left ventricular free wall thickness at end-diastole.interventricular septal thickness at end-diastole.Low sensitivities and specificities prevent outcome prediction in individual cats. Myocardial injury is part of the pathophysiology leading to disease progression and death. Left ventricular free wall thickness at end-diastole (LVFWd) at admission was correlated with cTnI at admission ( r = 0.35, P = .035), however no significant correlations ( r = 0.2–0.31, P = .074–.26) were found between changes in troponin concentrations and left ventricular thickness over time. In a model containing both markers, only cTnT remained significant ( P = .043). The final cTnT concentration was a significant predictor of death even when adjusting for the admission concentration ( P = .043). 026) as were the last available concentrations of each ( P = .016 and. Both were prognostic for death ( P = .032 and. Troponin concentrations at admission were median 0.14 ng/mL for cTnI, and 13 ng/L for cTnT. Correlations were used to examine associations between troponin concentrations and cardiac hypertrophy. Cox proportional hazards regression analysis was performed to evaluate prognostic potential of serum troponin concentrations at admission and subsequent examinations. Echocardiography, ECG, blood pressure, and serum cTnI and cTnT were evaluated at each visit. Cats with HCM were included consecutively and examined every 6 months. Presence of myocardial injury predicts long-term death in cats with hypertrophic cardiomyopathy (HCM), and ongoing myocardial injury reflects change in left ventricular wall thickness over time. Myocardial injury detected by cardiac troponin I and T (cTnI and cTnT) in cardiac disease is associated with increased risk of death in humans and dogs.
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