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BIOMARKERS OF CARDIOMYOCYTE INJURY AND STRESS IDENTIFY LEFT ATRIAL AND LEFT VENTRICULAR REMODELING AND DYSFUNCTION: A POPULATION-BASED STUDY

International Conference on Environmental Health & Safety

Susana Ravassa Albeniz

University of Navarra, Spain

Posters & Accepted Abstracts: Occup Med Health Aff

DOI: 10.4172/2329-6879.C1.029

Abstract
Background/Objectives: The validation of effective screening tools for the identification of patients with subclinical myocardial remodeling is a major clinical need. Thus, we explored the associations of circulating biomarkers of cardiomyocyte injury and stress with subclinical cardiac remodeling and dysfunction, and with biomarkers reflecting collagen turnover. Methods: We randomly recruited 727 subjects from a general population (51.2% women; mean age 51.3 years). Measurements included echocardiographic left atrial (LA) and left ventricular (LV) structure and function, quantification of high sensitivity cardiac Troponin T (hs-cTnT), NT-proBNP, and biomarkers of collagen type I and III turnover. Results: In unadjusted and adjusted analyses, the prevalence of LA enlargement (LAE), LV hypertrophy (LVH) and LV diastolic dysfunction (LVDD) increased with higher hs-cTnT (P�0.031). NT-proBNP was independently associated with LVDD (P=0.009). Both biomarkers combined yielded significant integrated discrimination and net reclassification improvements (P�0.014 and P�0.009, respectively) for LAE, LVH and LVDD, over the conventional risk factors, and were independently and positively associated with biomarkers of collagen type I turnover. In a sensitivity analysis, after excluding participants with previous cardiac diseases, our findings remained consistent. Conclusions: Our population-based study suggested that subclinical LV and LA remodeling were associated with hs-cTnT, and that, in combination with NT-proBNP, hs-cTnT showed incremental diagnostic utility over the conventional risk factors. Both biomarkers were associated with biomarkers of collagen type 1 turnover. Thus, biomarkers of cardiomyocyte microinjury and hemodynamic stress may stimulate fibrosis-related mechanisms and facilitate the diagnosis of subclinical LA and LV remodelling and dysfunction in the general population.
Biography

Email: sravassa@unav.es

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