To test the hypothesis that the prevalence of a cardiomyopathic syndrome in association with coronary artery disease is higher among diabetic patients, clinical, ventriculographic, and arteriographic features of coronary artery disease were evaluated in 84 patients with coronary artery disease. Forty-two diabetics were compared with 42 non-diabetics who were randomly selected and matched for age, sex, blood pressure, and serum lipids. The diabetic group represented all diabetic patients with angiographic coronary artery disease identified over a 6-year period who could be matched for these variables. The coronary circulation was divided into 6 arterial segments, and arteriograms were assigned a jeopardy score that expresses the number of segments jeopardised by signmficant proximal stenoses. Distal coronary artery disease was scored separately. The cardiomyopathic syndrome due to coronary artery disease was defined by evidence of chronic heartfailure in association with significant reduction of the left ventricular ejection fraction (<.048) caused by multiple and widespread left ventricular wall motion abnormalities. There was an increased prevalence of the syndrome in the diabetic group compared with the control group (20 patients vs 10 patients, P<0 05) and this was reflected in a lower mean ejection fraction in the diabetic group as a whole (0-47vs 0 56,P<005). There was also a higher prevalence ofmultiple myocardial infarcts (21 diabetics vs 9 controls with .2 myocardial infarctions, P<0 05) and anterior myocardial infarcts (23 diabetics vs 13 controls, P<0 05) in the diabetic group. There were no differences between the two groups in the prevalence of stable or unstable angina, persistent arrhythmias, or intraventricular conduction defects. The mean jeopardy score in patients with the cardiomyopathic syndrome was the same (10-.7±04 vs 10 6±0-3) whether diabetic or control. No patient, diabetic or control, with cardiomyopathy had a jeopardy score of < 8. Furthermore, the relation of cardiomyopathy to multiple myocardial infarctions was as strong in the diabetic patients (15 of 20 diabetics with cardiomyopathy had had .2 myocardial infarctions, 6 of 22 diabetics without cardiomyopathy had had >2myocardial infarctions; P<0-001) as it was in the overall study population. There was no significant difference in meanjeopardy score between diabetic and controlgroups as a whole (8 9± 0-5 vs 8-2± 0.5), but an increased fraction of the diabetic subpopulation with jeopardy scores of .8 had cardiomyopathy (20 of 30) compared with the control subpopulation with jeopardy scores of .8 (10 of 28). The prevalence ofcompletely occluded coronary arteries did not differ between diabetic and controlgroups. There was a higher prevalence of distal coronary artery disease in diabetic patients (24 diabetic vessels vs 10 control vessels), which was sigmificant, or not, depending on whether correction was made for non-visualised distal vessels. We conclude that there is an increased prevalence of the cardiomyopathic syndrome in diabetic patients with coronary artery disease, compared with non-diabetic patients with coronary artery disease, who come to angiography, and that this difference exists independently of hypertension and hyperlipidaemia. However, the cause of the cardiomyopathic syndrome, i.e. its relation to the extent ofproximal coronary artery disease and to the occurrence of multiple myocardial infarcts, is the same in both diabetic and non-diabetic patients.
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