Myocardial infarction enzymatic

The hrefly Inciferin system is very sensitive and can be conpled to any enzymatic reaction that prodnces or nses ATP. For example, creatine phosphokinase can be determined by this method and hence be nsed in the diagnosis of myocardial infarction and mnscle disorders. The creatine phosphokinase converts AMP into ATP which then nndergoes the reaction with Inciferin as shown in Fignre 3.25. ATP pro-dnction is essential for every known life form and the firefly Inciferin system can be nsed to check for microbial life. Hence systems have been developed that use a portable luminescence workstation to monitor sanitation in food manufacturing and to check for sterile environments in technological workplaces. The system can also be applied in checking cell viability, for instance in cell cultures and to measure the toxic effects of chemicals on cells. 

Stone GW, Mehran R, Dangas G, et al. Differential impact on survival of electrocardiographic Q-wave versus enzymatic myocardial infarction after percutaneous intervention, A device-specific analysis of 7174 patients. Circulation 2001 ... 

During platelet plug formation, the fibrinolytic pathway is locally activated. Plasminogen is enzymatically processed to plasmin (fibri-nolysin) by plasminogen activators present in the tissue. Plasmin interferes in clot propagation and dissolves the fibrin network as wounds heal. At present, a number of fibrinolytic enzymes are available for treatment of myocardial infarctions or pulmonary emboli (see p. 201). 

Elsman P, Van t Hof AW, de Boer MJ et al. Impact of infarct location on left ventricular ejection fraction after correction for enzymatic infarct size in acute myocardial infarction treated with primary coronary intervention. Am Heart J 2006 151 1239.e9-14. 

Anderson JL, Karagounis LA, Becker LC, Sorensen SG, Menlove RL. TIMI perfusion grade 3 but not grade 2 results in improved outcome after thrombolysis for myocardial infarction. Ventriculographic, enzymatic, and electrocardiographic evidence from the TEAM-3 Study. Circulation 1993 87 1829-1839. 

P. is - prostaglandin that is produced by enzymatic transformation of prostaglandin endoperoxides and which dilates blood vessels. P. is chemically unstable in aqueous solutions, but the mono sodium-salt is stable as a solid and in solution. In addition, p. shows antimetastatic effects and has been used for patients with acute myocardial infarction. It has also been postulated that p. acts to stimulate platelet adenylate cyclase and to prevent the action of thrombi in phospholipid breakdown as well as platelet aggregation. In clinical practice, it is used for preventing the loss of platelets in cases wdiere the blood comes into extracorporal contact with artificial surfaces, i.e., in hemodialysis, cardiopulmonary bypass, and charcoal column perfusion for treatment of liver failure. 

The importance of other factors additional to amount ofnecrosis has also been studied. In patients with first acute MI treated with PCI, LAD-related MI show for a similar amount of myocardial necrosis as determined by enzymatic infarct size, lower left-ventricular ejection fraction (LVEF) when compared to non-LAD-related MI. LVEF-measured 6-month post-MI showed a decrease, for every 1000 cumulative lactate dehydrogenase release, of 4.8% for LAD and 2.4% for non-LAD-related infarcts (p < 0.0001), and these results remain in the multivariate analysis (Elsman et al., 2006). 

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