C4 null alleles and myocardial infarction

The classical risk factors, hypercholesterolemia, smoking, hypertension and diabetes, explain only a part of the epidemiological features of atheroscl erotic coronary heart disease. Investigations in the past few years have sh own involvement of immunological mechanisms in atherosclerosis. Circulating immune complexes accelerate atherosclerosis both in experimental animal mo dels and in humans. The fourth component of complement (C4) plays an import ant role in the solubilisation and elimination of immune complexes. C4 cons ists of two allotypes, C4A and C4B. An earlier report showed an association between C4B null alleles (C4B*Q0) and myocardial infarction and to infarct ion related mortality. In the present investigation, C4A*Q0 and C4B*Q0 were studied in two population samples. The first (Group I) was a cross section al study of 100 consecutive males with myocardial infarction before the age of 45 years and 164 population based healthy controls, age and sex matched . The second (Group II) was a nested case control study in which a cohort o f 50 year-old males were followed for 20 years for development of myocardia l infarction between 50-60 and 60-70 years, and the results compared with t hose who did not develop MI. We observed no association of homozygous and/o r heterozygous C4A*Q0 or C4B*Q0 with myocardial infarction occurring in the age groups < 45, 50-60 and 60-70 years or with the infarction related mort ality (P > 0.05). The prevalence/frequency of C4A*Q0 and C4B*Q0 was not rel ated to the age at which MI occurred. The prevalence of C4A*Q0 was not affe cted by age. We thus conclude that partial deficiency of C4 does not appear to be a major risk factor for myocardial infarction. (C) 1999 Elsevier Sci ence Ireland Ltd. All rights reserved.