Why the study?
Does cardiac troponin I (cTnI) concentration help diagnose myocardial disease and predict survival in horses with cardiac disease?
Does cardiac troponin I (cTnI) concentration help diagnose myocardial disease and predict survival in horses with cardiac disease?
Cardiac troponin I is significantly elevated in horses with myocardial disease compared to healthy horses or those with structural heart disease or lone arrhythmias, though its association with survival remains unclear.
Answers are grounded in this paper and cite their sources.
cTnI elevation was associated with myocardial disease and nonsurvival in horses; hypothesis-generating for equine cardiac biomarkers pending prospective validation.
OBJECTIVES: To measure the cardiac troponin I (cTnI) concentration in horses and determine whether it could be used in the diagnosis of myocardial disease, as well as determining the association between cTnI and survival. DESIGN: Prospective, observational study. PROCEDURE: Physical examination, echocardiography, telemetric electrocardiography and postmortem were used to diagnose cardiac disease. Diagnoses were grouped as myocardial disease, structural heart disease or lone arrhythmia. Blood samples were collected at admission for cTnI analysis and the results were compared with those for 18 healthy horses. RESULTS: In total, 49 horses were admitted with cardiac disease. Elevated cTnI concentration (>0.03 ng/mL) was observed in a greater proportion of horses with myocardial disease (7/7), compared with healthy horses (0/18; P < 0.0001), horses with structural heart disease (7/25; P = 0.001), and horses with a lone arrhythmia (2/17; P = 0.0001). The median cTnI concentration for horses with myocardial disease was 17.5 ng/mL (range 0.78-49.87 ng/mL), which was higher than in the healthy horses (0.01 ng/mL, range 0.01-0.03 ng/mL; P < 0.0001). Of the 49 horses with cardiac disease, the median cTnI concentration for non-survivors (0.28 ng/mL, range 0.01-49.87 ng/mL) was higher than for survivors (0.01 ng/mL, range 0.01-30.31 ng/mL; P = 0.0035). However, the proportion of surviving horses with an elevated cTnI (10/39, 26%) was not significantly different from the proportion of non-surviving horses with an elevated cTnI (6/10, 60%; P = 0.060). CONCLUSIONS: cTnI is elevated in horses with myocardial disease and elevated to a lesser degree in some horses with structural heart disease or lone arrhythmias. The association between cTnI concentration and survival was not clear.
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Nath et al. (2012) studied this question.
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