The Journal of Thoracic and Cardiovascular Surgery, Vol 81, 408-418, Copyright © 1981 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Effect of left ventricular--to--aortic bypass on infarct size and infarct microcirculation in baboons
W Ruf, GT Smith, G Geary, V Pressler, RJ Anema, A Suehiro and JJ McNamara
A major diagonal branch of the left anterior descending coronary artery
(LAD) was acutely occluded in 17 baboons. Complete left ventricular (LV)
decompression was achieved with a left heart bypass (LHB) system in six
baboons while 11 baboons served as untreated controls. In the treated
group, LHB was initiated after 30 minutes of coronary occlusion. For a
period of 6 hours after occlusion, aortic pressure, LV pressure, left
atrial pressure, and cardiac output were monitored. During the same
monitoring period, electrograms were recorded from a high resolution matrix
of fixed epicardial electrodes. Regional myocardial blood flow was
determined prior to and at intervals following the initiation of LHB with
radioactive microspheres. Infarct size was assessed histologically from
serial cross sections of the left ventricle. The degree of salvage achieved
by LHB was assessed by comparing the epicardial area of infarction 6 hours
after occlusion (AI) to the area of epicardial St-segment elevation (STE)
30 minutes after occlusion (maxAST). In the LHB-treated group, 40.0% +/-
8.1% (SEM) of maxAST showed subsequent infarction; in the control group,
79.8% +/- 2.7% of maxAST showed eventual infarction (p less than 0.01). STE
overlying the region of ischemia in the LHB-treated group did not undergo
the spontaneous decline observed in the control group, which is normally
associated with the progression of necrosis. Regional myocardial blood flow
did not change significantly in the ischemic region during the period of
occlusion following LHB. LHB. The results suggest that LHB is capable of
substantial salvage of acutely ischemic myocardium by reducing myocardial
work and thus reducing myocardial oxygen requirements.