Drug-Induced Atrial Fibrillation Complicates the Results of Flap Surgery in a Rat Model

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To the Editor:
We read with interest the article entitled Drug-induced atrial fibrillation complicates the results of flap surgery in a rat model by Masanobu et al1 in Annals of Plastic Surgery. We appreciate the authors' excellent work, including the establishment of rat atrial fibrillation (AF) model and their investigation of the effect of drug-induced AF on flap survival in rats. However, there are several points attracting our attention, and we would like to express some opinions of ours.
In experiment 1, the intra-arterial blood pressure of 4 AF rats was monitored, showing no obvious decrease when compared with control group. Although in experiments 2 and 3, the effect of drug-induced AF on flap survival was observed and analyzed on another 17 rats. Also, the authors concluded that it might be the compensated peripheral vasoconstriction that maintained the arterial blood pressure and caused the low blood inflow to flaps. From our perspective of view, it might have been more reasonable if the arterial blood pressure and the survival of flaps have been observed in the same AF rats.
Furthermore, the authors mentioned in the discussion part that cardiac output in AF is reduced by inadequate left ventricular inflow due to the absence of atrial contribution of blood. Invalid atrial contraction indeed contributes to the decreased cardiac output, but the awfully irregular and feeble contraction of left ventricle is also a significant and more direct factor for the failure of aortic valve opening and the subsequent decreased ejection fraction.2
Atrial fibrillation is the commonest arrhythmia in clinical practice. It impairs organic blood flow through decreased total cardiac output, compensated peripheral vasoconstriction, massive endothelial damage, and systemic thromboembolism.3 Also, any of these underlying mechanisms may explain the diminished survival of flaps in AF rats. To thoroughly investigate the effect of AF on flap survival and its mechanism, more comprehensive analysis and direct measurements are suggested: (1) Recently, vector flow imaging is increasingly used to assess local blood velocity and other hemodynamic parameters, among which the implantable Doppler is an excellent example applied to evaluate the vitality of flaps.4 The result of this experiment could have been more persuasive if blood pressure or velocity of the left superficial inferior gastric vessels (for pedicled flaps) and the right femoral vessels (for free flaps) has been measured directly. (2) Atrial fibrillation patients are at high risk of thrombosis from atrial emboli. Thrombus formation, especially those occurring in major blood supplying vessels, is fetal for flaps. In this experiment, postoperative histologic examination of flaps for any thrombi could have provided strong evidence of AF diminishing flap survival. (3) Except from compensatory effect, massive vasoconstriction could also be resulted from systemic endothelial damage triggered by AF.5 Therefore, indicators of endothelial dysfunction, such as the asymmetric dimethylarginine, might be examined in further researches to help us fully understand the mechanism through which AF imposes its negative effects on flaps.
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