A Comparison of p53-induced Genes Activation in Patients With and Without Acute Myocardial Infarction
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.
|Study Design:||Observational Model: Case Control
Time Perspective: Prospective
|Official Title:||A Comparison of p53-induced Genes Activation as Possible Markers Differentiating Between Patients Presenting With Acute Myocardial Infarction and Controls|
- Expression of P53 induced genes in patients with and without acute myocardial infarction [ Time Frame: Up to 4 hours following recruitment ] [ Designated as safety issue: No ]
- Correlation between P53 associated gene expression with troponin level [ Time Frame: After 5 days from recruitment ] [ Designated as safety issue: No ]
|Study Start Date:||November 2010|
|Study Completion Date:||October 2011|
|Primary Completion Date:||October 2011 (Final data collection date for primary outcome measure)|
acute MI group
Patients presenting with acute ST elevation myocardial infarction, admitted to the intensive cardiac care unit and that are planned for emergency primary PCI
Other: Blood test
Patients undergoing a non-invasive evaluation of possible myocardial ischemia.
Other: Blood test
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.
Please refer to this study by its ClinicalTrials.gov identifier: NCT01191879
|Meir Medical Center|
|Kfar Saba, Israel|