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

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.

Inclusion criteria

Acute MI group:

Patient presenting with chest pain lasting for at leasY 1 hour and no more than 6 hours accompanied by 1 of the following ECG criteria:

• ST segment elevation of anterior or inferior wall (at least 2 consecutive leads)
• New LBBB

Controls:

• Patients undergoing non-invasive evaluation of possible myocardial ischemia

Exclusion criteria

• Chronic lung disease requiring chronic treatment
• Any malignancy in the 5 year prior to enrollment