Mechanisms and management of heart failure in active rheumatic carditis
Abstract
Fulminating active rheumatic carditis has been observed for over three decades in this environment with no recent alteration in either the incidence or the pattern of presentation. Heart failure (in this context defined as 'an inadequate circulation at rest together with a raised pulmonary venous pressure, with or without an associated high systemic venous pressure in the absence of haemodynamically significant tricuspid valve disease or pericardial effusion') is prevalent but occurs only when a haemodynamically important leftsided valve lesion supervenes. Regurgitation is the predominant valve lesion and involves principally the mitral valve. Mitral annular dilatation is marked and predisposes to lengthening - or rupture - of chordae tendineae and prolapse of the anterior leaflet. The resultant cardiac workoverload apparently perpetuates or aggravates the rheumatic activity. Heart failure, as defined, whether caused by or associated with active rheumatic carditis, makes surgical management of the valve lesion mandatory as a life-saving measure. Aggressive medical therapy for heart failure, which should include vasodilator drugs and especially angiotensinconverting enzyme inhibitors, provides temporary improvement only. Contrary to ongoing doctrine, treatment with steroid drugs in this context is neither life-saving nor beneficial.
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