Reactivity of the human internal thoracic artery to vasodilators in coronary artery bypass grafting

Aazami and Salehi must be commended for speculating that systolic coronary perfusion disturbance can be a factor in the occurrence of postoperative atrial fibrillation (AF) as a unique pathophysiological pathway by inducing functional atrial ischemia [1]. However, as their proposed pathophysiological mechanism still needs validation therefore at present the issue of whether or not we are missing a common pathophysiological pathway is irrelevant. They have also pointed out that unaccounted for confounding factors in randomised controlled trials (RCTs) such as more deliberate revascularization in on-pump coronary artery bypass grafting and nature of grafts may influence the incidence of postoperative AF. I will agree with Aazami and Salehi in this regard. Unfortunately confounding is perhaps the most significant dilemma even in well designed and analysed surgical RCTs. Despite randomisation being the ultimate method for arriving at comparable groups [2], because it indirectly matches for all prognostic variables, recognized and unrecognised, equipoise is impossible to achieve in surgical RCTs due to several hidden confounding factors. Hence, unless more sophisticated statistical methods and randomisation techniques are devised, bias in surgical RCTs cannot be completely eliminated although it can be minimized. Finally as for their view that efficient off-pump total arterial revascularization appears unconceivable at present owing to concerns about the increased risk of competitive flow with early arterial graft failure I will take this opportunity to highlight that plenty of evidence from RCTs as well as retrospective studies is available to validate that total arterial myocardial revascularization can be safely performed as an off-pump procedure, even in the treatment of multiple-vessel coronary disease [3,4]. In fact, off-pump composite total arterial grafting has become a routine these days with concerns about competitive flow, the mechanism of which is more complex than that in the individual graft, not yet proven [5]. It is important to remember that competitive flow is not only caused by the relation between the graft and its target coronary branch where competitive flow occurs, but also by the interactions of all anastomosed branches within the composite graft, the phasic delay between the in situ grafts, and the whole graft arrangement in the patient [5]. Therefore, prevention of competitive flow and graft occlusion depends entirely on adequate surgical strategy and manoeuvre rather than whether the revascularization is performed on-pump or off-pump.