ELECTRICAL REMODELING OF THE HUMAN ATRIUM - SIMILAR EFFECTS IN PATIENTS WITH CHRONIC ATRIAL-FIBRILLATION AND ATRIAL-FLUTTER

Objectives. This study sought to determine whether chronic atrial fibr illation (AF) and atrial flutter in patients lead to electrical remode ling of the human atrial myocardium, manifested by an abnormal relatio n between atrial cycle length and action potential duration (APD). Bac kground. Experimental studies in goats and isolated human atrial tissu e have shown that prolonged AF leads to persistent shortening of atria l refractoriness, a phenomenon referred to as electrical remodeling an d which helps to explain why AF begets AF. Direct data on human in sit u myocardium are still lacking. Methods. Using monophasic action poten tial recordings at two right atrial sites simultaneously, we determine d in 7 patients with chronic AF and 13 with chronic atrial flutter (3 weeks to 3 years in duration) the relation between paced cycle length and APD at 90% repolarization (APD90) 15 to 30 min after conversion to sinus rhythm. APD90 was measured during regularly paced cycle lengths (250 to 800 ms) to determine the steady state cycle length relation a nd during extrastimulus intervals (from 800 ms to refractoriness) at a basic cycle length of 600 ms to determine electrical restitution curv es. The same pacing protocols and measurements were performed in nine control patients with sinus rhythm and no overt atrial disease. Result s. In control patients, steady state APD90 increased steadily with inc reases in cycle length from 250 to 800 ms, reaching a maximal value of 325 +/- 41 ms (mean +/- SD) at a cycle length of 800 ms. In patients with cardioversion from atrial flutter or AF, the steady state cycle l ength-APD90 relation was shifted downward and flattened at cycle lengt hs >400 ms, reaching only 219 +/- 44 and 245 +/- 39 ms, respectively, at the 800 ms cycle length (p < 0.005 vs. control). The early time cou rse of electrical restitution (200- to 300-ms extrastimulus intervals) was similar between all three groups, but at extrastimulus intervals >350 ms, APD90 was shorter in both the AF and atrial putter groups tha n in the control group (p < 0.05). There were no significant differenc es between patients with cardioversion from atrial putter and those wi th cardioversion from AF. APD90 at a steady state cycle length of 600 ms showed no significant correlation with the duration of previous AF or atrial flutter. Conclusions. AF and atrial flutter lead to marked, quantitatively similar decreases in the right atrial APD during steady state pacing and extrastimulation a considerable time after cardiover sion. These data confirm that both AF and atrial flutter lead to elect rical remodeling in the human atrium, with a preponderance at longer c ycle lengths. It may be prudent to abort both types of arrhythmias ear ly to prevent electrical remodeling. (C) 1997 by the American College of Cardiology.