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Ann Thorac Surg 1998;66:726-732
© 1998 The Society of Thoracic Surgeons

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Original articles: Cardiovascular

Preconditioning during simulated MIDCABG attenuates blood flow defects and neutrophil accumulation

^a Division of Cardiothoracic Surgery, Department of Surgery, Emory University School of Medicine, Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, Crawford Long Hospital, Atlanta, Georgia, USA

Address reprint requests to Dr Vinten-Johansen, Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, Crawford Long Hospital, 550 Peachtree St NE, Atlanta, GA 30365-2225

Presented at the Forty-fourth Annual Meeting of the Southern Thoracic Surgical Association, Naples, FL, Nov 6–8, 1997.

Background. Ischemic preconditioning (IP) may be cardioprotective in minimally invasive direct coronary artery bypass where cardioplegia is not used. This study tested the hypothesis that IP of the area at risk (AAR) would attenuate postischemic injury from transient coronary artery occlusion.

Methods. In 19 anesthetized dogs, the left anterior descending coronary artery was occluded for 30 minutes (simulating coronary occlusion during anastomosis) followed by 3 hours of reperfusion. In 10 dogs, occlusion was preceded by 5 minutes of occlusion and 5 minutes of reperfusion (IP), whereas 9 other dogs had no IP (control, C).

Results. Thirty minutes of left anterior descending occlusion caused comparable dyskinesis (systolic shortening, sonomicrometry) in the AAR in C (baseline, 29% ± 3% to 3% ± 2%) and in IP (baseline, 29% ± 2% to -0.3% ± 2%). After 3 hours of reperfusion, systolic shortening was significantly depressed in C (20% ± 4%), and was not significantly improved by IP (24% ± 3%, p = 0.8 versus C). Postischemic diastolic stiffness in the AAR was not altered by IP versus C (0.60 ± 0.12 versus 0.41 ± 0.13). Plasma creatine kinase activity was similar between C and IP at the end of reperfusion (20 ± 11 versus 16 ± 5 U/g). Postischemic AAR blood flow (in milliliters per minute per gram of tissue) at 180 minutes of reperfusion decreased by 56% versus baseline in C (from 1.04 ± 0.4 to 0.46 ± 0.12; p < 0.05) compared with no change in IP (from 0.74 ± 0.23 to 0.60 ± 0.10), but there was no significant group difference at this time. Myeloperoxidase activity as an index of neutrophil accumulation in AAR was decreased in IP versus C (0.4 ± 0.09 versus 0.7 ± 0.04 U/µg tissue).

Conclusions. Ischemic preconditioning does not decrease postischemic wall motion and only modestly increases postischemic blood flow abnormalities in the AAR, but does significantly inhibit neutrophil accumulation.

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