Antimitochondrial autoantibodies in myocardial hypertrophy: Comparison between hypertrophic cardiomyopathy, hypertensive heart disease, and athlete's heart

Autore, Camillo; Fiorito, Silvana; Pelliccia, Antonio; Caselli, G.; Fragola, Pietro V.; Picelli, Antonella; Maccari, Anna Maria; Pocobelli, Donatella; Cannata, D; Sangiorgi, M

doi:10.1016/0002-8703(88)90623-0

Cited by 10 publications

(6 citation statements)

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“…In this subgroup of patients (ACA positive), the coex istence of two more features of autoimmunity raises the possibility of the involvement of an autoimmune mechanism in the pathogenesis of LVH [3,5]. These two findings are: (1) the observation that all ACA-positive patients were also AMA positive and (2) the finding that the ACA-positive subgroup of patients had higher C3c and C4 complement levels (ta bles 4,5).…”

Section: Discussionmentioning

confidence: 85%

“…Contributing factors in the development of LVH are multiple and controversial [5]. Recently, immunopathogenic mechanisms have also been postulated to be involved [3,6],…”

Section: Discussionmentioning

confidence: 99%

“…On the other hand, Autore et al [3] have reported the presence of autoantibodies against mitochondria in patients with cardio myopathies or hypertension with LVH, but not in athletes with LVH. These findings sug gest the possibility that autoimmune mecha nisms might be involved in the pathogenesis of LVH due to heart disease.…”

mentioning

confidence: 97%

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A Possible Role for Autoantibodies in Left Ventricular Hypertrophy

Boudonas

Boura²,

Lefkos³

et al. 1994

Cardiology

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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.

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Section: Discussionmentioning

confidence: 85%

“…Contributing factors in the development of LVH are multiple and controversial [5]. Recently, immunopathogenic mechanisms have also been postulated to be involved [3,6],…”

Section: Discussionmentioning

confidence: 99%

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A Possible Role for Autoantibodies in Left Ventricular Hypertrophy

Boudonas

Boura²,

Lefkos³

et al. 1994

Cardiology

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“…The main epitopes recognised by autoantibodies are coloured red, and the secondary, alternative, epitopes are coloured orange level and pattern of citrate synthase-specific antibody isotypes can be found in heart transplant patients. This imbalance may result in a shift towards an unfavourable, destructive, autoimmune response that-as the literature [10, 16,35] suggests-can take place in the formation of allograft vasculopathy.…”

Section: Discussionmentioning

confidence: 99%

“…Low-affinity IgM isotype autoantibodies are present in the human circulation against these structures to protect them from a targeting immune response [14]. Severe bacterial infection or tissue destruction can cause the formation of these low affinity molecules, but a parallel malfunction of the immune regulation may result in the appearance of high-affinity IgG or IgA isotype autoantibodies against these proteins [15,16], mediating further tissue destruction via an autoimmune response.…”

mentioning

confidence: 99%

Detection of citrate synthase-reacting autoantibodies after heart transplantation: an epitope mapping study

Petrohai¹,

Nagy²,

Bősze³

et al. 2005

Transpl Int

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Autoimmune mechanisms play an important role in the pathogenesis of allograft vasculopathy following heart transplantation, but the autoantigens involved have been only sparsely studied. Citrate synthase (CS) enzyme is a conserved molecule, and, as an important mitochondrial autoantigen, it is protected by the "immunological homunculus". Tissue destruction and alteration of the immune regulatory mechanisms can induce pathological immune response against CS in other autoimmune diseases. In our present study we aimed to detect CS-specific autoantibodies in heart transplant patients, therefore, prospective, randomised clinical tests were conducted on 33 heart transplant patients and compared with 130 healthy blood donors. The level and isotype of CS antibodies were detected by simple binding indirect enzyme-linked immunosorbent assay (ELISA). The epitope specificities of the autoantibodies were measured on synthetic overlapping peptide sequences of CS enzyme by an indirect multi-pin ELISA method. Mainly IgM isotype CS autoantibodies were found in healthy controls, while IgG was found at higher levels and frequency (four-times higher) in heart transplant patients. Autoantibodies of IgG isotype recognise different epitopes than do autoantibodies of IgM isotype, even within the same group and individual. New epitope-specific IgG and IgM isotype autoantibodies appeared in heart transplant patients when compared with the controls. Our findings suggest a possible role of CS-specific autoantibodies in the pathomechanism of allograft vasculopathy.

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