Exercise-Induced Cardiac Troponin Elevation: Evidence, Mechanisms, and Implications

Brief Myocardial Ischemia Produces Cardiac Troponin I Release and Focal Myocyte Apoptosis in the Absence of Pathological Infarction in Swine

Posttranslational modifications of cardiac troponin T: An overview

Multiorgan failure is a catastrophic consequence of heat stroke (HS) and considered the underlying etiology of mortality. Identifying novel biomarkers capable of predicting the extent of HS-induced...

https://www.physiology.org/doi/pdf/10.1152/japplphysiol.00365.2014

Cardiovascular and thermoregulatory biomarkers of heat stroke severity in a conscious rat model

Cardiac troponin is the biomarker of choice for the diagnosis of acute myocardial infarction. Recent consensus recommendations have adopted a concentration of troponin above the 99th percentile of a healthy population to diagnose myocardial infarction. Until recently, there was no assay capable of achieving recommended precision; however, with the development of "highly sensitive" troponin assays, it is now possible to accurately measure troponin concentrations at and below the current 99th percentile of a healthy population. These assays have enormous potential in not only identifying more patients with acute myocardial infarction, and providing superior risk prediction in those so afflicted, in addition highly sensitive troponins assays may be useful for long-term risk assessment of the patient with coronary disease. In this article, we will review the clinical applications, novel concepts, challenges, and limitations of using highly sensitive troponins assays.

Clinical applications of highly sensitive troponin assays.

Although measurement of troponin is widely used for diagnosing acute myocardial infarction (AMI), its diagnostic potential may be increased by a more complete characterization of its molecular appearance and degradation in the blood. The aim of this study was to define the time course of cardiac troponin I (cTnI) degradation in patients with acute ST-elevation myocardial infarction (STEMI). In the ASSENT-2 substudy, 26 males hospitalized with STEMI were randomized to 2 different thrombolytic drugs within 6 hours after onset of symptoms. Blood samples were obtained just before initiation of thrombolysis and at 30 minutes intervals (7 samples per patient). Western blot analysis was performed using anti-cTnI antibodies and compared with serum concentrations of cTnI. All patients exceeded the cTnI cutoff for AMI during the sampling period; at initiation of therapy, 23 had elevated cTnI values. All patients demonstrated 2 bands on immunoblot: intact cTnI and a single degradation product as early as 90 minutes after onset of symptoms. On subsequent samples, 15 of 26 patients showed multiple degradation products with up to 7 degradation bands. The appearance of fragments was correlated with higher levels of cTnI (P<0.001) and time to initiation of treatment (P=0.058). This study defines for the first time the initial time course of cTnI degradation in STEMI. Intact cTnI and a single degradation product were detectable on immunoblot as early as 90 minutes after onset of symptoms with further degradation after 165 minutes. Infarct size and time to initiation of treatment was the major determinant for degradation.

Time Course of Degradation of Cardiac Troponin I in Patients With Acute ST-Elevation Myocardial Infarction The ASSENT-2 Troponin Substudy

Introduction: Troponin has become the most important marker for diagnosing acute myocardial infarction, yet knowledge is scarce regarding appearance of specific degradation fragment

Cardiac Troponin I Degradation in Serum of Patients with Hypertrophic Obstructive Cardiomyopathy Undergoing Percutaneous Septal Ablation

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Time Course of Degradation of Cardiac Troponin I in Patients With Acute ST-Elevation Myocardial Infarction The ASSENT-2 Troponin Substudy

Cardiac Troponin I Degradation in Serum of Patients with Hypertrophic Obstructive Cardiomyopathy Undergoing Percutaneous Septal Ablation