No abstract

The severity and pattern of coronary artery disease in patients referred for investigation of the disease was compared between Asian and white patients living in Birmingham, matched for age, sex, blood pressure, and duration of symptoms, to investigate the clinical impression that Asians have worse, in particular worse distal, coronary artery disease than whites. Risk factors and outcome were also examined. The coronary angiograms of 34 Asians were compared blindly and repeatedly with those of 68 whites by two independent observers. Coronary artery disease was found to be quantitatively more severe in Asians, but the distribution of the disease was the same. Some risk factors were significantly different: fewer Asians were smokers; fasting cholesterol concentrations were higher in whites; and whites were heavier, with a larger body surface area. Follow up data showed that more Asians were refused coronary artery bypass surgery because of the severity of their disease.

Summary Thirty-four Asian patients with coronary artery disease (CAD) were each matched for age, sex, blood pressure and duration of symptoms with 2 white patients with CAD. Blind assessment of coronary arteriograms demonstrated significantly more severe disease in Asians but distribution of disease was similar in both groups. Assessment of risk factors showed that the Asian group had significantly more non-smokers, lower cholesterol levels and weighed less than whites.

SUMMARY Suppressor T lymphocyte function was examined in 11 patients with idiopathic congestive cardiomyopathy and in 11 age and sex matched patients with a similar degree of heart failure resulting from ischaemic heart disease. Suppressor T lymphocyte function was also assessed in a control population of 11 normal subjects. Suppressor T lymphocyte function was reduced in both groups of patients with heart failure but not significantly, and a wide range of suppression was demonstrated in all groups.These data do not support the hypothesis that there is a defect in T lymphocyte function in patients with congestive cardiomyopathy, but they do suggest that there may be a non-specific reduction in T lymphocyte suppressor function associated with heart failure in general.The aetiology of idiopathic congestive cardiomyopathy is, by definition, unknown and is likely to represent the end stage of several different pathogenic mechanisms."2 The possibility that immunological abnormalities may affect the pathogenesis of some cases has received much attention in recent years.34 There have been reports of impaired suppressor T lymphocyte function in patients with congestive cardiomyopathy and this could be the result of a quantitative or a qualitative abnormality.5'6 Such a defect might be determined genetically by predisposing an individual to viral infection, myocarditis, and subsequent development of cardiomyopathy.7 This hypothesis has not, however, been accepted by all workers8 and some studies have shown no specific abnormality of T lymphocyte function in congestive cardiomyopathy.9These doubts regarding the role of immunological abnormalities in the pathogenesis of congestive cardiomyopathy prompted a study to determine whether patients with congestive cardiomyopathy have a defect of suppressor T lymphocyte function that is specific to their disease.Requests for reprints to Dr Patricia J Lowry, Department of Cardiovascular Medicine, East Birmingham Hospital, Bordesley Green East, Birmingham B9 5ST.Accepted for publication 11 December 1986 Patients and methods PATIENTSEleven patients with idiopathic congestive cardiomyopathy (according to the classification of Goodwin and Oakley)' that was confirmed by cardiac catheterisation, coronary angiography, and left ventricular endomyocardial biopsy were studied and compared with eleven individually age and sex matched patients who had congestive cardiac failure of ischaemic origin, also confirmed at cardiac catheterisation. We also studied eleven healthy controls recruited from hospital staff with no personal or family history of ischaemic heart disease.The severity of congestive cardiac failure and the treatment regimens were similar in the patient groups (table). All patients in the heart failure groups were being treated with digoxin and warfarin. Ejection fractions were determined by volumes derived from end systolic and end diastolic frames acquired at left ventricular cineangiography. o METHODS Lymphocytes were separated from heparinised blood by density gradient cent...

SUMMARY Sera from patients with heart disease were examined by single sandwich indirect immunofluorescence for the presence of antibodies to human heart muscle. Endocardial biopsy specimens were also examined by direct inmunofluorescence for deposition of antibodies in vivo. No consistent or specific abnormality was found in the biopsy specimens or sera of patients with congestive cardiomyopathy. The presence of anti-heart antibodies in cardiac disease appears to reflect damage to cardiac muscle whatever the cause. Immunofluorescence is an insensitive test for anti-heart antibodies.It has been suggested that cardiac damage in congestive cardiomyopathy may be mediated by an autoimmine mechanism.I The role of humoral abnormalities, in particular type II hypersensitivity, has received considerable attention,2-4 but the results and their interpretation vary widely. Previous findings in our department (using baboon heart as substrate) suggested that the role of humoral autoimmunity as a primary cause of congestive cardiomyopathy is not proven5; we undertook a further study to confirm or refute the findings.Our aims were (a) to detect serum autoantibodies to human heart muscle, (b) to detect evidence of in vivo antibody fixation by cardiac antigens, and (c) to demonstrate immune complex deposition in and around myocardial vessels. Patients and methods SEROLOGICAL STUDYSera of 95 patients were examined for the presence of antiheart antibodies. Forty three had cardiomyopathy according to the classification of Goodwin and Oakley6: 28 had congestive cardiomyopathy diagnosed both clinically and by cardiac catheterisation and endomyocardial biopsy, with one exception in which the diagnosis was confirmed at necropsy and 15 had hypertrophic cardiomyopathy, in all but one of whom the diagnosis was confirmed at catheterisation. Nine of the 15 patients in the latter group had a left ventricular outflow tract obstruction detected at catheter-