Cumulative Troponin T Release after Acute Myocardial Infarction. Influence of Reperfusion

Abstract

For troponin T a characteristic biphasic change in the plasma time-concentration curve has been described, especially in patients with early reperfusion after thrombolytic therapy. As troponin T is bound to myofibrillar structures, treatment strategy or treatment outcome could influence the cumulative plasma release of this protein in a different way compared to the cumulative release of free cytoplasmic cardiac enzymes.The present study is the first study comparing the total quantity of troponin T released by the heart during the first 168 hours after acute myocardial infarction, both in patients treated with thrombolytic therapy (n = 16) and in patients not treated with thrombolytic therapy (n = 7). On the basis of clinical symptoms and coronary arteriogram within 24 hours, the patients treated with thrombolytic therapy were divided into two groups, reperfused (n = 9) and non-reperfused (n = 7). In the patients not treated with thrombolytic therapy, absence of spontaneous early reperfusion was judged only from clinical symptoms.Cumulative troponin T release into plasma was compared to the cumulative release of the cytoplasmic cardiac enzymes creatine kinase (EC 2.7.3.2) and hydroxybutyrate dehydrogenase (EC 1.1.1.27). Cumulative release, i.e., infarct size, was calculated using a two-compartment model for circulating proteins. Mean tissue contents, per gram wet weight, of 156 U/g for hydroxybutyrate dehydrogenase, 2.163 U/g for creatine kinase and 234 g/g for troponin T, were used to express infarct size in gram-equivalents of healthy myocardium per litre plasma (g-eq/1).Release rates were represented by the ratio of cumulative quantities released in 10 hours and 72 hours for creatine kinase and hydroxybutyrate dehydrogenase and in 10 hours and 168 hours for troponin T. Conclusions-Plasma time-concentration curves and release rates of troponin T in patients treated with thrombolytic therapy showing reperfusion differ significantly from those of patients not treated with thrombolytic therapy, showing no reperfusion.-Creatine kinase and hydroxybutyrate dehydrogenase release is completed within 72-100 hours in all patients, whereas troponin T release still continues after 168 hours.-Cumulative troponin T release at 168 hours is only a fraction (around 8%) of cumulative cytoplasmic enzyme release and the percentage released is not influenced by the treatment strategy or outcome, i. e., vessel patency.-Although troponin T release is only a fraction of the cumulative enzyme release (infarct size) there is a highly significant correlation between both, independent of the treatment strategy or treatment outcome.

Cardiac Magnetic Resonance Imaging Study for Quantification of Infarct Size Comparing Directly Serial Versus Single Time-Point Measurements of Cardiac Troponin T

“…The most accurate methods for estimation of infarct size in the pre-reperfusion era were based on complete recovery of CK or its isoforms (17,18) or LD isoenzymes released from the infarcted myocardial tissue (19,20). Measurement of maximum enzyme values of CK or CK-MB proves convenient but has a propensity to overestimate infarct size, particularly when spontaneous reperfusion, PCI, or thrombolysisinduced reperfusion leads to an earlier and higher maximum CK level at identical amounts of left ventricular impairment (21)(22)(23). In addition, the peak value is influenced by release ratio, which is much higher after reperfusion (24); the plasma half-life of the cardiac constituent (25); and the magnitude of the AMI itself (26 -28).…”

Relation of Cardiac Troponin I Measurements at 24 and 48 Hours to Magnetic Resonance–Determined Infarct Size in Patients With ST-Elevation Myocardial Infarction

“…In the absence of reperfusion the release pattern is characterized by a slow increase in plasma concentration which peaks at day 3 or 4 (49,124). Reperfusion therapy induces an early peak of both markers as the cytosolic pool is rapidly washed out, but there is no evidence that cumulative troponin release is impacted by reperfusion therapy (49,124,125). Evidence suggests that plasma levels are independent of reperfusion status from the first day and forward, largely reflecting the slow degradation and liberation of the structural pool (49,124).…”

Effect of Acute Phase Response on Cumulative Troponin T Release

“…However, the fact that similar estimates of infarct size are obtained for different enzymes indicate that, also in man, these cytoplasmic proteins are recovered completely in plasma within 72-100 hours after the onset of symptoms (4,19,20). The total activities of free cytosolic creatine kinase and HBDH lost from dog heart after permanent coronary occlusion (6) equalled the total release of these proteins into plasma.…”

“…In a recent study we found that the cumulative troponin T release in gram equivalents of cardiac tissue varied between 4 and 13% (range) of the cardiac enzyme release (4). As troponin T is bound to myofibrillar structures, differences in acute phase response might influence the release of this protein in a different way, when compared to the total plasma release of a free cytosolic cardiac marker like HBDH.…”