Cardiac Troponin I and T as Prognostic Markers in Cats with Hypertrophic Cardiomyopathy. (23rd July 2014)

• Record Type: Journal Article
• Authors: Langhorn, R.; Tarnow, I.; Willesen, J.L.; Kjelgaard‐Hansen, M.; Skovgaard, I.M.; Koch, J.
• Is Part Of: Journal of veterinary internal medicine. Volume 28:Number 5(2014:Sep./Oct.)
• Page Start: 1485
• Page End: 1491
• Publication Date: 2014-07-23
• Subjects: Veterinary medicine -- Periodicals; 636.0896
• DOI: 10.1111/jvim.12407
• Languages: English
• ISSNs: 0891-6640

Abstract

<abstract abstract-type="main" id="jvim12407-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="jvim12407-sec-0001" sec-type="section"> <title>Background</title> <p>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.</p> </sec> <sec id="jvim12407-sec-0002" sec-type="section"> <title>Hypothesis</title> <p>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.</p> </sec> <sec id="jvim12407-sec-0003" sec-type="section"> <title>Animals</title> <p>Thirty‐six cats with primary HCM.</p> </sec> <sec id="jvim12407-sec-0004" sec-type="section"> <title>Methods</title> <p>Prospective cohort study. Cats with HCM were included consecutively and examined every 6 months. Echocardiography, ECG, blood pressure, and serum cTnI and cTnT were evaluated at each visit. Cox proportional hazards regression analysis was performed to evaluate prognostic potential of serum troponin concentrations at admission and subsequent examinations. Correlations were used to examine associations between troponin concentrations and cardiac hypertrophy.</p> </sec> <sec id="jvim12407-sec-0005" sec-type="section"> <title>Results</title> <p>Troponin concentrations at admission were median [range] 0.14 [0.004–1.02] ng/mL for cTnI, and 13 [13–79.5] ng/L for cTnT. Both were prognostic for death (<italic>P</italic> = .032 and .026) as were the last available concentrations of each (<italic>P</italic> = .016 and .003). The final cTnT concentration was a significant predictor of death even when adjusting for the admission concentration (<italic>P</italic> = .043). In a model containing both markers, only cTnT remained significant (<italic>P</italic> = .043). Left ventricular free wall thickness at end‐diastole (LVFWd) at admission was correlated with cTnI at admission (<italic>r</italic> = 0.35, <italic>P</italic> = .035), however no significant correlations (<italic>r</italic> = 0.2–0.31, <italic>P</italic> = .074–.26) were found between changes in troponin concentrations and left ventricular thickness over time.</p> </sec> <sec id="jvim12407-sec-0006" sec-type="section"> <title>Conclusions and Clinical Importance</title> <p>Myocardial injury is part of the pathophysiology leading to disease progression and death. Low sensitivities and specificities prevent outcome prediction in individual cats.</p> </sec> </abstract>