Clinical trial NCT01191879: A Comparison of p53-induced Genes Activation in Patients With and Without Acute Myocardial Infarction
Official title: A Comparison of p53-induced Genes Activation as Possible Markers Differentiating Between Patients Presenting With Acute Myocardial Infarction and Controls
Study type: OBSERVATIONAL
Overall status: COMPLETED
Conditions: Acute Myocardial Infarction
Lead sponsor: Meir Medical Center
Sponsor class: OTHER
First posted: 2010-08-31
Enrollment: 79
Sex: MALE
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: no
Observational model: CASE_CONTROL
Time perspective: PROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: Aacute MI group- Patients with acute ST elevation MI planned for emergency primary PCI

Controls: Patients undergoing non-invasive evaluation of possible myocardial ischemia

Brief 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.

Detailed 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.

Eligibility criteria: 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

Primary outcomes:
measure: Expression of P53 induced genes in patients with and without acute myocardial infarction
timeFrame: Up to 4 hours following recruitment
Secondary outcomes:
measure: Correlation between P53 associated gene expression with troponin level
timeFrame: After 5 days from recruitment
Other outcomes:
Locations:
city: Kfar Saba
country: Israel
facility: Meir Medical Center
Study officials:
References:
citation: Ashur-Fabian O, Avivi A, Trakhtenbrot L, Adamsky K, Cohen M, Kajakaro G, Joel A, Amariglio N, Nevo E, Rechavi G. Evolution of p53 in hypoxia-stressed Spalax mimics human tumor mutation. Proc Natl Acad Sci U S A. 2004 Aug 17;101(33):12236-41. doi: 10.1073/pnas.0404998101. Epub 2004 Aug 9.