Abstract
BackgroundThere is increasing evidence that programmed cell death can be triggered during cardiopulmonary bypass (CPB) and may be involved in postoperative complications. The purpose of this study was to investigate whether apoptosis occurs during aortic valve surgery and whether modifying temperature during CPB has any influence on cardiomyocyte apoptotic death rate.Methods20 patients undergoing elective aortic valve replacement for aortic stenosis were randomly assigned to either moderate hypothermic (ModHT group, n = 10, 28°C) or mild hypothermic (MiHT group, n = 10, 34°C) CPB. Myocardial samples were obtained from the right atrium before and after weaning from CPB. Specimens were examined for apoptosis by flow cytometry analysis of annexin V-propidium iodide (PI) and Fas death receptor staining.ResultsIn the ModHT group, non apoptotic non necrotic cells (annexin negative, PI negative) decreased after CPB, while early apoptotic (annexin positive, PI negative) and late apoptotic or necrotic (PI positive) cells increased. In contrast, no change in the different cell populations was observed over time in the MiHT group. Fas expression rose after reperfusion in the ModHT group but not in MiHT patients, in which there was even a trend for a lower Fas staining after CPB (p = 0.08). In ModHT patients, a prolonged ischemic time tended to induce a higher increase of Fas (p = 0.061).ConclusionOur data suggest that apoptosis signal cascade is activated at early stages during aortic valve replacement under ModHT CPB. This apoptosis induction can effectively be attenuated by a more normothermic procedure.
Highlights
There is increasing evidence that programmed cell death can be triggered during cardiopulmonary bypass (CPB) and may be involved in postoperative complications
Recent reports have documented the prevalence of programmed cardiomyocyte death in open heart surgery under cardiopulmonary bypass (CPB), where it may contribute in parallel with necrosis to increase the bulk of myocardial death cells [3,4,5,6,7,8,9,10,11,12]
Groups were well matched in terms of age, sex, prevalence of cardiovascular risk factors and atrial fibrillation, preoperative left ventricular function, and duration of CPB and aortic crossclamping (Table 1)
Summary
There is increasing evidence that programmed cell death can be triggered during cardiopulmonary bypass (CPB) and may be involved in postoperative complications. Apoptosis that occurs in this clinical setting can be induced by a wide variety of conditions and agents, including reactive oxygen-derived species, calcium and pressure overload, mechanical stress, nitric oxide, tumor necrosis factor, and angiotensin II [2,13]. It remains unclear whether apoptosis is a primary or a secondary event within cardiac surgery, and while some authors have related it to postoperative myocardial stunning [9] and non cardiac complications [3,4]; others have observed that inhibition of apoptosis has no impact on postischemic left ventricle functional recovery [14]. The investigation of early apoptotic signs, such as the translocation of membrane phospholipids or the activation of intracellular proteins, using more accurate tools may overcome these limitations
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