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A Comparison of p53-induced Genes Activation in Patients With and Without Acute Myocardial Infarction

Acute Myocardial Infarction Clinical Trial

Official title:
A Comparison of p53-induced Genes Activation as Possible Markers Differentiating Between Patients Presenting With Acute Myocardial Infarction and Controls

Clinical Trial Summary

The purpose of this study is to compare p53-induced genes activation as possible markers differentiating between patients presenting with acute myocardial infarction and controls.

Clinical Trial Description

The diagnosis of acute myocardial infarction is based on the rise of bio-markers for cardiac necrosis such as troponin. While troponin measurement is highly sensitive for myocardial necrosis it has several limitations that influence its clinical use. First, since the troponin test is reliable only after 4-6 hours from symptoms onset, it has only limited value in the assessment of patients presenting earlier. Second, several clinical situations, most commonly renal dysfunction, are associated with increased troponin level and therefore may decrease the specificity of the test. Third, since troponin rise indicates myocardial infarction it is not useful in the common situations where there is myocardial ischemia without necrosis.

The P53 is a tumor suppressing gene activated in different stressful situations including hypoxia. This activation is associated with accelerated transcription (up to 30-50 folds from baseline) of different genes that are involved in apoptosis, DNA repair and in stopping the cell cycle. A study on pregnant women demonstrated high levels of fetal mRNA of these genes in maternal circulation. This gene expression correlated with other signs of fetal stress associated with hypoxia. Myocardial ischemia is another stressful event associated with tissue hypoxia. Nevertheless, the association of this gene expression with myocardial ischemia has not been investigated yet. ;

Study Design

Observational Model: Case Control, Time Perspective: Prospective

Related Conditions & MeSH terms

Clinical Trial Details
NCT number NCT01191879
Study type Observational
Source Meir Medical Center
Contact
Status Completed
Phase N/A
Start date November 2010
Completion date October 2011
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