Comparison of serum cardiac specific troponin‐I with creatine kinase, creatine kinase‐MB isoenzyme, tropomyosin, myoglobin and C‐reactive protein release in marathon runners: cardiac or skeletal muscle trauma?

Abstract

Problems arise in distinguishing skeletal from cardiac muscle trauma on the basis of serum enzyme tests following severe muscle exercise. The contributions of cardiac and skeletal sources have been assessed in eleven marathon runners by measuring pre- and post-race serum levels of cardiac-specific myofibrillar troponin-I together with total creatine kinase, creatine kinase-MB isoenzyme, myoglobin, myofibrillar tropomyosin and C-reactive protein. Total creatine kinase, creatine kinase-MB isoenzyme, tropomyosin and myoglobin were significantly elevated above pre-race levels in all runners between 1 h and 128 h post-race. Neither mean cardiac troponin-I nor C-reactive protein was elevated post-race. Nine out of sixty-three samples fulfilled conventional positive criteria for cardiac muscle damage on the basis of combined creatine kinase and creatine kinase-MB isoenzyme levels. Six runners had one or more positive samples. No samples had levels above twice the upper normal limit for either cardiac troponin-I or C-reactive protein. Correlation analysis of levels in each sample indicated skeletal and not cardiac muscle as the source of raised serum protein.

A Prospective Study of an Algorithm Using Cardiac Troponin I and Myoglobin as Adjuncts in the Diagnosis of Acute Myocardial Infarction and Intermediate Coronary Syndromes in a Veteran's Hospital

“…[19][20][21][22][23][24][25][26][27][28][29] Cardiac troponin I also remains elevated longer, usually up to 10-14 days.20 Recently it has also been shown that cTnI is an important prognostic indicator in patients presenting with unstable angina, even when CK-MB is not e l e~a t e d . l~\~&~~ Our study supports that notion.…”

Cardiac Troponin I and T Alterations in Dog Hearts With Myocardial Infarction: Correlation With Infarct Size

“…[10][11][12][13] Published studies have demonstrated the improved usefulness of cTnl and cTnT for the diagnosis of AMI [14][15][16][17][18] compared with creatine kinase MB, the most frequently used marker of AMI. [19][20][21][22] Increased serum concentrations of cTnl and cTnT have been shown to be more tissue specific for myocardial damage than other cardiac markers. [22][23][24][25] Furthermore, since the majority of cardiac troponins are myofibril bound, their release in serum may correlate with the extent of cardiac necrosis after myocardial infarction, providing a noninvasive method for assessing infarct size.…”

High-sensitivity cardiac troponin testing in routine practice: economic and organizational advantages

“…In the late 1980's a first assay (radioimmunoassay, RIA) for specific detection of cTn was made available, and shortly afterwards several more practical assays based on immunoenzymatic techniques were developed (1,2). The clinical adoption of cTn immunoassays was based on the assumption that the specific antibodies used in the assays were able to distinguish cTnI or cTnT from their skeletal muscle isoforms (2), thus enabling to reliably identify a cardiac myocyte injury.…”