Autoimmunity and heart diseases: pathogenesis and diagnostic criteria

Nussinovitch, Udi; Shoenfeld, Yehuda

doi:10.1007/s00005-009-0013-1

Cited by 43 publications

(36 citation statements)

References 59 publications

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“…Cardiac involvement in AA amyloidosis is rare and occurs late in the course of amyloidosis, suggesting that most affected individuals may fit into a subclinical stage. Ischemic cardiovascular disease, another adverse outcome of chronic inflammation, may also occur in FMF, as was reported for other diseases associated with a high inflammatory burden such as rheumatoid arthritis, psoriatic arthritis, and other inflammatory disease (10,11). Higher than normal prevalence of various markers, denoting likelihoods to develop ischemic heart disease, exist in FMF and further support this notion (12).…”

Section: Introductionsupporting

confidence: 67%

Late ventricular potentials in familial Mediterranean fever with and without AA amyloidosis

Nussinovitch¹,

Livneh²

2017

Eur J Rheumatol

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Data on increased rhythm and conduction disturbances in FMF are limited and conflicting. For instance, Akcay et al. (13) found that QT dispersion (QTd) and corrected dispersion (QTcd), which reflect cardiac repolarization heterogeneity and thereby suggest predisposition for cardiac arrhythmias, are increased in uncomplicated FMF. However, different methodologies have yielded normal QTd results in both uncomplicated and amyloidosis-affected FMF patients (14, 15). Limited information is found on depolarization-associated markers for arrhythmias. Low-amplitude, high-frequency waves-termed late ventricular potentials (LPs)-can be detected immediately adjacent to the QRS complex by signal-averaged electrocardiography Udi Nussinovitch 1 , Avi Livneh 2,3Original Article Abstract Objective: Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by episodic and chronic inflammation that may lead to both accelerated coronary atherosclerosis and cardiac AA amyloidosis. We hypothesized that late ventricular potentials (LPs), an established electrocardiographic susceptibility marker of ventricular arrhythmias, will be more common in FMF than in the adjusted normal population due to these two types of inflammation-associated cardiac effects. Therefore, we aimed to evaluate the occurrence of LPs in FMF patients with and without amyloidosis.Material and Methods: Signal-averaged electrocardiography was performed in consecutive patients with FMF using the Frank corrected orthogonal lead system. At least 200 consecutive beats were digitally recorded and averaged, and the presence of LPs was determined according to acceptable thresholds.Results: There were 54 patients with colchicine-treated FMF, of whom 14 had biopsy-proven AA amyloidosis. None of the uncomplicated FMF patients and 2 of the 14 FMF amyloidosis patients had abnormal or borderline LPs. Conclusion:Based on LPs as a susceptibility marker for arrhythmia, FMF patients, including the large majority of FMF patients with amyloidosis, are seemingly not at an increased risk to develop arrhythmias.

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Section: Introductionsupporting

confidence: 67%

Late ventricular potentials in familial Mediterranean fever with and without AA amyloidosis

Nussinovitch¹,

Livneh²

2017

Eur J Rheumatol

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“…Several autoimmune diseases have been related to heart failure (13,28,40). Furthermore, increased immune markers such as sIL-2R and neopterin as well as the presence of specific cardiac autoantibodies have been identified in patients with DCM (1,6,8,23,29).…”

Section: Discussionmentioning

confidence: 99%

Differences in Virus Prevalence and Load in the Hearts of Patients with Idiopathic Dilated Cardiomyopathy with and without Immune-Mediated Inflammatory Diseases

Dennert¹,

Paassen²,

Wolffs³

et al. 2012

Clin. Vaccine Immunol.

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dInfections with cardiotrophic viruses and immune-mediated responses against the heart have been suggested to play a dominant role in the pathogenesis of idiopathic dilated cardiomyopathy (DCM). Furthermore, immune-mediated inflammatory diseases (IMIDs) may result in DCM. It has not previously been assessed whether DCM patients with and without an IMID have different prevalences and quantities of cardiotrophic viruses in the heart. Therefore, we compared the profiles of cardiotrophic viruses in heart tissue of DCM patients with and without an IMID. Serum and myocardial tissue samples were obtained from 159 consecutive patients with DCM and 20 controls. Patients were subdivided into three groups, the first two based on the presence (n ‫؍‬ 34) or absence (n ‫؍‬ 125) of an IMID and the third being a control group. The parvovirus B19 virus genome was detected in equal quantities in the non-IMID DCM patients (100/125) and the control group (15/20) but in lower quantities in the IMID patients (21/34, P ‫؍‬ 0.02). Both the non-IMID and IMID DCM patients demonstrated increased myocardial inflammation compared to controls: 12.5 ؎ 1.8 and 14.0 ؎ 3.2 CD45-positive inflammatory cells, respectively, versus 5.1 ؎ 0.7 for the controls (P < 0.05 for both). Importantly, significantly higher parvovirus B19 copy numbers could be amplified in non-IMID than in IMID patients (561 ؎ 97 versus 191 ؎ 92 copies/g DNA, P < 0.001) and control subjects (103 ؎ 47 copies/g DNA, P < 0.001). The present study shows decreased parvovirus B19 prevalence and copy numbers in hearts of DCM patients with an IMID compared to those without an IMID. These findings may suggest that DCM patients with an IMID have a different pathophysiologic mechanism from that which is present in the virus-induced form of DCM.

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“…31,32 Because pre-existing autoimmune memory likely persists post-transplant, it could negatively affect transplant outcome. To address this, we reanalyzed our data and assessed whether pretransplant autoantibodies that persisted posttransplant were strongly associated with the development of TG.…”

Section: Pretransplant Autoantibody Repertoires In Kidney Transplant mentioning

confidence: 99%

Antibodies Reactive to Non-HLA Antigens in Transplant Glomerulopathy

Dinavahi¹,

George

Tretin³

et al. 2011

Journal of the American Society of Nephrology

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Although T and B cell alloimmunity contribute to transplant injury, autoimmunity directed at kidneyexpressed, non-HLA antigens may also participate. Because the specificity, prevalence, and importance of antibodies to non-HLA antigens in late allograft injury are poorly characterized, we used a protein microarray to compare antibody repertoires in pre-and post-transplant sera from several cohorts of patients with and without transplant glomerulopathy. Transplantation routinely induced changes in antibody repertoires, but we did not identify any de novo non-HLA antibodies common to patients with transplant glomerulopathy. The screening studies identified three reactivities present before transplantation that persisted after transplant and strongly associated with transplant glomerulopathy. ELISA confirmed that reactivity against peroxisomal-trans-2-enoyl-coA-reductase strongly associated with the development of transplant glomerulopathy in independent validation sets. In addition to providing insight into effects of transplantation on non-HLA antibody repertoires, these results suggest that pretransplant serum antibodies to peroxisomal-trans-2-enoyl-coA-reductase may predict prognosis in kidney transplantation.

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Autoimmunity and heart diseases: pathogenesis and diagnostic criteria

Cited by 43 publications

References 59 publications

Late ventricular potentials in familial Mediterranean fever with and without AA amyloidosis

Late ventricular potentials in familial Mediterranean fever with and without AA amyloidosis

Differences in Virus Prevalence and Load in the Hearts of Patients with Idiopathic Dilated Cardiomyopathy with and without Immune-Mediated Inflammatory Diseases

Antibodies Reactive to Non-HLA Antigens in Transplant Glomerulopathy

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