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J Thorac Cardiovasc Surg 1999;117:447-453
© 1999 Mosby, Inc.
SURGERY FOR ADULT CARDIOVASCULAR DISEASE |
From the Departments of Thoracic Surgerya and Cardiothoracic Anesthesia,b Karolinska Hospital, Stockholm, Sweden.
Supported by grants from the Wallenberg Foundation, the Swedish Heart-Lung Foundation, the Swedish Medical Research Council, and funds from the Karolinska Institute.
Received for publication June 1, 1998. Revisions requested Aug 19, 1998. Revisions received Sept 8, 1998. Accepted for publication Oct 7, 1998. Address for reprints: Göran Källner, MD, Department of Cardiothoracic Surgery and Anesthesiology, Karolinska Institute at Huddinge University Hospital, S-141 86 Huddinge, Sweden.
Objective: Because of adverse effects of cardiopulmonary bypass and the prospect of shortening intensive care and hospital stay, coronary artery bypass grafting without cardiopulmonary bypass is gaining increased attention. The impact of the localized myocardial ischemia that is inherent in these procedures has not been thoroughly investigated in human beings. We have investigated metabolic changes, possible myocardial damage, and myocardial outflow of the vasodilator calcitonin gene-related peptide during coronary artery bypass grafting without cardiopulmonary bypass.
Methods: Coronary sinus and arterial blood was sampled before coronary arterial occlusion, after 10 minutes of ischemia, and after 1 and 10 minutes of reperfusion in 9 consecutive patients (mean age 70 ± 5 years) who had an anastomosis performed to the left anterior descending artery without cardiopulmonary bypass.
Results: No perioperative myocardial infarctions occurred. The arteriovenous difference in lactate decreased during ischemia, to reach a minimum after 1 minute of reperfusion (0.17 ± 0.25 vs 0.15 ± 0.25 mmol/L before ischemia; P = .008). Myocardial lactate extraction decreased (from 11.2 ± 13.6 µmol/min before ischemia to 3.0 ± 7.0 µmol/min after 1 minute of reperfusion; P = .012), that is, a net production of lactate. The arteriovenous difference in calcitonin gene-related peptide decreased from 0.1 ± 2.6 pmol/L before ischemia to 30.5 ± 26.5 pmol/L (P = .008) after 1 minute of reperfusion.
Conclusions: The localized myocardial ischemia associated with these procedures causes metabolic changes in the myocardium, but no myocardial damage. The ischemia-related outflow of calcitonin gene-related peptide indicates that the vasodilating and cardioprotective properties of this peptide that are known from animal studies may be of importance in myocardial ischemia in human beings.
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