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J Thorac Cardiovasc Surg 1994;107:220-225
© 1994 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Intraoperative myocardial ischemia detection with laser-induced fluorescence

Boston, Mass.

From the Department of Surgery, Harvard Medical School, The Division of Cardiac Surgery, Brigham and Women's Hospital, and Wellman Laboratory of Photomedicine,^a Harvard Medical School, Boston, Mass.

Received for publication Sept. 2, 1992. Accepted for publication Mar. 1, 1993. Address for reprints: Lawrence H. Cohn, MD, Chief, Division of Cardiac Surgery, Brigham and Women's Hospital, 75 Francis St., Boston, MA 02115.

Abstract

Myocardial ischemia can be detected at the mitochondrial level by measuring shifts in nicotinamide adenine dinucleotide and its reduced form. Using a pulsed nitrogen laser and an optical multichannel analyzer, we monitored myocardial metabolism by measuring laser-induced nicotinamide adenine dinucleotide (reduced form) fluorescence in a large animal model of acute ischemia. Eight opened-chest sheep underwent occlusion of branches of the left anterior descending coronary artery, establishing a 15% infarct of the left ventricle. For the simulation of the clinical scenario, after 60 minutes of occlusion, the animals were supported by cardiopulmonary bypass, the aorta was crossclamped, and cold crystalloid cardioplegic solution was administered. The occlusion was removed after 10 minutes, and two additional doses of cardioplegic solution were delivered at 10-minute intervals. The aortic crossclamp was released, and a 30-minute period of reperfusion on bypass ensued. The hearts were then weaned off bypass and allowed to recover. Laser-induced fluorescence was measured inside, outside, and along the border of the infarct. Baseline measurements were made before occlusion, immediately after occlusion, and then at 5, 10, and 20 minutes after occlusion. The results show that immediately after occlusion there is a 200% ± 30% (mean ± standard deviation) increase in laser-induced fluorescence in the infarct zone, a 110% ± 30% increase along the border, and no significant change in the area outside the infarct. The fluorescence in the infarct reaches a plateau in 5 minutes at 270% ± 30%, where it remains for all areas until the aortic crossclamp is removed. Fluorescence then drops to 70% ± 20%whereas along the border it reaches peak near end ischemia of 110% ± 40%. With the first dose of cardioplegic solution, fluorescence increases outside the infarct and decreases inside the infarct and along the border to 120% ± 30% and finally returns to baseline after 5 minutes of recovery. All of these shifts in laser-induced fluorescence were statistically significant (p < 0.01). The changes noted with doses of cardioplegic solution reflect the hypothermic and hyperkalemic effects on the myocardium. Laser-induced flurescence provides and sensitive and specific method of monitoring myocardial ischemia during the operation. It also provides instantaneous feedback of metabolic changes that may be useful in evaluating the effects of different cardioplegic regimens and in monitoring reperfusion injury. (J THORAC CARDIOVASC SURG 1994;107:220-5)

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