Autoimmune Mechanisms Underlying Dilated Cardiomyopathy

Yoshikawa, Tsutomu; Baba, Akira; Nagatomo, Yuji

doi:10.1253/circj.cj-08-1151

Cited by 79 publications

(52 citation statements)

References 37 publications

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“…The results of the 6-min walk test and plasma brain natriuretic peptide levels improved immediately after treatment in most patients. 19 No significant differences were observed in other parameters, although all parameters tended to improve. Mean LVEF, however, was significantly improved 3 months after the last session in comparison to pretreatment levels (from 18±8% to 22±10%, P<0.01).…”

Section: Resultsmentioning

confidence: 88%

Complete Elimination of Cardiodepressant IgG3 Autoantibodies by Immunoadsorption in Patients With Severe Heart Failure

Baba

Amaki

Shimada

et al. 2010

Circ J

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Background: Cardiodepressant IgG3 autoantibodies (CD-Abs) can be targeted by apheresis. Using blinded measurements of CD-Abs before and after immunoadsorption (IA), the cardiac function of patients who did or did not achieve complete CD-Abs elimination was compared. Methods and Results:Autoantibodies were completely removed from 18 patients with heart failure (New York Heart Assocation class 3 or 4, left ventricular ejection fraction (LVEF) <30%) using a selective IgG3 adsorption column. All patients had anti-β1-adrenergic and/or M2-muscarinic autoantibodies before IA, and all LVEF were measured on radionuclide ventriculography. CD-Abs were measured before and after IA, and patient status was blinded until all measurements were collected. Treatment was defined as complete when CD-Abs status changed from positive to negative after IA. Other instances were defined as incomplete. Six-min walk test results and brain natriuretic peptide levels improved significantly after IA (P<0.01). The increase in LVEF 3 months after IA was significantly greater after complete treatment in comparison to the incomplete treatment group (19±8-29±9% vs 18±9-17±8%, P<0.01). Cardiac insufficiency events were also more frequent in the incomplete treatment group. Conclusions:Complete elimination of CD-Abs with apheresis may be related to improved cardiac function in the treatment of heart failure. (Circ J 2010; 74: 1372 - 1378

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Section: Resultsmentioning

confidence: 88%

Complete Elimination of Cardiodepressant IgG3 Autoantibodies by Immunoadsorption in Patients With Severe Heart Failure

Baba

Amaki

Shimada

et al. 2010

Circ J

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“…2,19 Cardiac troponin T variants produced by aberrant splicing of multiple exons in animals have been related to high rates of DCM. 20 However, there has not been a report of a transgenic animal model for cTnC dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Conditional Antisense-Knockdown of Zebrafish Cardiac Troponin C as a New Animal Model for Dilated Cardiomyopathy

Lin

Tsai

et al. 2009

Circ J

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“…DCM is a disease that may result from a variety of underlying pathologies. Recent reports revealed both inflammatory processes related to infections with cardiotrophic viruses and autoimmune mechanisms as major predisposing factors in the pathogenesis of this disease (5,11,22,24,(31)(32)(33)44). It would seem important to distinguish an immunemediated inflammatory disorder from infectious cardiac disease, since there is growing evidence that for selected patients, specific treatment strategies may be effective only if based on their immunological and virological characterization (12,16,21).…”

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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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Autoimmune Mechanisms Underlying Dilated Cardiomyopathy

Cited by 79 publications

References 37 publications

Complete Elimination of Cardiodepressant IgG3 Autoantibodies by Immunoadsorption in Patients With Severe Heart Failure

Complete Elimination of Cardiodepressant IgG3 Autoantibodies by Immunoadsorption in Patients With Severe Heart Failure

Conditional Antisense-Knockdown of Zebrafish Cardiac Troponin C as a New Animal Model for Dilated Cardiomyopathy

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

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