EVIDENCE AGAINST A MYOCARDIAL FACTOR AS THE CAUSE OF LEFT-VENTRICULARDILATION IN ACTIVE RHEUMATIC CARDITIS

Citation
Mr. Essop et al., EVIDENCE AGAINST A MYOCARDIAL FACTOR AS THE CAUSE OF LEFT-VENTRICULARDILATION IN ACTIVE RHEUMATIC CARDITIS, Journal of the American College of Cardiology, 22(3), 1993, pp. 826-829
Citations number
23
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
22
Issue
3
Year of publication
1993
Pages
826 - 829
Database
ISI
SICI code
0735-1097(1993)22:3<826:EAAMFA>2.0.ZU;2-6
Abstract
Objectives. The aim of this study was to determine whether left ventri cular dilation and congestive heart failure in patients with acute rhe umatic fever with carditis are accompanied by left ventricular contrac tile dysfunction. Background. Acute rheumatic fever with carditis invo lves both the myocardium and endocardium, with consequent valvular reg urgitation. The relative contribution of volume overload induced by va lvular regurgitation and myocardial dysfunction due to rheumatic myoca rditis to the overall degree of left ventricular dilation and congesti ve 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 regurgi tation or combined mitral and aortic regurgitation. Echocardiographic analysis of left ventricular dimensions and systolic performance was p erformed before and after isolated mitral or combined mitral and aorti c valve replacement and the results were compared with those in 19 con trol 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 compare d 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 shorteni ng decreased significantly postoperatively (38 +/- 6% to 32 +/- 6%, p < 0.001), the postoperative percent fractional shortening did not diff er from that in control subjects (32 +/- 6% vs. 33 +/- 1%, p = NS). Co nclusions. The results of this study indicate that left ventricular di lation and heart failure in patients with acute rheumatic carditis rar ely occur in the absence of hemodynamically significant regurgitant va lve lesions. Furthermore, rapid reduction in left ventricular dimensio ns and preservation of fractional shortening after isolated mitral or combined mitral and aortic valve replacement suggest that rheumatic ca rditis is not accompanied by any significant degree of myocardial cont ractile dysfunction.