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J Am Coll Cardiol, 1993; 22:575-580
© 1993 by the American College of Cardiology Foundation
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Plasma atrial natriuretic peptide response to direct current cardioversion of atrial fibrillation in patients with mitral stenosis

H Fujiwara, F Ishikura, S Nagata, S Beppu, and K Miyatake

Department of Medicine, National Cardiovascular Center, Osaka, Japan.

OBJECTIVES. The purpose of this study was to evaluate the effect of direct current cardioversion therapy on the plasma concentration of atrial natriuretic peptide and to determine the main factors that influence the change in plasma atrial natriuretic peptide levels in patients with atrial fibrillation. BACKGROUND. In atrial arrythmias, whether the fast atrial rate itself or the associated elevation of atrial pressure, or both, contributes to the increase in atrial natriuretic peptide is a subject of debate. METHODS. In 15 patients with mild mitral stenosis, plasma atrial natriuretic peptide levels were measured and transmitral flow pattern was obtained by continuous wave Doppler echocardiography immediately before cardioversion and at 5 min, 4 h, 24 h and 5 days after direct current cardioversion. Mean mitral pressure gradient and atrial filling fraction were calculated on the basis of transmitral flow. RESULTS. In three patients who did not have a successful return to sinus rhythm, plasma atrial natriuretic peptide levels remained elevated after cardioversion. In 12 patients who maintained sinus rhythm, plasma atrial natriuretic peptide levels were significantly reduced from 79 +/- 29 to 36 +/- 11 pg/ml 4 h after cardioversion to sinus rhythm. However, the mitral pressure gradient did not change significantly during the observation period. There were progressive increases in atrial filling fraction throughout the observation period. From 4 h to 5 days after direct current cardioversion, plasma atrial natriuretic peptide levels gradually increased concomitantly with the recovery of atrial mechanical function. CONCLUSION. The reduction of plasma atrial natriuretic peptide levels after direct current cardioversion might be due to recovery from the high rate of atrial firing and not to an alteration in the mitral pressure gradient. Direct current cardioversion itself does not seem to influence atrial natriuretic peptide secretion. The increase in atrial natriuretic peptide levels from 4 h to 5 days after cardioversion concomitantly with an increase in atrial filling fraction may be due to recovery of atrial mechanical function.


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