Chest, Vol 100, 303-306, Copyright © 1991 by American College of Chest Physicians

ARTICLES

Cardiac biopsy in patients with "primary" atrial fibrillation. Histologic evidence of occult myocardial diseases

A Frustaci, M Caldarulo, A Buffon, F Bellocci, R Fenici and D Melina
Department of Cardiology, Catholic University, Rome, Italy.

Fourteen patients (ten men and four women; mean age, 37 years) with lone atrial fibrillation (AF) (1 to 18 months' duration) were evaluated by thyroid function tests, two-dimensional echocardiography, hemodynamics, coronary angiography, and left ventricular endomyocardial biopsy, because of unresponsiveness to the usual antiarrhythmic therapy. The results of the T3, T4, TSH, and TRH tests were normal in all patients; cardiac valves and ventricular and atrial sizes (left atrium less than 40 mm) were within the normal limits; also normal were LVEDP (less than or equal to 10 mm Hg) and EF (greater than 0.50). Histologic findings were abnormal in all cases, with three patients showing cardiomyopathic changes, three other patients showing active myocarditis (lymphocytic in two and eosinophilic in one), and eight patients with nonspecific necrosis or fibrosis or both. Steroids (prednisone; 50 mg/m2 of body surface area daily) used in addition to antiarrhythmic therapy in patients with eosinophilic and lymphocytic active myocarditis were able to cause reversion to sinus rhythm, while the other patients continued to have AF. This study documents that occult myocardial diseases (myocarditis, cardiomyopathy, and nonspecific necrosis or fibrosis) can underlie "primary" AF. The addition of steroids to antiarrhythmic therapy in patients with refractory AF and histologic evidence of active myocarditis seems to be useful in controlling the arrhythmia.

This article has been cited by other articles:

				S. Verheule, T. Sato, T. Everett IV, S. K. Engle, D. Otten, M. Rubart-von der Lohe, H. O. Nakajima, H. Nakajima, L. J. Field, and J. E. Olgin Increased Vulnerability to Atrial Fibrillation in Transgenic Mice With Selective Atrial Fibrosis Caused by Overexpression of TGF-{beta}1 Circ. Res., June 11, 2004; 94(11): 1458 - 1465. [Abstract] [Full Text] [PDF]

				A. Goette, M. Arndt, C. Rocken, T. Staack, R. Bechtloff, D. Reinhold, C. Huth, S. Ansorge, H. U. Klein, and U. Lendeckel Calpains and cytokines in fibrillating human atria Am J Physiol Heart Circ Physiol, July 1, 2002; 283(1): H264 - H272. [Abstract] [Full Text] [PDF]

				C. H. Zachary and S. E. Cyran Spontaneous-Onset Atrial Fibrillation in a Toddler with Review of Mechanisms and Etiologies Clinical Pediatrics, August 1, 2000; 39(8): 453 - 459. [Abstract] [PDF]

				A. Frustaci, C. Chimenti, F. Bellocci, E. Morgante, M. A. Russo, and A. Maseri Histological Substrate of Atrial Biopsies in Patients With Lone Atrial Fibrillation Circulation, August 19, 1997; 96(4): 1180 - 1184. [Abstract] [Full Text]