Literature DB >> 18672196

Clinical significance of troponin I efflux and troponin autoantibodies in patients with dilated cardiomyopathy.

Kati H Miettinen1, Susann Eriksson, Jarkko Magga, Petri Tuomainen, Johanna Kuusisto, Esko J Vanninen, Anu Turpeinen, Kari R Punnonen, Kim Pettersson, Keijo J Peuhkurinen.   

Abstract

BACKGROUND: The appearance of circulating autoantibodies against cardiac troponin I (cTnAbs) in patients with heart failure has been reported. We sought to evaluate the role of circulating cardiac troponin I (cTnI) and cTnAbs in the pathophysiology and prognosis of idiopathic dilated cardiomyopathy. METHODS AND
RESULTS: Circulating concentrations of cTnI and the presence of cTnAbs were determined in 95 patients with idiopathic dilated cardiomyopathy. The patients underwent laboratory testing, echocardiography, cardiopulmonary exercise testing, gated single photon emission computed tomography, and both-sided cardiac catheterization during a 3-day study period. Compared with cTnI- patients, the hearts of cTnI+ patients (cTnI > or = 0.01 ng/mL, n = 19) were significantly more dilated (left ventricular end-diastolic diameter 67 vs 61 mm, P < .05; left ventricular end-systolic dimension, 55 vs 49 mm, P < .01; echocardiography) and demonstrated greater intracardiac volumes (left ventricular end-diastolic volume 161 vs 132 mL, P = .060; left ventricular end-systolic volume 112 vs 82 mL, P < .05; gated single photon emission computed tomography), more disturbed systolic (ejection fraction 27 vs 33%, P < .05; gated single photon emission computed tomography) and cardiac sympathetic (123I-metaiodobenzylguanidine washout: 41% vs 34%; P < .05) function, and higher levels of vasoactive peptides (N-terminal proatrial natriuretic peptide 1030 vs 558 pmol/L, P < .05; N-terminal pro-B type natriuretic peptide 337 vs 115 pmol/L, P < .05). In addition, during a median follow-up time of 4.1 years, cTnI+ patients had clinical end points (cardiovascular death, heart transplantation, or clinical need for an automatic implantable cardioverter defibrillator) more often than cTnI- patients (37% vs 8%, P < .01). The presence of circulating cTnAbs (n = 15) was not associated with patients' clinical status or outcome.
CONCLUSION: Patients with idiopathic dilated cardiomyopathy with cTnI efflux demonstrate more prominent changes in the indices of left ventricular remodeling and function than patients without signs of cTnI efflux. Moreover, elevated serum cTnI is associated with poor clinical outcome. The presence of circulating cTnAbs seems to have less utility in the clinical assessment of these patients. However, their pathogenic role in disease progression in the long term cannot be excluded.

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Year:  2008        PMID: 18672196     DOI: 10.1016/j.cardfail.2008.02.009

Source DB:  PubMed          Journal:  J Card Fail        ISSN: 1071-9164            Impact factor:   5.712


  9 in total

Review 1.  The natural history of acute dilated cardiomyopathy.

Authors:  G William Dec
Journal:  Trans Am Clin Climatol Assoc       Date:  2014

Review 2.  Autoantibodies and cardiovascular dysfunction: cause or consequence?

Authors:  Yuji Nagatomo; W H Wilson Tang
Journal:  Curr Heart Fail Rep       Date:  2014-12

Review 3.  The diagnostic and clinical significance of anti-muscarinic receptor autoantibodies.

Authors:  Udi Nussinovitch; Yehuda Shoenfeld
Journal:  Clin Rev Allergy Immunol       Date:  2012-06       Impact factor: 8.667

Review 4.  Cardiac troponins and autoimmunity: their role in the pathogenesis of myocarditis and of heart failure.

Authors:  Ziya Kaya; Hugo A Katus; Noel R Rose
Journal:  Clin Immunol       Date:  2009-05-14       Impact factor: 3.969

Review 5.  Anti-cardiac troponin antibodies in clinical human disease: a systematic review.

Authors:  Eduardo M Vilela; Rita Bettencourt-Silva; J Torres da Costa; Ana Raquel Barbosa; Marisa P Silva; Madalena Teixeira; João Primo; Vasco Gama Ribeiro; José Pedro L Nunes
Journal:  Ann Transl Med       Date:  2017-08

6.  Intermittent levosimendan treatment in patients with severe congestive heart failure.

Authors:  Petri O Tuomainen; Jarkko Magga; Pekka Timonen; Kati Miettinen; Minna Kurttila; Esko Vanninen; Tomi Laitinen; Kirsi Timonen; Kari Punnonen; Ilkka Parviainen; Ari Uusaro; Olli Vuolteenaho; Matti Kivikko; Keijo Peuhkurinen
Journal:  Clin Res Cardiol       Date:  2013-03-17       Impact factor: 5.460

7.  Autoantibodies and Cardiomyopathy: Focus on Beta-1 Adrenergic Receptor Autoantibodies.

Authors:  Wai Hong Wilson Tang; Sathyamangla V Naga Prasad
Journal:  J Cardiovasc Pharmacol       Date:  2022-09-01       Impact factor: 3.271

8.  Cardiac troponin I autoantibody induces myocardial dysfunction by PTEN signaling activation.

Authors:  Yu Wu; Yang-Hua Qin; Yang Liu; Li Zhu; Xian-Xian Zhao; Yao-Yang Liu; Shi-Wen Luo; Gu-Sheng Tang; Qian Shen
Journal:  EBioMedicine       Date:  2019-08-29       Impact factor: 8.143

9.  Troponin and anti-troponin autoantibody levels in patients with ventricular noncompaction.

Authors:  Hatice Betül Erer; Tolga Sinan Güvenç; Ahu Sarbay Kemik; Hale Yaka Yılmaz; Şeref Kul; Servet Altay; Nurten Sayar; Yüksel Kaya; Mehmet Eren
Journal:  PLoS One       Date:  2013-02-28       Impact factor: 3.240

  9 in total

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