The effects of mechanical cardiac stabilization on left ventricular performance
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Updated: Oct 28, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
Published on: April 8, 2013
W R Burfeind1, F G Duhaylongsod, D Samuelson
1Department of Surgery, DUMC-3457, Durham, NC 27710, USA.
Objective:
Mechanical cardiac stabilization is beneficial for precise coronary anastomoses on the beating heart. However, the effect of mechanical cardiac stabilization on hemodynamics, left ventricular performance, and the degree of injury to underlying tissue are uncertain.
Methods:
Twelve swine (20-30 kg) underwent median sternotomy and a mechanical stabilizing device (United States Surgical, Norwalk, CT) was positioned astride a segment of left anterior descending coronary artery (LAD). Coronary blood flow was measured by Doppler. Sonomicrometry crystals were placed distal to the stabilizer in a region of myocardium subtended by the LAD, and a left ventricular micromanometer was inserted. Regional myocardial function was determined using the preload recruitable stroke work (PRSW) relationship. Data were acquired at three time points: 20 min before (PRE) and after placing the stabilizer (EXPT); and 20 min after removing the stabilizer (POST). Tissue subjacent to the stabilizer was then biopsied. Means +/- standard deviation are reported.
Results:
The mechanical stabilizer caused a decrease in cardiac output from 4.2+/-1.5 to 3.6+/-1.3 l/min (P < 0.05), which returned to baseline values after its removal. Regional myocardial function (percent systolic shortening and MW and x-intercept of the PRSW relationship) was unchanged. Blood pressure, heart rate, and LAD blood flow remained constant. Histologic findings included a layer of myocyte necrosis less than 1 mm in depth immediately beneath the stabilizer.
Conclusions:
These data demonstrate that mechanical stabilization of the LAD may temporarily decrease cardiac output. This is not attributed to impaired contractility or ischemia, but is secondary to direct ventricular compression with reduced stroke volume. Injury to underlying tissue is negligible.
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