Prospective Study Correlating Fibrinopeptide A, Troponin I, Myoglobin, and Myosin Light Chain Levels With Early and Late Ischemic Events in Consecutive Patients Presenting to the Emergency Department With Chest Pain

Abstract

Background-Although thrombus formation plays a major role in acute coronary syndromes, few studies have evaluated a thrombus marker in risk stratification of patients with chest pain. Furthermore, the relation between markers that reflect myocardial injury and thrombus formation that may predict events in a heterogeneous patient population is unknown. This study correlated markers of thrombus and myocardial injury with early and late ischemic events in consecutive patients with chest pain. Methods and Results-Serum troponin I (TnI), myoglobin, and myosin light chain levels were obtained from 247 patients and urinary fibrinopeptide A (FPA) from 178 of the 247. By multivariate analysis, patients with an elevated FPA level were 4.82 times more likely to die or have myocardial infarction, unstable angina, and coronary revascularization at 1 week (Pϭ0.002, 95% CI 1.78, 13.03), whereas those with an elevated TnI (Ͼ0.2 ng/mL) were 9.41 times more likely (PϽ0.001, 95% CI 2.84, 31.17). At 6 months (excluding the index event), an elevated FPA level was an independent predictor of events, with an odds ratio of 9.57 (PϽ0.001, C1 3.29, 27.8), and was the only marker to predict a shorter event-free survival (PϽ0.001). The other markers did not independently correlate with cardiac events, although MLC incrementally increased early predictive accuracy in combination with the FPA and TnI. Conclusions-Elevated FPA and TnI correlated with cardiac events during the initial week in patients presenting to the Emergency Department with chest pain. FPA predicted adverse events and a shorter event-free survival at 6 months.

Beckman Access versus the Bayer ACS:180 and the Abbott AxSYM cardiac Troponin-I real-time immunoassays: an observational prospective study

“…Levels of cTnI are, on average, detectable four to six hours from the onset of chest pain, peaking in twelve hours and remaining elevated for three to ten days, making it an ideal marker for the detection of both acute as well as delayed AICS presentations [26]. Also, cTnI has been shown to be more sensitive than CK-MB mass assays for the detection of subsequent myocardial events in those patients presenting to the ED with chest pain [5,27]. …”

Progressive troponin I loss impairs cardiac relaxation and causes heart failure in mice

“…TnI is the inhibitory subunit that can bind to actin-tropomyosin and prevent muscle contraction by inhibition of actin-activated myosin (actomyosin) ATPase activity (33). TnI has received considerable attention as a serum biomarker of myocardial tissue damages (2,31) and as a key phosphoprotein that regulates cardiac contractile function (13,40). Its role in mediating cardiac dysfunction in humans and experimental animals is controversial and continues to be actively investigated.…”

Thrombin-induced Rapid Geranylgeranylation of RhoA as an Essential Process for RhoA Activation in Endothelial Cells

“…tion, platelet aggregation, and activation of the coagulation cascade, all of which contribute to the pathogenesis of coronary atherosclerosis and acute coronary syndrome (1)(2)(3). Moreover, thrombin has been shown to induce the rapid activation of small GTPase RhoA, which is involved in endothelial dysfunction including hyperpermeability and impaired nitric oxide synthesis (4 -9).…”