Cardiac Muscle Injury Research Articles

Significance of elevated MB creatine kinase in patients after cardiac catheterization.

To clarify the etiology of elevations in plasma MB creatine kinase (CK) in patients after cardiac catheterization, we studied 32 consecutive patients undergoing cardiac catheterization and coronary arteriography. Total CK and MB CK were within the normal range in all patients prior to catheterization. Total CK activity rose from a mean of 61.46 +/- 33.8 IU/1 (SD) to 141 +/- 105 in the first sample after catheterization (p less than .005) and 121.6 +/- 92.4 in the second catheterization sample (p less than .0005). The MB CK activity also rose from a mean of 3.2 +/- 1.6 IU/1 prior to catheterization to a maximum value of 5.0 +/- 2.9. The mean increase in MB CK, though statistically significant (p less than .005), was only 1.8 IU/1. Only one patient's value for MB CK rose to outside of the normal range (greater than 12) likely due to cardiac injury. Thus, our data document that marked elevations in MB CK after cardiac catheterization are unusual. They likely represent cardiac muscle injury rather than MB CK released due to skeletal muscle injury induced by the catheterization itself.

Experimental reversal of acute coronary thrombotic occlusion and myocardial injury in animals utilizing streptokinase

Fresh autologous thrombus, 1.0 to 1.5 ml, was injected into the left anterior descending and/or left diagonal coronary arteries of 19 open-chest dogs to produce evolving acute myocardial infarction (AMI). Thrombotic obstruction was documented by coronary angiography. Multilead epicardial ECGs showed ST segment elevations of affected left ventricular (LV) areas within 2 minutes after thrombus injection, and LV segmental wall cyanosis with hypocontraction was observed within 10 minutes in the myocardial areas supplied by the thrombosed artery. Ten animals then received an initial dose of streptokinase (STK), 250,000 U (intravenous), followed by STK, 1000 to 3000 U/min (intracoronary), while nine control dogs untreated with STK received normal saline infusion. All but one STK-treated animal (all nine animals receiving intracoronary STK) had reestablishment of blood flow in the previously occluded vessels within 1 1 2 hours , disappearance of ventricular cyanosis, return of normal LV contractile function, and normalization of elevated ST segments within 1 hour after intracoronary STK thearpy. In contrast, in the non-STK-treated control group, all animals had continued coronary obstruction, progressive ST elevations, and worsening LV cyanosis and hypocontraction until death or for more than 3 hours post thrombus; three control animals died of ventricular fibrillation (VF) within 1 hour of thrombus occlusion, three more died of VF within 2 hours post thrombus, and only three survived beyond 2 hours post thrombus. Postmortem examination of non-STK-treated animals revealed extensive residual coronary thrombus. All intracoronary STK-treated animals evidenced absence of residual thrombus at postmortem examination. These data provide clinically relevant evidence that early intracoronary STK effects thrombolysis in AMI by reopening coronary vessels occluded by fresh thrombus, thereby protecting myocardium from further ischemia and necrosis, preserving LV function, and also reversing cardiac muscle injury.

Influence of glucose availability on reversibility of membrane and cellular injury in hypoxic cardiac muscle: K.P. Burton, H.K. Hagler, G.H. Templeton, J.T. Willerson and L.M. Buja. The University of Texas Health Science Center at Dallas, Dallas, Texas 75235

Influence of glucose availability on reversibility of membrane and cellular injury in hypoxic cardiac muscle: K.P. Burton, H.K. Hagler, G.H. Templeton, J.T. Willerson and L.M. Buja. The University of Texas Health Science Center at Dallas, Dallas, Texas 75235

Electron microscope observations on freezing injury in cardiac muscle

Electron microscope observations on freezing injury in cardiac muscle

Myofibrillar degeneration: a common form of cardiac muscle injury.

Myofibrillar degeneration: a common form of cardiac muscle injury.