, and chamber function during initial upright tilt correlate with positive tilt responses in syncope patients.
  • These findings suggest that LV hypercontractility or increased systolic wall stress do not trigger neurally mediated syncope via LV mechanoreceptor activation.