Abstract 13743: Urinary N-terminal Fragment of Titin Predicts Mortality in Dilated Cardiomyopathy

Background: Titin, a giant sarcomeric protein, functions as a scaffold in striated muscle. Titin is involved in myocardial passive tension and viscoelasticity, and associated with myocardial stiffness and hypertrophy. Mutations in titin gene have been identified in cardiac myopathies such as dilated cardiomyopathy (DCM). It has been recently reported that in damaged muscle, the N-terminal fragment of titin (Titin-N) is cleaved by calpain-3, and the resulting fragments are excreted into the urine via glomerular filtration. We aimed to investigate the impact of urinary Titin-N on prognosis of DCM. Methods and Results: We measured urinary levels of Titin-N/creatinine (U-TN/Cr; pmol/mg/dl) in 102 DCM patients, and followed up all the patients (mean 1167 days). These patients were divided into 3 groups based on the U-TN/Cr: 1st (U-TN/Cr <3.35, n=34), 2nd (3.35≤ U-TN/Cr <7.26, n=34) and 3rd (7.26≤ U-TN/Cr, n=34) tertiles. Left ventricular ejection fraction (LVEF) and right ventricular fractional area change did...