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Ventricular arrhythmia is the main cause of sudden cardiac death. Intracardiac strain, myocardial and extracellular matrix remodelling, and subsequent myocardial fibrosis are involved in arrhythmia pathogenesis. The present study investigates the relationship between cardiac fibrosis [procollagen type I aminoterminal peptide (PINP), procollagen type III aminoterminal peptide (PIIINP), TIMP1, membrane metalloproteinase I], pressure overload [brain natriuretic peptide (BNP)] inflammation [high sensitivity (hs)-C-reactive protein] serum markers, and the incidence of ventricular tachycardia (VT) in implantable cardioverter-defibrillators (ICD) recipients.

Serum BNP, hs-C-reactive protein, procollagen to assess the risk of ventricular tachycardia in ICD recipients after myocardial infarction