(DOWNLOAD) "Cardiac Troponins I and T in Patients with Suspected Acute Coronary Syndrome: A Comparative Study in a Routine Setting (Enzymes and Protein Markers) (Report)" by Clinical Chemistry * Book PDF Kindle ePub Free
eBook details
- Title: Cardiac Troponins I and T in Patients with Suspected Acute Coronary Syndrome: A Comparative Study in a Routine Setting (Enzymes and Protein Markers) (Report)
- Author : Clinical Chemistry
- Release Date : January 01, 1998
- Genre: Chemistry,Books,Science & Nature,
- Pages : * pages
- Size : 232 KB
Description
In recent years, cardiospecific proteins of the troponintropomyosin complex in the contractile system of the cardiomyocytes [cardiac troponin I (cTnI)3 and cardiac troponin T (cTnT)] have challenged creatine kinase isoenzyme MB (CK-MB) as the "gold standard" for the early biochemical detection of acute myocardial injury (1-3), and they appear also to be superior to LD-1 in the late diagnosis of acute myocardial infarction (AMI) (4). An additional feature of cTnT is the ability to detect myocardial injury in some of the patients with unstable angina pectoris (UAP) (5-7). Because these patients bear a substantial risk for developing adverse events such as AMI, cTnT and, more recently, cTnI have been proposed to be of value in risk stratification of patients with UAP in view of the possible benefit of an early intervention with antithrombotic therapy (8-10). The cardiospecificity of cTnT compared with cTnI has recently been questioned (11). cTnT is regularly increased in patients with end-stage renal failure (12). In some instances, re-expression in skeletal muscle of the fetal gene for cTnT may occur and form a potential source of nonspecific cTnT with respect to myocardial injury (13). Such re-expressions seem to be possible in such chronic myopathies as muscle dystrophy and polymyositis (14). The first generation of the cTnT assay lacked absolute specificity for the cardiac isoform and allowed interference by skeletal muscle troponin T (TnT) in conditions such as rhabdomyolysis (15). The second generation of the assay system is claimed to be absolutely specific for the myocardial isoform of TnT (16). However, cTnT is still detectable in many cases of end-stage renal failure, to a lesser extent than the first generation but to an extent far more frequent than cTnI (17). The mechanism behind this situation is unclear at the present time; however, a recent a Nonstandard abbreviations: cTn1, cardiac troponin 1; cTnT, cardiac troponin T; CK, creatine kinase; CK-MB, creatine kinase MB isoenzyme; AMI, acute myocardial infarction; UAP, unstable angina pectoris; TnT, troponin T; CK-MBm, creatine kinase MB mass concentration; ECG, electrocardiogram; and URL, upper reference limit of a healthy population. report indicates the presence of some cTnT in skeletal muscle biopsies from patients with end-stage renal failure (13). The specificity of cTnT for the detection of myocardial injury has therefore been debated from both a practical and a theoretical point of view (11). However, studies in unselected patients are few, and the practical impact of these specificity considerations is not known at the present time.
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