Cardiac troponins are sensitive and specific markers of myocardial injury. The troponin concentration can be thought of as a quantitative measure of the degree of injury sustained by the heart, however, it provides no information on the cause of injury or the mechanism of troponin release. Conventionally, the cardiac troponins have been used for diagnosis of acute myocardial infarction in humans and have become the gold standard biomarkers for this indication. They have become increasingly recognized as an objective measure of cardiomyocyte status in both cardiac and noncardiac disease, supplying additional information to that provided by echocardiography and ECG. Injury to cardiomyocytes can occur through a variety of mechanisms with subsequent release of troponins. Independent of the underlying disease or the mechanism of troponin release, the presence of myocardial injury is associated with an increased risk of death. As increasingly sensitive assays are introduced, the frequent occurrence of myocardial injury is becoming apparent, and our understanding of its causes and importance is constantly evolving. Presently troponins are valuable for detecting a subgroup of patients with higher risk of death. Future research is needed to clarify whether troponins can serve as monitoring tools guiding treatment, whether administering more aggressive treatment to patients with evidence of myocardial injury is beneficial, and whether normalizing of troponin concentrations in patients presenting with evidence of myocardial injury is associated with reduced risk of death.

Background: In noncardiac critical disease in humans, myocardial injury as detected by cardiac troponin I and T (cTnI and cTnT) has been linked to high intensive care unit (ICU) death independent of prognostic composite scoring.Hypothesis: Presence of myocardial injury predicts short-term death in critically ill dogs with systemic inflammation and provides additional prognostic information when combined with established canine prognostic composite scores.Animals: Forty-two dogs admitted to the ICU with evidence of systemic inflammation and no primary cardiac disease. Methods: Prospective cohort study. Blood samples were obtained at ICU admission for the measurement of cTnI and cTnT, C-reactive protein, and several cytokines. The acute patient physiologic and laboratory evaluation (APPLE) score and the survival prediction index were calculated within the first 24 hours of admission. Receiver operating characteristic (ROC) curves were used to examine the prognostic capacity of each biomarker and severity score. Multiple logistic regression analysis was performed to evaluate whether cardiac markers significantly contributed to severity scores.Results: Twenty-eight day case fatality rate was 26% (11/ Conclusions and Clinical Importance: Markers of myocardial injury predict short-term death in dogs with systemic inflammation and cTnI significantly contributes to the APPLE score.

BackgroundMyocardial 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.HypothesisPresence 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.AnimalsThirty‐six cats with primary HCM.MethodsProspective 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.ResultsTroponin 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 (P = .032 and .026) as were the last available concentrations of each (P = .016 and .003). The final cTnT concentration was a significant predictor of death even when adjusting for the admission concentration (P = .043). In a model containing both markers, only cTnT remained significant (P = .043). 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.Conclusions and Clinical ImportanceMyocardial injury is part of the pathophysiology leading to disease progression and death. Low sensitivities and specificities prevent outcome prediction in individual cats.

The results confirm the ADVIA Centaur CP TnI-Ultra assay as a valuable tool for assessing cTnI and thus myocardial injury in dogs and cats.

Objective -To investigate the presence of myocardial injury in dogs hospitalized for snake envenomation and to examine its relationship with systemic inflammation.Design -Prospective case-control study.Setting -University teaching hospital and small animal referral hospital.Animals -Dogs naturally envenomed by the European viper (Vipera berus) (n=24), African puff adder (Bitis arietans) (n=5), or snouted cobra (Naja annulifera) (n=9).Interventions -Blood was collected from dogs envenomed by V. berus at admission, 12-24 hours post-admission, and 5-10 days post-admission. Blood was collected from dogs envenomed by B. arietans or N. annulifera at admission, and 12, 24, and 36 hours post-admission.Measurements and Main Results -Concentrations of cardiac troponin I (cTnI), a marker of myocardial injury, and C-reactive protein (CRP), a marker of systemic inflammation, were measured in each blood sample. Evidence of myocardial injury was found in 58% of dogs envenomed by V. berus at one or more time-points. A significant correlation between cTnI and CRP concentrations was found at all time-points. Evidence of myocardial injury was found in 80% of dogs envenomed by B. arietans at one or more time-points; however, no correlation was found between cTnI and CRP concentrations. Evidence of myocardial injury was found in 67% of dogs envenomed by N. annulifera at one or more time-points. A significant correlation between cTnI and CRP concentrations was found at admission, but not at other time-points.Conclusions -Myocardial injury frequently occurred in dogs with snake envenomation. While the degree of systemic inflammation was significantly correlated with degree of myocardial injury in V. berus envenomation at all time-points, this was not the case in dogs envenomed by N. annulifera or B. arietans. This could be due to differences in the toxic substances of the snake venoms or to differences in the cytokines induced by the venom toxins.