Cardiac specific troponin-I release in canine experimental myocardial infarction: Development of a sensitive enzyme-linked immunoassay

Cummins, Bernadette; Cummins, Peter L.

doi:10.1016/s0022-2828(87)80572-2

Cited by 80 publications

(42 citation statements)

References 37 publications

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“…Concentrations begin to increase and peak at 12–48 hours and then decrease after 5–10 days 31. A canine model of acute myocardial infarction showed similar release times, but the peak occurred earlier (range, 10–16 hours) 32. A study of dogs with GDV identified peak serum cTnI concentrations between 48 and 72 hours, after surgery.…”

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confidence: 93%

Serum Cardiac Troponin I Concentrations in Dogs with Systemic Inflammatory Response Syndrome

Hamacher¹,

Dörfelt²,

Müller³

et al. 2015

Veterinary Internal Medicne

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BackgroundMyocardial injury can be detected by cardiac troponin I (cTnI) concentration, which appears to be a predictor of short‐term death in critically ill patients. It is unknown if the best prognostic indicator of short‐term survival is cTnI measurement at admission or at later time points.Hypothesis/ObjectivesMeasuring cTnI with a high‐sensitivity (HS) test at different time points after admission may be a better short‐term prognostic indicator than a single cTnI measurement at admission in dogs with systemic inflammatory response syndrome (SIRS).AnimalsProspective, observational clinical study of 60 dogs with SIRS.MethodsCardiac troponin I concentration was measured in 133 serum samples, collected at days 1, 2, 3, and 5. Additionally, the acute patient physiologic and laboratory evaluation (APPLE) fast score was evaluated at admission. Prognostic capabilities of cTnI measurement and APPLE fast score for 28‐day mortality were assessed by receiver operating characteristic curve analysis.ResultsForty‐one dogs with SIRS that survived 28 days had significantly lower serum cTnI concentrations at admission (median, 0.09 ng/mL; P = .004) and at the peak time point (median, 0.23 ng/mL; P = .01) compared to 19 nonsurvivors (median at admission, 0.63 ng/mL; median at peak, 1.22 ng/mL). Area under the curve to predict survival, using cTnI was similar at admission (0.732) and at peak (0.708), and was 0.754 for the APPLE fast score.Conclusions and Clinical ImportanceIncreased cTnI concentration in dogs with SIRS is associated with poor outcome. Daily follow‐up measurement of cTnI concentration provides no additional prognostic information for short‐term mortality.

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confidence: 93%

Serum Cardiac Troponin I Concentrations in Dogs with Systemic Inflammatory Response Syndrome

Hamacher¹,

Dörfelt²,

Müller³

et al. 2015

Veterinary Internal Medicne

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“…10 The similarity of the canine heart to the human heart has resulted in the use of dogs as an experimental model for induced myocardial infarction, in which cTnT and cTnI have been found to be sensitive and specific biomarkers of cardiac injury. [13][14][15][16][17] A limited number of clinical studies on cardiac troponins in dogs have been published in recent years. [18][19][20][21][22][23] Results of these studies indicate that cardiac troponins may be helpful in the identification of myocardial contusion, myocarditis, and congestive heart failure, doxorubicin-induced cardiotoxicity, and in distinguishing between idiopathic pericardial effusion and pericardial effusion caused by hemangiosarcoma.…”

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confidence: 99%

Cardiac Troponins as Indicators of Acute Myocardial Damage in Dogs

Burgener

Kovačević²,

Mauldin

et al. 2006

Veterinary Internal Medicne

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Cardiac troponin I (cTnI) and T (cTnT) have a high sequence homology across phyla and are sensitive and specific markers of myocardial damage. The purpose of this study was to evaluate the Cardiac Reader, a human point-of-care system for the determination of cTnT and myoglobin, and the Abbott Axsym System for the determination of cTnI and creatine kinase isoenzyme MB (CK-MB) in healthy dogs and in dogs at risk for acute myocardial damage because of gastric dilatationvolvulus (GDV) and blunt chest trauma (BCT). In healthy dogs (n 5 56), cTnI was below detection limits (,0.1 mg/L) in 35 of 56 dogs (reference range 0-0.7 mg/L), and cTnT was not measurable (,0.05 ng/mL) in all but 1 dog. At presentation, cTnI, CK-MB, myoglobin, and lactic acid were all significantly higher in dogs with GDV (n 5 28) and BCT (n 5 8) than in control dogs (P , .001), but cTnT was significantly higher only in dogs with BCT (P 5 .033). Increased cTnI or cTnT values were found in 26 of 28 (highest values 1.1-369 mg/L) and 16 of 28 dogs (0.1-1.7 ng/mL) with GDV, and in 6 of 8 (2.3-82.4 mg/L) and 3 of 8 dogs (0.1-0.29 ng/mL) with BCT, respectively. In dogs suffering from GDV, cTnI and cTnT increased further within the first 48 hours (P , .001). Increased cardiac troponins suggestive of myocardial damage occurred in 93% of dogs with GDV and 75% with BCT. cTnI appeared more sensitive, but cTnT may be a negative prognostic indicator in GDV. Both systems tested seemed applicable for the measurement of canine cardiac troponins, with the Cardiac Reader particularly suitable for use in emergency settings.

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“…However, the correlation between serum Tm or TnT levels and infarct size has not been examined, 5,6 and release of TnI did not always correlate well with infarct size. 8 Although the appearance of myofibrillar proteins in serum indicates that these proteins were degraded within the heart during myocardial ischemia, these studies provide little information about changes in myofibrillar proteins and their inherent function within the heart.…”

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confidence: 99%

Alterations in myofibrillar function and protein profiles after complete global ischemia in rat hearts.

Westfall

Solaro

1992

Circulation Research

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We studied changes in myofibrillar function and protein profiles after complete global ischemia with anoxia in rat hearts. Hearts were exposed to global ischemia and anoxia (CGI) In a few studies using coronary artery ligation, degradation of specific myofibrillar proteins was observed, although the identity of various protein fragments was uncertain.23 Evidence for changes in the composition and function of specific myofibrillar proteins has not been examined in globally ischemic rat hearts.

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Cardiac specific troponin-I release in canine experimental myocardial infarction: Development of a sensitive enzyme-linked immunoassay

Cited by 80 publications

References 37 publications

Serum Cardiac Troponin I Concentrations in Dogs with Systemic Inflammatory Response Syndrome

Serum Cardiac Troponin I Concentrations in Dogs with Systemic Inflammatory Response Syndrome

Cardiac Troponins as Indicators of Acute Myocardial Damage in Dogs

Alterations in myofibrillar function and protein profiles after complete global ischemia in rat hearts.

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