Eosinophilia and heart disease

Abstract

The clinical presentations of endomyocardial fibrosis are well known as a result of the comprehensive descriptions from Uganda (Shillingford and Somers, 1961; Connor et al., 1967) and from Nigeria (Parry and Abrahams, 1963). The features vary greatly with the sites of the intracardiac lesions. Chronic right-sided disease may obliterate the cavity of the right ventricle almost completely without killing the patient who classically presents with proptosis and tense ascites. The condition may mimic constrictive pericarditis (Somers et al., 1968) or present with pericardial effusion. Left-sided disease may simulate other cardiomyopathies and present with heart failure (Falase et al., 1976). Tricuspid and/or mitral regurgitation (Clark et al., 1956; Fowler and Somers, 1968) may be dominant and scar excision with valve replacement has recently been employed successfully (Cachera et al., 1976). Rarely, the condition simulates primary pulmonary hypertension (Davies et al., 1965) or an intracardiac tumour (Van der Hauwaert et al., 1965). Clubbing and cyanosis are common with severe right-sided disease and secondary infective endocarditis is not unknown on the mitral valve (Falase et al., 1976). The main haemodynamic effect of the cardiac disorder (with or without persisting eosinophilia) is to restrict the filling and output of the ventricles, but the effect of this restriction is only felt in advanced cases and asymptomatic milder cases who do not seek treatment would evade recognition in societies whose patients are medically less sophisticated than our own. This could, perhaps, explain the absence of descriptions of mild endomyocardial fibrosis from those centres in tropical Africa from which the 'classical' forms were described and the late appearance of endomyocardial fibrosis in temperate climes where severe forms of the disorder are rare. The European patients with endomyocardial fibrosis have started to emerge pari passu with the more thorough diagnostic investigations of asymptomatic patients which are now usual. The name 'primary restrictive cardiomyopathy' was recently coined to describe British patients believed to have a mild burned out form of Loffler's disease (Oakley, 1974), but, in such cases, proof of this is dependent on cardiac biopsy or accidental death from some non-cardiac cause. The balance of the argument suggests that endomyocardial fibrosis represents both a later evolutionary phase and a milder burned out form of the disease which Loffler described. It is probable that the eosinophil is usually though not invariably involved; the underlying pathological processes are still unknown and further study and analysis of these conditions remain to be done.