• Dietmar Krüger, Abdolhamid Sheikhzadeh, Ulrich Stierle, and Rüdiger Simon.
• Department of Cardiology, University Hospital Kiel, Schittenhelmstr. 12, 24105 Kiel, Germany. krueger@cardio.uni-kiel.de
• Int. J. Cardiol. 2005 Feb 15;98(2):285-90.

BackgroundMyoglobin, cardiac troponin-T and creatine phosphokinase are biochemical indicators of acute coronary syndromes, however, the clinical significance in myocardial ischemia is not well established. Our aim was to elucidate their release kinetics in a well-defined short-lasting myocardial ischemia.MethodsA coronary sinus lactate study with incremental atrial pacing was performed in 27 patients with significant coronary stenosis. Troponin-T, myoglobin and creatine phosphokinase samples were withdrawn from the coronary sinus and a peripheral vein before, 1, 5, 10, 30, 45 min and 1, 2, 3, 6, 12 h after pacing.ResultsPacing stress induced a severe myocardial ischemia with a duration of 5.8+/-1.6 min, angina pectoris in 22/27, significant ST-segment depressions in 25/27 patients (0.34+/-0.11 mV) and a frank cardiac lactate production of 37.6+/-19.9%. Serum troponin-T levels as well as creatine phosphokinase were normal at baseline and remained unchanged. A transient rise of myoglobin after 1 h with a peak coronary sinus concentration after 2 h (101.5+/-39.0 microg/l) and peripheral venous concentration (90.5+/-32.5 microg/l) after 3 h (134.3% and 120.7%, respectively, of the upper normal limit, p<0.002) followed myocardial ischemia. In a control group of 20 patients without heart disease all variables remained unchanged.ConclusionsSevere short-lasting myocardial ischemia did not enhance troponin-T or creatine phoshokinase concentrations, whereas a transient slight cardiac release of myoglobin with a delay of 1 h and a coronary sinus peak concentration after 2 h was detected. This may be due to a rapid reperfusion effect on ischemic myocardium or minor damaged single myocardial cells.

16 keywords...

hide…