Abstract

In atrial fibrillation, exercise capacity is often reduced. This is usually ascribed to a decreased cardiac output as compared with sinus rhythm. Very few studies, however, have focused on changes in the peripheral blood flow during atrial fibrillation as a potential mechanism for exercise limitation. The aim of the present study was to determine the effect of conversion of atrial fibrillation to sinus rhythm on peripheral blood flow. Calf blood flow, using an electrocardiogram-triggered venous occlusion plethysmograph, and peak oxygen consumption (peak VO2), using treadmill exercise testing, were studied in 28 patients with chronic atrial fibrillation eligible for electrical cardioversion. Measurements were performed before cardioversion, and repeated 1 day and 1 month thereafter. Calf blood flow at rest, maximal calf blood flow, and minimal calf vascular resistance during the hyperaemic response immediately following 700 J of calf exercise were determined plethysmographically. One day and 1 month after cardioversion, 23 and 14 patients were still in sinus rhythm, respectively. In patients who still had sinus rhythm after 1 month, maximal calf blood flow increased from 33.7 +/- 12 to 40.0 +/- 13 ml. 100 ml-1.min-1 (P < 0.01) and minimal calf vascular resistance fell from 3.2 +/- 0.9 to 2.7 +/- 0.7 mmHg. ml-1. 100 ml-1. min-1 (P < 0.01); peak VO2 increased from 21.3 +/- 4 to 24.2 +/- 5 ml. min-1. kg-1 (P < 0.001). Calf blood flow at rest did not improve. In contrast, no significant changes in maximal calf blood flow, minimal calf vascular resistance and peak VO2 occurred in patients who had atrial fibrillation 1 month after cardioversion. A significant correlation was found between changes in maximal calf blood flow and peak VO2 1 month after cardioversion (r = 0.53, P < 0.01). One day after cardioversion, no changes in calf blood flow or peak VO2 were found, either in patients with sinus rhythm or atrial fibrillation. In conclusion, transition from chronic atrial fibrillation to sinus rhythm is associated with a (delayed) improvement in maximal calf blood flow, minimal calf vascular resistance, and peak VO2. Our findings suggest that increase in vasodilatory reserve capacity may contribute to the improvement of exercise capacity after cardioversion of atrial fibrillation.

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