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

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

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 Overview

• Status: Completed
• Conditions: Acute Myocardial Infarction
• Intervention / Treatment: Other: Blood test

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.

• Study Type: Observational
• Enrollment (Actual): 79

Contacts and Locations

Study Locations

• Israel
  • Kfar Saba, Israel
    • Meir Medical Center

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: 18 years and older (Adult, Older Adult)
• Accepts Healthy Volunteers: No
• Genders Eligible for Study: Male

• 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

Description

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

Study Plan

How is the study designed?

Design Details

• Observational Models: Case-Control
• Time Perspectives: Prospective

Number of groups / cohorts

2

Cohorts and Interventions

Group / Cohort	Intervention / Treatment
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; Blood test
Controls; Patients undergoing a non-invasive evaluation of possible myocardial ischemia.	Other: Blood test; Blood test

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Time Frame
Expression of P53 induced genes in patients with and without acute myocardial infarction	Up to 4 hours following recruitment

Secondary Outcome Measures

Outcome Measure	Time Frame
Correlation between P53 associated gene expression with troponin level	After 5 days from recruitment

Collaborators and Investigators

• Sponsor: Meir Medical Center

Publications and helpful links

General Publications

• 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.

Study record dates

Study Major Dates

• Study Start: November 1, 2010
• Primary Completion (Actual): October 1, 2011
• Study Completion (Actual): October 1, 2011

Study Registration Dates

• First Submitted: August 8, 2010
• First Submitted That Met QC Criteria: August 30, 2010
• First Posted (Estimate): August 31, 2010

Study Record Updates

• Last Update Posted (Estimate): October 31, 2012
• Last Update Submitted That Met QC Criteria: October 30, 2012
• Last Verified: October 1, 2012

More Information

Terms related to this study

• Additional Relevant MeSH Terms: Ischemia; Pathologic Processes; Necrosis; Myocardial Ischemia; Heart Diseases; Cardiovascular Diseases; Vascular Diseases; Myocardial Infarction; Infarction
• Other Study ID Numbers: MRNA-MI-1

Drug and device information, study documents

• Studies a U.S. FDA-regulated drug product: No
• Studies a U.S. FDA-regulated device product: No
• product manufactured in and exported from the U.S.: No