CLINICAL STUDY: RHEUMATIC FEVER
Left ventricular mechanics during and after acute rheumatic fever: contractile dysfunction is closely related to valve regurgitation
Thomas L. Gentles, FRACP* b, ,d,
Steven D. Colan, MD, FACC,d,
Nigel J. Wilson, MRCP* b,
Renelle Biosa* b and
John M. Neutze, MD, FRACP* b,d
* Department of Pediatric Cardiology, Green Lane Hospital, Auckland, New Zealand
b Departments of Pediatrics and Medicine, University of Auckland, Auckland, New Zealand
Department of Cardiology, Children’s Hospital, Boston, Massachusetts, USA
d Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA
Manuscript received February 28, 2000;
revised manuscript received August 9, 2000,
accepted September 14, 2000.
Reprint requests and correspondence: Dr. Thomas Gentles, Department of Cardiology, Green Lane Hospital, Green Lane Road, Auckland 3, New Zealand
tomg{at}ahsl.co.nz
OBJECTIVES
The purpose of this study was to characterize left ventricular (LV) mechanics during acute rheumatic fever (ARF) and to define factors influencing remodeling after the acute event.
BACKGROUND
Acute rheumatic fever is associated with varying degrees of valvulitis and myocarditis, but the impact of these factors on LV mechanics is poorly defined.
METHODS
Echocardiograms and clinical data were reviewed in 55 patients aged 11.2 ± 2.6 years during ARF. Valve regurgitation was absent or mild in 33 (group I) and moderate or severe in 22 (group II). Forty-two children (75%) underwent a further examination after ARF.
RESULTS
Group I patients demonstrated a mildly elevated LV size during ARF and had normal indexes at follow-up. Group II patients demonstrated a markedly elevated LV size (end-diastolic dimension z-score 3.6 ± 1.8, p < 0.01 compared with the normal population) and decreased shortening fraction (z-score –0.8 ± 1.4, p < 0.05). The stress-velocity index, a z-score describing the velocity of shortening-afterload relationship, was normal in group II patients with mitral regurgitation (–0.2 ± 1.2, p = NS) but was depressed in those with aortic regurgitation or both (–1.4 ± 1.4, p < 0.01). At follow-up the stress-velocity index remained depressed (–1.2 ± 1.0, p < 0.01) and had deteriorated in those treated nonsurgically compared with those treated surgically (interval change nonsurgical –0.7 ± 1.2 vs. surgical 1.3 ± 1.3, p = 0.005).
CONCLUSIONS
The evolution of contractile dysfunction during and after ARF is dependent on the degree and type of valve regurgitation and may be influenced by surgical intervention. These findings suggest that mechanical factors are the most important contributors to myocardial damage during and after ARF.
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Abbreviations and Acronyms
| | ARF | = acute rheumatic fever | | AR | = aortic regurgitation | | EDh/D | = End-diastolic wall thickness:chamber dimension ratio | | ESSc | = circumferential end-systolic wall stress | | LV | = left ventricle | | MR | = mitral regurgitation | | SF | = shortening fraction | | SVI | = stress-velocity index | | VCFC | = rate-corrected mean velocity of circumferential fiber shortening |
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