Author + information
- Received March 5, 1997
- Revision received July 7, 1997
- Accepted August 21, 1997
- Published online December 1, 1997.
- Michael R Franz, MD, PhD, FACCA,* (, )
- Pamela L Karasik, MDA,
- Cuilan Li, PhDA,
- Jean Moubarak, MDA and
- Mary Chavez, CVTA
- ↵*Dr. Michael R. Franz, Cardiology Division, Veteran Affairs Medical Center, 50 Irving Street, NW, Washington, DC 20422.
Objectives. This study sought to determine whether chronic atrial fibrillation (AF) and atrial flutter in patients lead to electrical remodeling of the human atrial myocardium, manifested by an abnormal relation between atrial cycle length and action potential duration (APD).
Background. Experimental studies in goats and isolated human atrial tissue have shown that prolonged AF leads to persistent shortening of atrial refractoriness, a phenomenon referred to as electrical remodeling and which helps to explain why AF begets AF. Direct data on human in situ myocardium are still lacking.
Methods. Using monophasic action potential recordings at two right atrial sites simultaneously, we determined 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 and during extrastimulus intervals (from 800 ms to refractoriness) at a basic cycle length of 600 ms to determine electrical restitution curves. The same pacing protocols and measurements were performed in nine control patients with sinus rhythm and no overt atrial disease.
Results. In control patients, steady state APD90 increased steadily with increases 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 length–APD90 relation was shifted downward and flattened at cycle lengths >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 course 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 flutter groups than in the control group (p < 0.05). There were no significant differences between patients with cardioversion from atrial flutter and those with 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 cardioversion. These data confirm that both AF and atrial flutter lead to electrical remodeling in the human atrium, with a preponderance at longer cycle lengths. It may be prudent to abort both types of arrhythmias early to prevent electrical remodeling.
- Received March 5, 1997.
- Revision received July 7, 1997.
- Accepted August 21, 1997.
- The American College of Cardiology