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IPMJ-Iraqi Postgraduate Medical Journal. 2009; 8 (4): 309-313
in English | IMEMR | ID: emr-102179

ABSTRACT

It have been suggested that pre-treatment with a statin agent prior to myocardial infarction limits myocardial creatine kinase release, and thus may act to limit myocardial infarct size in humans. To examine the effect of very early statin initiation for AMI, to the extent of myonecrosis as manifested by peak serum creatine kinase levels. Patients with AMI admitted to Al-Kindy teaching hospital cardiac care unit from February 2007 through February 2008, who fulfilled the inclusion criteria cited in the present study, were randomly assigned into two study groups. The statin group patients have received a single oral dose of 40 mg atorvastatin at time of admission and repeated for the next days until discharge, patients not receiving statin serves as controls. Blood samples were obtained upon admission and every 8 h for another three consecutive samples to identify peak creatine kinase levels. Patients who had statin therapy initiated immediately after hospital admission have similar peak creatine kinase concentrations as compared to those not receiving statin therapy [1020 +/- 621 IU/L vs. 911 +/- 591 IU/L,P= 0.332]. Statin initiation in AMI patients fails to show any observable effect on creatine kinase release, which can be attributed to the need of an extended period for the statin agent to achieve the predictable outcome and suggesting the necessity of statin pretreatment in patients at high risk for AMI


Subject(s)
Humans , Male , Female , Myocardial Infarction/drug therapy , Creatine Kinase/drug effects , Pyrroles , Stroke Volume , Creatine Kinase/metabolism , Treatment Outcome
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