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Our main goal is to create a prospective cohort of 1500 patients with a first large myocardial infarction allowing us, in a second step, to identify susceptibility genes for the progression of patients towards chronic heart failure using a candidate gene/candidate pathway approach. Our main hypothesis is that there is, for a given initial biomechanical stress (duration of the ischemic episode, size of the infarcted area, etc.), a variation in the individual susceptibility to develop left ventricular remodelling and to progress towards heart failure, and that this variation is linked to genetic variants between individuals.
The research program comprises 4 phases: a selection phase at D0-D1, a pre-inclusion and an inclusion phase at D4±2, a visit at M6, and a 5 year follow up phase.
Visit at Day 0 - Day 1:
- The first 12-lead ECG, to be included in the observation book, is performed.
- The first blood sample is taken.
Visit at Day 4±2:
- The first transthoracic echocardiography is performed in all patients selected.
- In the presence of at least 3 akinetic LV segments at the transthoracic echocardiography, the patient is included.
- Demographic data, medical and surgical anteriority, detailed circumstances of occurrence of the MI and any other relevant information is obtained during an interview.
- The second 12-lead ECG is performed.
- The second blood sample is taken.
- The first MRI is performed (optional)
Visit at 6 months:
- The second transthoracic echocardiography is performed.
- The third 12-lead ECG is performed.
- The third blood sample is taken.
- A 24-hour Holter-ECG monitoring is performed (optional)
- The second MRI is performed (optional)
Five year follow up:
Each patient included at day 4±2 will be contacted by phone 1, 2, 3, 4 and 5 years post-MI to obtain information regarding cardiovascular events and hospitalizations. If the patient cannot be contacted directly, we will try to contact a member of his/her family or his/her family physician.
Control: Uncontrolled, Intervention Model: Single Group Assignment, Masking: Open Label
ST-segment Elevation Myocardial Infarction (STEMI)Q-wave MI
Pr Jean-Jacques MERCADIER
Not yet recruiting
Assistance Publique - Hôpitaux de Paris
Published on BioPortfolio: 2014-08-27T03:14:06-0400
Despite progress in pre-hospital care, ambulance logistics, pharmacotherapy and PPCI techniques, ST-segment elevation myocardial infarction (STEMI) continues to confer a substantial burden...
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A clinical syndrome defined by MYOCARDIAL ISCHEMIA symptoms; persistent elevation in the ST segments of the ELECTROCARDIOGRAM; and release of BIOMARKERS of myocardial NECROSIS (e.g., elevated TROPONIN levels). ST segment elevation in the ECG is often used in determining the treatment protocol (see also NON-ST ELEVATION MYOCARDIAL INFARCTION).
A myocardial infarction that does not produce elevations in the ST segments of the ELECTROCARDIOGRAM. ST segment elevation of the ECG is often used in determining the treatment protocol (see also ST Elevation Myocardial Infarction).
MYOCARDIAL INFARCTION in which the anterior wall of the heart is involved. Anterior wall myocardial infarction is often caused by occlusion of the left anterior descending coronary artery. It can be categorized as anteroseptal or anterolateral wall myocardial infarction.
A malformation that is characterized by a muscle bridge over a segment of the CORONARY ARTERIES. Systolic contractions of the muscle bridge can lead to narrowing of coronary artery; coronary compression; MYOCARDIAL ISCHEMIA; MYOCARDIAL INFARCTION; and SUDDEN CARDIAC DEATH.
MYOCARDIAL INFARCTION in which the inferior wall of the heart is involved. It is often caused by occlusion of the right coronary artery.
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