Elsevier

American Heart Journal

Volume 138, Issue 2, August 1999, Pages 303-308
American Heart Journal

Ventricular remodeling in active myocarditis,☆☆,,★★

https://doi.org/10.1016/S0002-8703(99)70116-XGet rights and content
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Abstract

Background Remodeling of the left ventricle with the development of a spherical cavity occurs in dilated cardiomyopathy and is associated with a poor long-term prognosis. The early effects of myocarditis on left ventricular geometry have not been previously described or correlated with clinical outcome. Methods The baseline echocardiograms of 35 patients with biopsy-confirmed myocarditis were compared with 20 normal controls. Left ventricular end-diastolic volume, long axis length, and mid-cavity diameter were measured. The degree of sphericity was expressed as the ratio of the mid-cavity diameter to the long axis length. Left ventricular ejection fraction was assessed by radionuclide angiography. Results In patients with myocarditis, mean left ventricular volume of 81 ± 29 mL/m2 was significantly greater than 50 ± 8 mL/m2 in controls (P = .001). Chamber dilatation occurred primarily along the mid-cavity diameter, which measured 5.3 ± 0.8 cm in patients with myocarditis versus 4.2 ± 0.4 cm in controls (P = .001). The degree of left ventricular sphericity in patients with myocarditis, 0.64 ± 0.08, was significantly greater than that of controls, 0.54 ± 0.04 (P = .001). When patients were stratified according to left ventricular volume, patients with increased left ventricular volume (>75 mL/m2) were associated with a more spherical chamber and lower left ventricular ejection fraction than patients with a more normal left ventricular volume (≤75 mL/m2). Conclusions Active myocarditis is associated with early left ventricular remodeling and the development of a spherical chamber. These changes correlate with ventricular dilatation and reduced left ventricular ejection fraction. (Am Heart J 1999;138:303-8.)

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From the aEvans Memorial Department of Clinical Research and the Section of Cardiology, Department of Medicine, Boston Medical Center; the bCardiac Unit, Massachusetts General Hospital, Boston; and the cSection of Cardiology, Department of Medicine, University of Arizona, Tucson.

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Supported by a grant from the National Heart, Lung, and Blood Institute (R01-HL34744).

Reprint requests: Lisa A. Mendes, MD, Division of Cardiology, Boston Medical Center, One Boston Medical Center Place, E Newton Street Campus, Boston, MA 02118.

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