Stubbs, Peter John; (1995) Cardiac troponin t and myocardial damage. Doctoral thesis (M.D), UCL (University College London).

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Abstract

An accurate diagnosis of patients presenting with chest pain is required for appropriate patient management and to define prognosis. Current methods used to diagnose myocardial infarction were reviewed and an assessment of the biochemical markers currently available for identifying myocyte damage revealed a potential role for a more cardiac specific marker. Further review of current strategies to risk stratify patients with unstable angina identified a continuing problem between available investigations and predictive power for future cardiac events. An assay for the cardiac specific protein Troponin T (cTnT) has recently become available and its potential role in acute coronary syndromes was studied. The cardiac specificity of cTnT was compared with creatine kinase MB isoenzyme (CK- MB) concentration measurement for the differential diagnosis of elevated creatine kinase (CK) produced by arduous physical training in 219 Royal Marine Commandos with no evidence of cardiovascular disease. CK was elevated up to 22.6 times and CK-MB mass up to 6.6 times the upper reference limit. Only 2 individuals had detectable cTnT, neither exceeded 0.2 micrograms/litre. Cardiac Troponin T was considered to be superior and more cardiac specific than the other biochemical markers. The potential role of cTnT measurement in the differential diagnosis of suspected ischaemic myocardial damage was examined in 93 consecutive patients admitted to a Coronary Care Unit. The study showed that the cut off value should be 0.2 micrograms/litre, and that a single measurement at either 12-24 hours from admission or 12-48 hours from the onset of chest pain will confirm or exclude myocardial infarction. Cardiac Troponin T was also identified in a subset of patients with unstable angina and the prognostic potential and usefulness in risk stratification was examined. 183 patients admitted with unstable angina were followed for a median of 1032 days. The presence of cTnT in the serum when tested at 12-24 hours from admission in this syndrome identified a high risk subgroup that had a higher frequency of cardiac death. Its presence also identified a subgroup that had a higher frequency of coronary revascularisation, cardiac death or revascularisation and cardiac death or readmission with non fatal myocardial infarction as first events. Further studies were undertaken to try and identify a pathophysiological explanation for the adverse prognosis of this subgroup. The angiographic culprit lesion morphological findings were compared in 46 unstable angina patients during the repair phase of the syndrome. No major differences in the extent or severity of coronary artery disease, or the location or morphological findings of the culprit lesion between the cTnT positive and cTnT negative unstable angina patients were identified. Activation of coagulation on admission in unstable angina in relation to cTnT concentrations were studied in 96 patients by examining variations m prothrombin fragment 1+2 and fibrinogen concentrations. No significant differences were observed between the two unstable angina groups. Variations in Lipoprotein (a) concentrations in patients admitted with unstable angina in relation to cardiac Troponin T levels were examined. Lipoprotein (a) concentrations were significantly higher in the cTnT positive than in the cTnT negative unstable angina patients and these findings represent the first demonstration of a risk factor that may play a role in the pathogenesis of this acute coronary syndrome subgroup. The cardiac specificity and long diagnostic window of the biochemical marker cardiac Troponin T offers advantages over existing biochemical markers for the confirmation of myocardial infarction. The identification by its presence in the acute syndrome of unstable angina of a high risk subgroup justifies its routine measurement in clinical practice.

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