IMMUNOPATHOGENIC MECHANISMS IN HYPERTENSION

There is a growing interest in immunologically-mediated lesions in the cardiovascular system, as there has been evidence that there are anti mitochondrial antibodies (AMA) in patients with hypertrophic cardiomyo pathy or hypertensives with left ventricular hypertrophy (LVH). We hav e also very recently published findings from our laboratory that hyper tensives with LVH have a considerable quantity of anticardiac antibodi es (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 inclu ded in the study. Group A comprised 37 patients (20 men, 17 women, mea n 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 normo tensive subjects (8 men, 7 women, mean age 47.7 +/- 8.7 years). Cellul ar 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 pre sence of autoantibodies against both specific (myocardial) and nonspec ific antigens, by means of the indirect immunofluorescence technique. Eighty per cent of patients with essential hypertension showed a posit ive cellular response (MIF) against an arterial wall antigen compared to the patients with secondary hypertension or the control group. More over, patients with essential hypertension and LVH had the highest inc idence of specific (anticardiac, ACA) and nonspecific autoantibodies a nd the highest C-3c and C-4 complement component levels compared to pa tients without LVH or the control group. Most of the ACA positive pati ents were also AMA positive, while the ACA negative patients were AMA negative as well. Defects in cell-mediated immunity against arterial w all 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 hy pertension, we suggest that, in some cases of essential hypertension, delayed hypersensitivity reactions possibly contribute to the pathogen esis of hypertension. Autoimmune mechanisms are discussed on the basis of common epitopes shared between heart and arterial tissue.