Abstract
This editorial refers to ‘Cavotricuspid isthmus dependent flutter is associated with an increased incidence of occult coronary artery disease’ by J.P. de Bono et al., on page 1774 de Bono et al. 1 report the coronary angiogram results on 138 patients undergoing ablation for typical atrial flutter (AFL, n ¼ 37) or atrial fibrillation (AF, n ¼ 61), in comparison to a control group of patients undergoing ablation for supraventricular tachycardia (SVT) or idiopathic right ventricular outflow tract tachycardia (RVOT-VT) (n ¼ 40). The demographic data for these groups were statistically similar, and the groups were evenly matched for age and coronary disease risk factors. The authors observed that patients undergoing ablation for typical AFL had a significantly higher incidence of occult (i.e. asymptomatic) coronary artery disease (CAD, P ¼ 0.005) compared with those undergoing ablation for AF, SVT, or RVOT-VT. Specifically, 54% of the AFL patients had coronary atheroma, compared with 26% of the patients with AF and 21% of the patients with SVT or RVOT-VT. No difference was noted in the incidence of coronary atheroma in patients with AF compared with those with SVT or RVOT-VT (P ¼ 0.68). However, the majority of the CAD detected was mild non-obstructive plaque, 75% in AFL patients, 44% in AF patients, and 67% in patients with SVT or RVOT-VT. The authors conclude that there may be a mechanistic link between the right atrial substrate underlying typical AFL and that it may be responsible for a higher incidence of CAD in these patients, when compared with similar age- and CAD risk factormatched patients with AF, SVT, or RVOT-VT. What specific mechanistic link this might be, however, is not determined by this strictly observational report. The authors note that there is a close relationship between AF and AFL, with pulmonary vein ectopy commonly triggering both AF and AFL. 2 However, although not all patients with AFL have AF, most patients with AF have AFL at one time or another. 2 Thus, the authors note that patients with typical AFL probably have a substrate that ‘specifically allows initiation and maintenance of AF’. This has been previously shown to be true, with slower conduction velocity noted in the right atrium in the medial cavo-tricuspid isthmus (CTI) and inferior septum compared with other areas in the atrium, and slower conduction in the CTI in patients with AFL compared with those with SVT. 3,4 The mechanism responsible for this slower conduction velocity is not known 3,4 and has never been specifically studied. Thus, the findings of this study are intriguing, suggesting that underlying CAD could be a possible causative factor, leading to ischaemia and fibrosis of the right atrium. Unfortunately, it appears that the CAD in most patients with AFL in this study was very mild, and not likely to cause ischaemia. Therefore, an alternative explanation must be sought if this phenomenon is true, and not just a chance observation due to the small number of patients included in this study.
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