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Ann Thorac Surg 2003;75:1252
© 2003 The Society of Thoracic Surgeons
Department of Thoracic Surgery, Karolinska Hospital, Stockholm 17176, Sweden
e-mail: jarle.vaage{at}ks.se
Experimentally preconditioning is the most powerful mode of protection against ischemia-reperfusion injury known. In cardiac surgery with cardiopulmonary bypass and cardioplegia, most studies conclude that preconditioning improves myocardial preservation [1]. Only a few investigations have studied ischemic preconditioning in off-pump coronary artery bypass grafting (OPCAB) [2, 3], and the present study is an important contribution to this line of research. It is a timely and well-conducted study, which is the only one conducted on OPCAB with multivessel disease and multiple distal anastomoses. There was, however, no effect of preconditioning, which is in disagreement with another recent paper [3].
The two studies have used different preconditioning models, and nobody knows which one is optimal in humans. Animal studies have shown that protection is dependent on the preconditioning model. The endpoints are release of biochemical markers [3], metabolic parameters (this study), or cardiovascular performance [3]. Laurikka and colleagues [3] found less release of troponin I and higher stroke volume index in the preconditioned group during the early postoperative period. However, all other hemodynamic parameters were similar, so even in that work [3] the effect of preconditioning in OPCAB is almost negligibleand also distinctly less than what that group found after on-pump surgery with the same preconditioning model [1].
The conclusion must be that preconditioning is not very effective in OPCAB. Why does preconditioning not work in OPCAB when it is so effective in experimental studies of regional ischemia-reperfusion? The explanation may be the endpoints. In the experimental studies, the sustained ischemia is always longer than in OPCAB and the endpoint is always myocardial necrosis or infarct size. Is there no or only negligible necrosis in uncomplicated OPCAB? There is stunning in OPCAB, and animal studies have shown that early preconditioning has probably no effect on stunning [2, 4], although there is some evidence that delayed preconditioning may attenuate stunning. Since preconditioning is cardioprotective in coronary bypass surgery with cardiopulmonary bypass, does this mean that there is more necrosis after cardioplegia than in OPCAB? Some proponents of OPCAB may agree on this.
The main conclusion is that early ischemic preconditioning is not cardioprotective in OPCAB. However, since preconditioning also may attenuate postischemicpostoperative arrhythmias [5], there may still be a general indication for preconditioning in OPCAB. Additionally preconditioning of the mainstem of the right coronary artery may reduce the effects on the conduction system if this artery is occluded during OPCAB? These questions have not yet been addressed.
References
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