The Role of Autoantibodies in Arrhythmogenesis

Li, Jin

doi:10.1007/s11886-020-01430-x

Cited by 18 publications

(17 citation statements)

References 72 publications

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“…Their levels correlate with premature ventricular contraction count in ACM patients, and in vitro analyses revealed their ability to functionally affect gap junctions. This is in line with the increasingly recognized ability of autoantibodies in arrhythmia stimulation through ion channels interference [ 156 ]. Moreover, DSG2 autoantibodies may attack the desmosomes and the whole intercalated discs, further weakening these structures.…”

Section: Autoimmune Response Hypothesis In Endurance Athletessupporting

confidence: 67%

Cardiac Biomarkers and Autoantibodies in Endurance Athletes: Potential Similarities with Arrhythmogenic Cardiomyopathy Pathogenic Mechanisms

Stadiotti

Lippi

Maione

et al. 2021

IJMS

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The “Extreme Exercise Hypothesis” states that when individuals perform training beyond the ideal exercise dose, a decline in the beneficial effects of physical activity occurs. This is due to significant changes in myocardial structure and function, such as hemodynamic alterations, cardiac chamber enlargement and hypertrophy, myocardial inflammation, oxidative stress, fibrosis, and conduction changes. In addition, an increased amount of circulating biomarkers of exercise-induced damage has been reported. Although these changes are often reversible, long-lasting cardiac damage may develop after years of intense physical exercise. Since several features of the athlete’s heart overlap with arrhythmogenic cardiomyopathy (ACM), the syndrome of “exercise-induced ACM” has been postulated. Thus, the distinction between ACM and the athlete’s heart may be challenging. Recently, an autoimmune mechanism has been discovered in ACM patients linked to their characteristic junctional impairment. Since cardiac junctions are similarly impaired by intense physical activity due to the strong myocardial stretching, we propose in the present work the novel hypothesis of an autoimmune response in endurance athletes. This investigation may deepen the knowledge about the pathological remodeling and relative activated mechanisms induced by intense endurance exercise, potentially improving the early recognition of whom is actually at risk.

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Section: Autoimmune Response Hypothesis In Endurance Athletessupporting

confidence: 67%

Cardiac Biomarkers and Autoantibodies in Endurance Athletes: Potential Similarities with Arrhythmogenic Cardiomyopathy Pathogenic Mechanisms

Stadiotti

Lippi

Maione

et al. 2021

IJMS

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“…This suggests that fibrosis and calcification ensue rapidly after the start of inflammation in utero in the early second trimester, with no evidence of cardiac dysfunction or valve regurgitation on an echocardiogram. Numerous studies on animals, including murine, rat, guinea pig, and rabbit models and fetal hearts, have demonstrated that anti-Ro/SSA antibodies from mothers’ sera cause CHB by transplacental passage as early as 11 weeks of gestation [ 28 ]. Various immunohistochemistry data speculate that this leads to inhibition of the calcium channels of the fetal heart or apoptotic cell accumulation that induces macrophage infiltration and the release of cytokines, which cause fibrosis and calcification [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Endocardial Fibroelastosis as an Independent Predictor of Atrioventricular Valve Rupture in Maternal Autoimmune Antibody Exposed Fetus: A Systematic Review with Clinicopathologic Analysis

et al. 2023

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Background: Neonatal lupus (NL) is a clinical syndrome that develops in the fetus as a result of maternal autoimmune antibodies. Congenital complete heart block (CHB) is the most common manifestation, while extranodal cardiac manifestations of NL, such as endocardial fibroelastosis (EFE) and myocarditis, are rare but more serious. Less is known about this atrioventricular valve rupture due to valvulitis as a consequence of maternal autoantibodies. We have described a case of cardiac neonatal lupus with an antenatally detected CHB patient who developed mitral and tricuspid valve chordal rupture at 45 days of age. We compared the cardiac histopathology and the fetal cardiac echocardiographic findings of this case with another fetus that was aborted after being antenatally diagnosed with CHB but without valvar rupture. A narrative analysis after a systematic review of the literature regarding atrioventricular valve apparatus rupture due to autoimmune etiology along with maternal characteristics, presentation, treatment, and outcome have been discussed in this article. Objectives: To describe published data on atrioventricular valve rupture in neonatal lupus, including clinical presentation, diagnostic evaluation, management, and outcomes. Methods: We conducted a PRISMA-compliant descriptive systematic examination of case reports that included accounts of lupus during pregnancy or in the newborn period that resulted in an atrioventricular valve rupture. We gathered information on the patient’s demographics, the details of the valve rupture and other comorbidities, the maternal therapy, the clinical course, and the results. We also used a standardized method to evaluate the cases’ quality. A total of 12 cases were investigated, with 11 cases drawn from 10 case reports or case series and 1 from our own experience. Results: Tricuspid valve rupture (50%) is more common than mitral valve rupture (17%). Unlike mitral valve rupture, which occurs postnatally, the timing of tricuspid valve rupture is perinatal. A total of 33% of the patients had concomitant complete heart block, while 75% of the patients had endocardial fibroelastosis on an antenatal ultrasound. Antenatal changes pertaining to endocardial fibroelastosis can be seen as early as 19 weeks of gestation. Patients with both valve ruptures generally have a poor prognosis, especially if they occur at close intervals. Conclusion: Atrioventricular valve rupture in neonatal lupus is rare. A majority of patients with valve rupture had antenatally detected endocardial fibroelastosis in the valvar apparatus. Appropriate and expedited surgical repair of ruptured atrioventricular valves is feasible and has a low mortality risk. Rupture of both atrioventricular valves occurring at close intervals carries a high mortality risk.

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“…Adult AV node is thought to be more resistant to anti-SSA as it has a higher expression of calcium channels (compared with fetal AV node) 11. AV block (secondary to anti-SSA-induced inflammation) may also be reversible with immunosuppressants if caught early in the process prior to occurrence of irreversible damage 12…”

Section: Discussionmentioning

confidence: 99%

Sjogren syndrome presenting as atrioventricular block in an adult

et al. 2022

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A woman in her late teens with a history of Juvenile idiopathic arthritis (JIA) and ongoing sicca symptoms presented with syncope. Upon admission, she was found to be bradycardic with a second-degree atrioventricular (AV) block. After infectious, structural and metabolic aetiologies had been ruled out, she was worked up for rheumatologic causes.Our patient had elevated titres of anti-Sjogren syndrome (SS) antibodies anti-Ro antibodies and was diagnosed with AV block secondary to SS. She was treated with a permanent pacemaker. Patient was followed up in clinic where she denied further syncopal episodes and was started on secretagogues for sicca symptoms.

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The Role of Autoantibodies in Arrhythmogenesis

Cited by 18 publications

References 72 publications

Cardiac Biomarkers and Autoantibodies in Endurance Athletes: Potential Similarities with Arrhythmogenic Cardiomyopathy Pathogenic Mechanisms

Cardiac Biomarkers and Autoantibodies in Endurance Athletes: Potential Similarities with Arrhythmogenic Cardiomyopathy Pathogenic Mechanisms

Endocardial Fibroelastosis as an Independent Predictor of Atrioventricular Valve Rupture in Maternal Autoimmune Antibody Exposed Fetus: A Systematic Review with Clinicopathologic Analysis

Sjogren syndrome presenting as atrioventricular block in an adult

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