الفهرس 
Coronary thrombolysis by use of streptokinaseOnly 14 pages are availabe for public view
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Abstract
Infarct size is the most important single factor influencing prognosis after acute myocardial infarction but its determination by clinical chemical means is difficult. Total releases of creatine kinase or its MB isoenzyme correlate well with the size of myocardial infarction c-reactive protein is synthesized in the liver and its synthesis is stimulated by a number of diseases, including AMI.(acute myocardial infarction). It has been shown that then rise in c-reactive protein during infarction correlates with the activity of serum creatine kinase. Rapid perfusion of an infarcted myocardium could diminish the stimulus for c-reactive protein synthesis in the liver by altering the development of the infarction. If this is the case, successful thrombolytic treatment of acute MI should have a similar effect. This study aimed to measure accurately and quanti-tatively serum CRP in both streptokinase and non-streptokinase treated patients with AMI to recognize any difference between both groups and to correlate the concentration of CRP and serum CPK and if this level can be used as a prognostic parameter and to assess the efficacy of streptokinase therapy. Twenty patients with acute MI were selected for this study. Ten of them treated conventionally without streptokinase therapy, and the other ten subjected to streptokinase therapy. To all of them the following
had been done :
Full medical history and clinical examination.
-12 leads ECG
-Estimation of CRP and CPK in their
-Other routine investigation s (Blood
serum triglycer ides.
sera.
Sugar, Serum Cholesterol and
The results of this study demonstrated that:
In patients with acute MI treated conventionally, serum CRP was detected in all patients and the peak levels were in the third day in most of patients. In patients who showed smooth recovery, CRP showed a fairly fall from its peak values towards its normal values in the subsequent days. Serum CPK showed similar pattern. In complicated patients, CRP showed a persistent rise or secondary peak. Corresponding rise of serum enzyme CPK indicating extension of MI while corresponding fall of CPK indicating complications other than MI (for examples, deep venous thrombosis, embotic manifestation). There is no correlation between levels of serum CRP CPK in the 1st 24 hrs from the is correlation between peak levels
and corresponding serum enzyme onset of chest pain while there of CRP and CPK.
In patients subjected to streptokinase therapy, 2 subgroups detected, subgroup A with successful therapy and subgroup B with failed therapy. In subgroup A serum CRP was detected in all patients, and its level showed moderate rise detected in the third day in the majority of patients. This group showed good early and smooth recovery and CRP showed a fairly fall towards normal values in subsequent day. CPK showed early peak levels in the first 24 hours them fall to words normal values in subsequent days. There is no correlation between levels of serum CRP and corresponding serum enzyme CPK during the first 24 hrs from onset of chest pain while there is a significant correlation between peak levels of CRP and serum enzyme CPK. Subgroup B behaved like group I treated conventionally without streptokinase therapy.