Correlation of Antemortem Serum Creatine Kinase, Creatine Kinase-MB, Troponin I, and Troponin T with Cardiac Pathology

Abstract

Background: Spurious increases in serum troponins, especially troponin T, have been reported in patients with and without acute myocardial syndromes. Methods: We studied 78 autopsied patients without clinical myocardial infarction (MI) and correlated histologic cardiac findings with antemortem serum creatine kinase (CK), its MB isoenzyme (CK-MB), cardiac troponin I (cTnI), and cardiac troponin T (cTnT). Results: There was no significant myocardial pathology in 15 patients. Cardiac pathologies were in five groups: scarring from previous MI or patchy ventricular fibrosis (n = 9), recent MI (n = 27), healing MI (n = 7), degenerative myocyte changes consistent with congestive heart failure (CHF; n = 12), and other cardiac pathologies (n = 8). The median concentrations in the five groups were not significantly different for either CK or CK-MB. Compared with the no-pathology group, only the MI group was significantly different for cTnI, and the MI and other pathology groups were significantly different for cTnT. For patients with MI, 22%, 19%, 48%, and 65% had increased CK, CK-MB, cTnI, and cTnT, respectively; for CHF and other cardiac pathologies combined, the percentages were 28%, 17%, 22%, and 50%. For patients with increased cTnI, 72% and 28% had MI and other myocardial pathologies, respectively; patients with increased cTnT had 64% and 36%, respectively. Patients without myocardial pathology had no increases in CK-MB, cTnI, or cTnT. Conclusions: All patients with increased serum CK-MB, cTnI, and cTnT had significant cardiac histologic changes. The second-generation cTnT assay appears to be a more sensitive indicator of MI and other myocardial pathologies than the cTnI assay used in this study.

Correlation of Serum Cardiac Troponin I and Myocardial Damage in Cattle with Monensin Toxicosis

“…Moreover, we identified a higher sensitivity of cTnI to detect myocardial injury as compared with CK as described by other investigators. 4 Serum cTnI increased earlier after monensin intoxication and an association among cTnI concentration, ventricular dysfunction, and myocardial necrosis was detected, whereas CK was not correlated to any of these measures. This finding is in accordance with previous studies which have shown that CK lacks specificity for myocardial cell injury and that the measurement of CK is not sensitive enough to detect micropathology of the heart in cattle.…”

“…Flunixin-meglumine f (1.1 mg/kg, IV) was given for pyrexia and alleviation of gastrointestinal pain as needed. Blood was collected from the indwelling jugular catheter at 4,6,8,12,16,20,24,36,48,72, and 80 hours (Group A) and at 12, 24, 36, 48, 72, 96, 120, and 144 hours (Group B) after monensin administration for serum biochemical analyses and cTnI measurement. The blood was divided equally and put into tubes without anticoagulant.…”

Cardiac troponins and renal disease

“…Post-mortem evidence suggests the presence of micro-infarction in patients with elevated serum troponins. 81 It is possible that patients with ESRD may sustain repeated subclinical microinfarctions.…”

Comparison of Canine Cardiac Troponin I Concentrations as Determined by 3 Analyzers

“…C ardiac troponin I (cTnI) is a highly sensitive and specific blood marker for the noninvasive diagnosis of increased cardiomyocyte permeability and, as such, has become very important for the early detection of myocardial infarction in human beings. [1][2][3][4][5][6] Although myocardial infarction is uncommon in veterinary medicine, some dogs and cats with conditions involving myocardial damage, such as hypertrophic cardiomyopathy, unclassified cardiomyopathy, dilated cardiomyopathy, subaortic stenosis, mitral valve degeneration, gastric dilatation-volvulus, blunt thoracic trauma, and babesiosis have been found to have high cTnI concentrations. [7][8][9][10][11][12] Cardiac troponin I analyzers have not been standardized and because each company can use a potentially different and proprietary target amino acid in the assay, values obtained on 1 analyzer may not be directly comparable to values obtained on a different analyzer.…”