Aims: 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.
Methods and results: Serum markers were collected in 121 patients implanted for spontaneous sustained VT and a prior history of myocardial infarction. VT incidence was obtained during ICD interrogation. Over a 1 year period, 38 patients (31%) experienced at least 1 VT. In a multivariate analysis, a left ventricular ejection fraction <0.35 (OR = 2.19, 95%CI 1.00-4.79, P = 0.049), an increased serum BNP (OR = 3.75, 95%CI 1.46-9.67, P = 0.014), an increased hs-C-reactive protein (OR = 3.2, 95%CI 1.26-8.10, P = 0.006), an increased PINP (OR = 3.71, 95%CI 1.40-9.88, P = 0.009), and a decreased PIIINP (OR = 0.21, 95%CI 0.08-0.59, P = 0.003) were associated with a higher VT incidence.
Conclusion: In coronary artery disease patients: (1) BNP is not only a marker of left ventricular dysfunction, but also a marker of VT; (2) combined 'high PINP and low PIIINP' is a strong VT marker; and 3) inflammatory process is involved in VT pathogenesis.