A Possible Role for Autoantibodies in Left Ventricular Hypertrophy

Abstract

The purpose of the study was to investigate the possible role of autoantibodies in the development and type of left-ventricular hypertrophy (LVH). Three groups of subjects were studied:15 patients with hypertrophic cardiomyopathy (HCM; 11 males, 4 females; mean age 50.0 ± 16..3 years); (b) 15 patients with essential hypertension (10 males, 5 females; mean age 56.8 ± 13.5 years) with normal renal function and serum electrolytes and (c) 15 male athletes (mean age 20.8 ± 5.9 years). The control group consisted of 15 normal subjects with no sign of heart disease. The following indices of cardiac performance were determined by means of echocardiography: end-diastolic and end-systolic diameters, interventricular septum thickness, left-ventricular (LV) wall thickness, LV mass and LV mass index. The immunologic parameters studied included autoantibodies against (a) specific (anticardiac cell; ACA) and nonspecific (antimitochondrial cell; AMA) autoantigens according to a conventional indirect immunofluorescence technique. (1) Higher values for LV mass and LV mass index were observed in HCM. (2) The incidence of specific and nonspecific autoantibodies in hypertensive patients and in patients with HCM was significantly higher compared to athletes and controls. All ACA-positive individuals (5 with HCM, 3 with hypertension and 1 athlete) were AMA positive as well, while all ACA-negative individuals were also AMA negative. The ACA-positive individuals had higher C3c and C4 levels compared to the ACA-negative individuals. An autoantibody-mediated immunopathogenic role is discussed in the development and type of myocardial hypertrophy. Left-ventricular hypertrophy (LVH) due to heart disease (cardiomyopathies, hypertension or aortic stenosis) is considered as a pathological process followed by fibrosis and structural muscle changes [1]. On the contrary, LVH in athletes is considered as a ‘physiological’ myocardial response to exercise [2]. On the other hand, Autore et al. [3] have reported the presence of autoantibodies against mitochondria in patients with cardiomyopathies or hypertension with LVH, but not in athletes with LVH. These findings suggest the possibility that autoimmune mechanisms might be involved in the pathogenesis of LVH due to heart disease In this study we sought for the presence of autoantibodies against both specific and nonspecific antigens in athletes and patients with LVH of different origins, such as hypertrophic cardiomyopathy (HCM) or hypertension, in order to investigate the possible involvement of these autoantibodies in the development of LVH.

Proteomic and Structural Manifestations of Cardiomyopathy in Rat Models of Obesity and Weight Loss

“…Inflammation is involved in cardiac remodeling and activation of complement cascade accompanies cardiovascular disturbances both in humans and rodents ( 96 , 97 ). C3 level has been shown to be elevated in serum of patients with left ventricular hypertrophy ( 98 ), in hypertensive patients ( 99 ) and more recently was recognized as a marker of hypertrophic cardiomyopathy ( 100 ). However we could not point at the immune proteins as biomarkers for monitoring the cardiac recovery because we observed upregulation of complement cascade proteins in cardiac muscle but not in the plasma.…”

Antigenic stimulation in T‐cell cultures in cardiomyopathies: differences in cytokine profiles

“…Cardiomyopathies might also be organ‐specific autoimmune disorders, perhaps in genetically predisposed individuals (Popovici et al , 1996; Badorff et al , 1997). In both HCM and DCM patients, autoimmune phenomena have been described (Boudonas et al , 1994; Badorff et al , 1997). Differences or similarities between these diseases and the other organ‐specific autoimmune diseases have not so far been described.…”

“…Autoimmune mechanisms are likely to be involved in the process of disease development (Caforio et al 1996; Rose & Hill, 1996; Penninger et al , 1997; Matsumori, 1996; Schwimmbeck et al , 1996; Badorff et al , 1997). We have previously described cellular and humoral autoimmune reactivity against arterial and myocardial antigens in patients with hypertrophic cardiomyopathy (HCM) (Boudonas et al , 1994; Lefkos et al , 1995). The purpose of the present study is to investigate which pattern of immune response (Th 1 or Th 2 ) type is involved in the autoimmune process and/or what differences, if any, exist between HCM and dilated cardiomyopathy (DCM), by analysing the basic cytokines secreted from phytohaemagglutinin (PHA)‐cultured T cells, in the presence of relevant myocardial antigens.…”

The Time Has Come to Explore Plasma Biomarkers in Genetic Cardiomyopathies

“…Some small HCM cohort studies have been performed in the past, revealing, among other effects, an increase in the number of patients with elevated AAbs against G-proteincoupled β1 and Muscarin-2 receptors (β1-AAb and M2-AAb) [151][152][153]. A recent study with 134 HCM patients (and 40 controls) confirmed these past results and also showed that the concentration of M2-AAb in HCM patients with a family history of SCD or atrial fibrillation was significantly higher [154].…”