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

NCT ID: NCT01191879

Last Updated: 2012-10-31

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

79 participants

Study Classification

OBSERVATIONAL

Study Start Date

2010-11-30

Study Completion Date

2011-10-31

Brief Summary

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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

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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.

Conditions

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Acute Myocardial Infarction

Study Design

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Observational Model Type

CASE_CONTROL

Study Time Perspective

PROSPECTIVE

Study Groups

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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

Blood test

Intervention Type OTHER

Blood test

Controls

Patients undergoing a non-invasive evaluation of possible myocardial ischemia.

Blood test

Intervention Type OTHER

Blood test

Interventions

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Blood test

Blood test

Intervention Type OTHER

Eligibility Criteria

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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
Minimum Eligible Age

18 Years

Eligible Sex

MALE

Accepts Healthy Volunteers

No

Sponsors

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Meir Medical Center

OTHER

Sponsor Role lead

Responsible Party

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Responsibility Role SPONSOR

Locations

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Meir Medical Center

Kfar Saba, Israel, Israel

Site Status

Countries

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Israel

References

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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.

Reference Type BACKGROUND
PMID: 15302922 (View on PubMed)

Other Identifiers

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MRNA-MI-1

Identifier Type: -

Identifier Source: org_study_id