Cardiac troponin I concentrations in horses with colic

• Autores: Olga M. Seco Díaz
• Localización: JAVMA: Journal of the American Veterinary Medical Association, ISSN-e 0003-1488, Vol. 245, Nº. 1, 2014, págs. 118-125
• Idioma: inglés
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• Resumen

  • Objective—To determine prevalence of myocardial injury in horses with colic on the basis of high concentrations of cardiac troponin I (cTnI), frequency of cardiac arrhythmias within the first 24 to 48 hours after hospital admission or surgery because of colic, and associations between high cTnI concentrations and cardiac arrhythmias, clinical course, and outcome (survival to discharge from hospital vs nonsurvival [death or euthanasia]).

    Design—Prospective observational study.

    Animals—111 horses with colic.

    Procedures—Blood was drawn at admission and 12 and 24 hours after admission if horses were treated medically or 12 and 24 hours after surgery if treated surgically. A 24-hour ambulatory ECG was recorded beginning the morning after admission in medically treated cases or after surgery and evaluated for arrhythmias. Clinical and clinicopathologic data and outcome were obtained. Associations between cTnI concentrations and other variables were determined.

    Results—An abnormal cTnI concentration (≥ 0.10 ng/mL) at admission was significantly associated with the occurrence of ventricular arrhythmias, outcome, and surgical treatment.

    Conclusions and Clinical Relevance—The data suggested that horses with colic and high cTnI concentrations at admission were more likely to have ventricular arrhythmias and have a less favorable prognosis for recovery. High cTnI concentrations in horses with colic were suggestive of myocardial damage.

    Cardiac arrhythmias have been reported in horses with gastrointestinal tract disorders.1–4 These arrhythmias can be caused by metabolic or electrolyte disturbances, hypovolemia, toxemia, and drugs such as inhalation anesthetics or can be associated with primary myocardial injury.4 Horses with acute colic often have endotoxemia, particularly those with strangulating gastrointestinal lesions or enterocolitis.5,6 Such horses may be more likely to develop cardiovascular complications associated with endotoxemia, including cardiac arrhythmias and myocardial injury.3 The prevalence of cardiac arrhythmias or cardiac damage in these horses is unknown and is probably underestimated. Ventricular arrhythmias have been reported in horses with strangulating and nonstrangulating small or large intestinal disorders, proximal enteritis, and salmonellosis.1–4 Myocardial degeneration and fibrosis have been documented in horses with duodenitis-proximal jejunitis and ventricular arrhythmias.4 Myocardial necrosis has been seen in horses with endotoxemia and large colon torsion.3,7 Primary myocardial disease is a diagnosis of exclusion that is usually made in patients with cardiac arrhythmias without other apparent causes. Echocardiograms in horses with myocarditis are usually normal other than abnormalities caused by the arrhythmia, unless there is severe myocardial injury.7,8 Serum concentration of CK-MB (the cardiac isoenzyme of CK) and serum lactate dehydrogenase activity (hydroxybutyrate dehydrogenase or lactate dehydrogenase 1 and 2) have been used in the past for diagnosis of myocardial cell injury; however, their sensitivity and specificity for diagnosis of myocardial cell damage in horses have been questioned.5,9,10 Cardiac troponin I is a sensitive and specific marker for myocardial injury in humans and dogs and more recently has been used with success in horses to detect myocardial damage.11–18 The primary objectives of the study reported here were to determine prevalence of myocardial injury in horses with colic on the basis of high concentrations of cTnI, frequency of cardiac arrhythmias within the first 24 to 48 hours after hospital admission, and associations between high cTnI concentrations and cardiac arrhythmias, clinical course, and outcome (survival to discharge from hospital vs nonsurvival [death or euthanasia]). Secondary objectives were to determine whether high concentrations of cTnI were associated with other clinical, laboratory, or physical examination findings typically associated with endotoxemia and whether there was a significant difference in cTnI concentration depending on the type or severity of disease. Our hypothesis was that cTnI concentration would be high (> 0.1 ng/mL) in horses with severe colic such as strangulating gastrointestinal tract lesions or enterocolitis and that cTnI concentration would be superior to CK-MB concentration for the detection of associated myocardial damage.