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Comparative Study
. 1993 Sep;22(3):826-9.
doi: 10.1016/0735-1097(93)90197-9.

Evidence against a myocardial factor as the cause of left ventricular dilation in active rheumatic carditis

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Free article
Comparative Study

Evidence against a myocardial factor as the cause of left ventricular dilation in active rheumatic carditis

M R Essop et al. J Am Coll Cardiol. 1993 Sep.
Free article

Abstract

Objectives: The aim of this study was to determine whether left ventricular dilation and congestive heart failure in patients with acute rheumatic fever with carditis are accompanied by left ventricular contractile dysfunction.

Background: Acute rheumatic fever with carditis involves both the myocardium and endocardium, with consequent valvular regurgitation. The relative contribution of volume overload induced by valvular regurgitation and myocardial dysfunction due to rheumatic myocarditis to the overall degree of left ventricular dilation and congestive heart failure in these patients is unknown.

Methods: To investigate this, we evaluated 32 patients (15 male, 17 female, mean age 14 +/- 3 years) with documented active carditis and congestive heart failure. All 32 patients were found to have significant isolated mitral regurgitation or combined mitral and aortic regurgitation. Echocardiographic analysis of left ventricular dimensions and systolic performance was performed before and after isolated mitral or combined mitral and aortic valve replacement and the results were compared with those in 19 control subjects matched for age, gender and body surface area.

Results: Both preoperative left ventricular end-diastolic diameter and percent fractional shortening were significantly increased in patients compared with control subjects (57 +/- 7 vs. 43 +/- 3 mm, p < 0.001, and 38 +/- 6% vs. 33 +/- 1%, p < 0.001, respectively). After valve replacement, left ventricular end-diastolic diameter decreased significantly (57 +/- 7 to 47 +/- 6 mm, p < 0.001). Although percent fractional shortening decreased significantly postoperatively (38 +/- 6% to 32 +/- 6%, p < 0.001), the postoperative percent fractional shortening did not differ from that in control subjects (32 +/- 6% vs. 33 +/- 1%, p = NS).

Conclusions: The results of this study indicate that left ventricular dilation and heart failure in patients with acute rheumatic carditis rarely occur in the absence of hemodynamically significant regurgitant valve lesions. Furthermore, rapid reduction in left ventricular dimensions and preservation of fractional shortening after isolated mitral or combined mitral and aortic valve replacement suggest that rheumatic carditis is not accompanied by any significant degree of myocardial contractile dysfunction.

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