There is a growing interest in immunologically-mediated lesions in the cardiovascular system, as there has been evidence that there are antimitochondrial
antibodies (AMA) in patients with
hypertrophic cardiomyopathy or hypertensives with
left ventricular hypertrophy (LVH). We have also very recently published findings from our laboratory that hypertensives with LVH have a considerable quantity of anticardiac
antibodies (ACA) in their serum. The aim of this study was to investigate the possible involvement of autoimmune mechanisms in the pathogenesis and evolution of hypertensive disease. Three groups of subjects were included in the study. Group A comprised 37 patients (20 men, 17 women, mean age 50.5 +/- 8.5 years) with mild to moderate
essential hypertension, 19 without echocardiographic evidence of LVH, and 18 with LVH. Group B comprised 10 patients (6 men, 4 women, mean age 45.1 +/- 8.7 years) with secondary
hypertension. The control group (C) comprised 15 normotensive subjects (8 men, 7 women, mean age 47.7 +/- 8.7 years). Cellular immunity against arterial wall
antigen was studied in all subjects by means of migration inhibitory factor (MIF) against relevant
antigen preparation. Sera from Group A and C subjects were tested for the presence of
autoantibodies against both specific (myocardial) and nonspecific
antigens, by means of the indirect immunofluorescence technique. Eighty per cent of patients with
essential hypertension showed a positive cellular response (MIF) against an arterial wall
antigen compared to the patients with secondary
hypertension or the control group. Moreover, patients with
essential hypertension and LVH had the highest incidence of specific (anticardiac, ACA) and nonspecific
autoantibodies and the highest C3c and
C4 complement component levels compared to patients without LVH or the control group. Most of the ACA positive patients were also AMA positive, while the ACA negative patients were AMA negative as well. Defects in cell-mediated immunity against arterial wall
antigen(s) may be the cause or the effect of
hypertension. On the basis of our findings that there was no delayed type
hypersensitivity response to arterial wall
antigen(s) in the patients with secondary
hypertension, we suggest that, in some cases of
essential hypertension,
delayed hypersensitivity reactions possibly contribute to the pathogenesis of
hypertension. Autoimmune mechanisms are discussed on the basis of common
epitopes shared between heart and arterial tissue.