PATIENTS AND METHOD: In consideration of own investigations and analysis of the most important publications of other authors, a critical interpretation of the concentrations of Troponin T (cut off: < 1 microgram/l) and Troponin I (cut off: < 0.4 microgram/l) was done in patients with acute and chronic muscle diseases, with chronic renal failure, with acute myocardial infarction, and stable and unstable angina pectoris, after coronary angioplasty, following cardiac surgery and critical care patients. RESULTS: In all cases with acute damage of the skeletal muscles (post operationem) the concentrations of TnT and TnI were in normal ranges. - In patients with chronic muscle diseases (M. Duchenne, Dermatomyositis) in 75% the TnT concentrations increased, while TnI concentrations were < 0.4 microgram/l. - In end stage renal disease patients undergoing chronic maintenance hemodialysis we found in 39% constantly elevated concentrations of TnT. TnI in all cases were in normal range. - In acute myocardial infarction in 97% of all patients both Troponins were increased, beginning 2 to 4 hours after onset. A normalization was observed between the 5th and 9th day. Very important is the differentiation between stable, and instable angina pectoris. In stable angina the concentration of both Troponins were in normal range, in contrast in 33 to 41% of all patients with unstable angina TnT and TnI were increased, in 9 to 16% even if the ECG showed no alteration. Elevated TnT or TnI concentrations predicted a significantly increased mortality. After coronary angioplasty and heparin treatment all patients had once more an elevation of TnT and TnI 8 and 27 hours after the invasive therapy. One of these substantial reasons for these minor myocardial cell necrosis is beside the endothelial injury the activation of the platelets and the coagulation system. - During the therapy with hirudin increases of TnT and TnI was not observed. Following cardiac surgery (ACVB) 6 to 48 hours after aortic unclamping 76 patients with TnI < 1 microgram/l had no perioperative myocardial infarction, while 14 patients with TnI concentrations > 1 microgram/l in 71.4% (n = 10) developed an acute infarction. - In patients in critical care units we observed only increased TnI concentrations in shock, especially in septic shock with multiple organ failures.
PATIENTS AND METHOD: In consideration of own investigations and analysis of the most important publications of other authors, a critical interpretation of the concentrations of Troponin T (cut off: < 1 microgram/l) and Troponin I (cut off: < 0.4 microgram/l) was done in patients with acute and chronic muscle diseases, with chronic renal failure, with acute myocardial infarction, and stable and unstable angina pectoris, after coronary angioplasty, following cardiac surgery and critical care patients. RESULTS: In all cases with acute damage of the skeletal muscles (post operationem) the concentrations of TnT and TnI were in normal ranges. - In patients with chronic muscle diseases (M. Duchenne, Dermatomyositis) in 75% the TnT concentrations increased, while TnI concentrations were < 0.4 microgram/l. - In end stage renal diseasepatients undergoing chronic maintenance hemodialysis we found in 39% constantly elevated concentrations of TnT. TnI in all cases were in normal range. - In acute myocardial infarction in 97% of all patients both Troponins were increased, beginning 2 to 4 hours after onset. A normalization was observed between the 5th and 9th day. Very important is the differentiation between stable, and instable angina pectoris. In stable angina the concentration of both Troponins were in normal range, in contrast in 33 to 41% of all patients with unstable angina TnT and TnI were increased, in 9 to 16% even if the ECG showed no alteration. Elevated TnT or TnI concentrations predicted a significantly increased mortality. After coronary angioplasty and heparin treatment all patients had once more an elevation of TnT and TnI 8 and 27 hours after the invasive therapy. One of these substantial reasons for these minor myocardial cell necrosis is beside the endothelial injury the activation of the platelets and the coagulation system. - During the therapy with hirudin increases of TnT and TnI was not observed. Following cardiac surgery (ACVB) 6 to 48 hours after aortic unclamping 76 patients with TnI < 1 microgram/l had no perioperative myocardial infarction, while 14 patients with TnI concentrations > 1 microgram/l in 71.4% (n = 10) developed an acute infarction. - In patients in critical care units we observed only increased TnI concentrations in shock, especially in septic shock with multiple organ failures.