The use of troponin measurements in patients with unstable angina

Abstract

Appreciation of the reasons why elevations of tissue is damaged [8–10]. This issue in regard to cardiac troponin I (cTnI) and T (cTnT) provide cTnT is more complex. It appears that at least some important prognostic information can only be underof the cardiac isoforms that are expressed in the heart stood if one understands the basis for the use of these are expressed in skeletal muscle during development markers. Thus, it is important to briefly recount some [11,12]. Whether these are the isoforms that are basic information. detected by the antibodies currently used for assays is more controversial and some have argued that they may well be undetected fetal forms that are present in 1. Basic biology both skeletal muscle and cardiac muscle [13]. Nonetheless, these facts have led to some concern that The troponins are part of a trimolecular complex some of the elevations of cTnT in patients with renal that are responsible for regulating the calcium mefailure and skeletal muscle injury may be due to diated interaction of actin and myosin [1,2]. From the coexpression of this marker in skeletal muscle [14– perspective of being highly specific biomarkers, cTnT 18]. This has led to the contention that cTnT may and cTnI are the products of unique genes and their have less robust specificity for cardiac injury than cardiac isoforms are substantially different from their cTnI. Definitive studies in this regard have yet to be skeletal muscle isoforms [3–5]. This is not the case published. for troponin C where the cardiac form is the same as the form found in vascular smooth muscle [6]. Thus, both cTnI and cTnT have the potential for having 2. Clinical specificity of the troponins unique specificity for cardiac injury. The data in regard to specificity are more fully developed for Multiple studies have confirmed that the troponins cTnI and suggest that the cardiac isoform is not are more specific for cardiac injury than MBCK [19]. expressed outside of the heart at any time during Increases are far less common in patients with acute neonatal development [7]. For this reason, not only or chronic skeletal muscle injury, marathon runners, would cTnI not be expected to exist in skeletal and the like. In studies where cardiac injury is muscle as has been shown by several investigations, diagnosed independently, cTnI is not found to be but it also should not be reexpressed in response to elevated in patients with acute or chronic skeletal tissue injury where fetal forms are often found when muscle injury, marathon runners or patients with renal failure in the absence of evidence of myocardial