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Abstract
Objectives. Alterations of collagen metabolism present in heart failure promote the fibrotic substrate for the development of atrial fibrillation (AF). Myocardial collagen I synthesis and degradation can be assessed indirectly by circulating biomarkers such as the carboxy terminal propeptide (PICP) and carboxy-terminal telopeptide (CITP), respectively. Design. We examined myocardial collagen type-I metabolism in 143 patients with systolic heart failure (New York Heart Association Class 2–4) in relation to coexisting AF. Results. Mean age was 75 years, blood pressure 134/80 mm Hg, ejection fraction 34%, serum PICP 81 μg/L and CITP 8.3 μg/L, and median plasma brain natriuretic peptide 215 pg/L; 77 were in AF. PICP and CITP were related to left atrial diameter (r = 0.22, P = 0.013, and r = 0.26, P = 0.003) and CITP to pulmonary capillary wedge pressure and C-reactive protein (r = 0.19, P = 0.044, and r = 0.29, P = 0.003). A logistic regression suggested that PICP (odds ratio per 1 μg/L change 1.01, P = 0.012) and left ventricular end-diastolic volume (odds ratio per 1 mL change 0.98, P < 0.001) were independently associated with coexisting AF. Conclusion. Collagen type-I metabolism is associated to left atrial size. Heart failure patients with coexisting AF exhibit more altered collagen type-I metabolism than patients in sinus rhythm. This might represent more severe atrial and ventricular fibrosis.
Trial registration: ClinicalTrials.gov identifier: NCT01671995.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
This work was supported by the Regional agreement on medical training and clinical research (ALF) between Stockholm County Council and Karolinska Institutet; Karolinska Institutet Research Foundations; the Agreement between the Foundation for Applied Medical Research (FIMA) and Unión Temporal de Empresas project Centro de Investigación Médica Aplicada (CIMA); the Red Temática de Investigación Cooperativa en Enfermedades Cardiovasculares (RECAVA) from the Instituto de Salud Carlos III, Ministry of Science and Innovation, Spain [RD06/0014/0008]; and the European Commission [FP7-HEALTH-2010-261409, FP7-HEALTH-2011-278249, FP7-HEALTH-2012-305507, and FP7-HEALTH-2013-602904].