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Troponin Release and Reversible Left Ventricular Dysfunction After Transient Pressure Overload.

Brian R Weil1, Gen Suzuki2, Rebeccah F Young2

  • 1Department of Physiology and Biophysics, University at Buffalo, Buffalo, New York; Clinical and Translational Research Center of the University at Buffalo, Buffalo, New York.

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Summary

Elevated left ventricular preload can cause cardiac troponin I (cTnI) release and myocyte apoptosis without ischemia. This finding helps explain cTnI elevations in patients without signs of myocardial ischemia.

Keywords:
cardiac troponin Icardiomyocyte apoptosisleft ventricular preloadmyocardial stretchmyocardial stunningpressure overload

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Area of Science:

  • Cardiology
  • Cardiovascular Physiology
  • Biomarker Research

Background:

  • Previous studies showed ischemia causes cardiac troponin I (cTnI) release and myocyte apoptosis without necrosis.
  • The effect of other stresses on cTnI release and apoptosis without ischemia was unclear.

Purpose of the Study:

  • To investigate if increased left ventricular (LV) preload causes cTnI release and myocyte apoptosis in the absence of ischemia.

Main Methods:

  • Swine underwent phenylephrine infusion to increase LV end-diastolic pressure (LVEDP) to ~30 mm Hg.
  • Serial cTnI levels, echocardiographic function, and myocardial tissue apoptosis/necrosis were assessed over 24 hours.

Main Results:

  • Phenylephrine increased LVEDP and blood pressure without causing ischemia.
  • Transiently elevated LVEDP led to significant cTnI release and myocyte apoptosis.
  • LV ejection fraction was depressed but recovered within 24 hours, with no necrosis observed.

Conclusions:

  • Transient preload elevation induces cTnI release, myocyte apoptosis, and reversible cardiac stunning without ischemia.
  • Preload-induced myocyte injury may explain elevated cTnI in the absence of clinical myocardial ischemia.