Brief Report: Antisynthetase Syndrome–Associated Myocarditis

Sharma, Kavita; Orbai, Ana‐Maria; Desai, Dipan; Cingolani, Oscar H.; Halushka, Marc K.; Christopher‐Stine, Lisa; Mammen, Andrew L.; Wu, Kathérine C.; Zakaria, Sammy

doi:10.1016/j.cardfail.2014.07.012

Cited by 27 publications

(12 citation statements)

References 62 publications

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“…to 4% and it is not linked to autoantibody specificity (50). In a French retrospective study of 12 cases of myocarditis in AS patients, myocarditis was a part of the first AS manifestations in 42%.…”

Section: Antisynthetase Syndromementioning

confidence: 98%

Myocarditis in auto-immune or auto-inflammatory diseases

Comarmond

Cacoub

2017

Autoimmunity Reviews

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Myocarditis is a major cause of heart disease in young patients and a common precursor of heart failure due to dilated cardiomyopathy. Some auto-immune and/or auto-inflammatory diseases may be accompanied by myocarditis, such as sarcoidosis, Behçet's disease, eosinophilic granulomatosis with polyangiitis, myositis, and systemic lupus erythematosus. However, data concerning myocarditis in such auto-immune and/or auto-inflammatory diseases are sparse. New therapeutic strategies should better target the modulation of the immune system, depending on the phase of the disease and the type of underlying auto-immune and/or auto-inflammatory disease.

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Section: Antisynthetase Syndromementioning

confidence: 98%

Myocarditis in auto-immune or auto-inflammatory diseases

Comarmond

Cacoub

2017

Autoimmunity Reviews

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“…Beside the classical skeletal muscular manifestation, cardiac involvement is rare but may expose IIM patients to threatening complications. The MSA anti-SRP antibody is associated with a risk of cardiac complication [41] and several reports have also shown cardiac involvement in anti-synthetase syndrome [42]. Two MAA have further been reported with increased risk of cardiac involvement: anti-mitochondrial and anti-PM/Scl antibodies [43,44].…”

Section: Clinical Phenotypementioning

confidence: 99%

Diagnostic Utility of Auto-Antibodies in Inflammatory Muscle Diseases

Allenbach

Benveniste

2015

Journal of Neuromuscular Diseases

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To date, there are four main groups of idiopathic inflammatory myopathies (IIM): polymyositis (PM), dermatomyositis (DM), immune-mediated necrotizing myopathy (IMNM) and sporadic inclusion body myositis; based on clinical presentation and muscle pathology. Nevertheless, important phenotypical differences (either muscular and/or extra-muscular manifestations) within a group persist. In recent years, the titration of different myositis-specific (or associated) auto-antibodies as a diagnostic tool has increased. This is an important step forward since it may facilitate, at a viable cost, the differential diagnosis between IIM and other myopathies. We have now routine access to assays for the detection of different antibodies. For example, IMNM are related to the presence of anti-SRP or anti-HMGCR. PM is associated with anti-synthetase antibodies (anti-Jo-1, PL-7, PL-12, OJ, and EJ) and DM with anti-Mi-2, anti-SAE, anti-TIF-1-␥ and anti-NXP2 (both associated with cancer) or anti-MDA5 antibodies (associated with interstitial lung disease). Today, over 30 myositis specific and associated antibodies have been characterised, and all groups of myositis may present one of those auto-antibodies. Most of them allow identification of homogenous patient groups, more precisely than the classical international classifications of myositis. This implies that classification criteria could be modified accordingly, since these auto-antibodies delineate groups of patients suffering from myositis with consistent clinical phenotype (muscular and extra-muscular manifestations), common prognostic (cancer association, presence of interstitial lung disease, mortality and risk of relapse) and treatment responses. Nevertheless, since numerous auto-antibodies have been recently characterised, the exact prevalence of myositis specific antibodies remains to be documented, and research of new auto-antibodies in the remaining seronegative group is still needed.

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“…Reasons to suspect a genetic susceptibility in infectious myocarditis may derive from twin studies (usually newborn or children) [16][17][18], familial clustering suggesting genetic determinants or predisposing genetic factors [19][20][21], and rare Mendelian diseases [22,23] as well as endemic infections linked to both pathogen and population genetic make-up [24]. The topic must be discussed with caution so as not to transform infectious diseases into genetic ones, especially as the distinction between genetic susceptibility from exclusive environmental factors that might aggregate within families can be difficult.…”

Section: Infectious Myocarditis and Geneticsmentioning

confidence: 99%