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Related Experiment Videos

Right ventricular dysfunction persists following brief right ventricular pressure overload

C Greyson1, Y Xu, J Cohen

  • 1San Francisco Department of Veterans Affairs Medical Center, CA, USA. greyson@cardio.ucsf.edu

Cardiovascular Research
|May 1, 1997
PubMed
Summary

Acute pulmonary hypertension causes persistent right ventricular (RV) contractile dysfunction. This dysfunction remains even after normal loading conditions are restored, indicating lasting impairment of RV function.

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Area of Science:

  • Cardiovascular Physiology
  • Pulmonary Circulation
  • Cardiac Mechanics

Background:

  • Acute pulmonary hypertension can lead to right ventricular (RV) contractile failure.
  • Complete recovery of RV function after acute pulmonary hypertension is often assumed upon normalization of loading conditions, but this has not been thoroughly investigated.

Purpose of the Study:

  • To test the hypothesis that acute RV pressure overload results in RV contractile dysfunction that persists after control loading conditions are re-established.

Main Methods:

  • Eighteen pigs underwent 1-hour pulmonary artery constriction to induce acute pulmonary hypertension.
  • RV free wall function was assessed using pressure-segment length loops and preload recruitable stroke work relations.
  • Global RV function was evaluated using stroke work versus end-diastolic pressure relations.

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Main Results:

  • RV systolic shortening decreased during pulmonary artery constriction but normalized after release.
  • Despite normalized pressures, persistent RV contractile dysfunction was observed, with reduced RV free wall systolic shortening, regional external work, and global RV stroke work.
  • The depressed regional work was linked to a shift in the preload recruitable stroke work relation, not RV ischemia.

Conclusions:

  • Acute pulmonary hypertension induces RV contractile dysfunction that lasts for at least 2 hours after loading conditions return to normal.
  • This persistent dysfunction is not caused by RV ischemia during the pressure overload period.