Multi-Analyte, Genetic, and Thrombogenic Markers of Atherosclerosis (MAGMA)
Recruitment status was: Recruiting
About 13 million people in the United States have coronary artery disease (CAD). It is the leading cause of death in both men and women.
Coronary artery disease (CAD) occurs when the blood vessels that supply blood to the heart muscle (the coronary arteries) become hardened and narrowed. The arteries harden and narrow due to buildup of fatty and calcified material called plaque on their inner walls. The buildup of plaque is also called atherosclerosis. This is a process which starts early in life, but can be influenced by multiple factors.
Several factors increase the risk of developing atherosclerosis. They include high blood pressure, smoking, diabetes, high cholesterol and being related to someone who had a heart attack or a stroke. The more risk factors you have, the greater the chance that you have severe atherosclerosis. Some of the risk factors cannot be modified, like age and family history of early heart disease. The influenceable factors include high blood pressure, high blood cholesterol, high blood sugar, cigarette smoking, overweight or obesity, and lack of physical activity.
Nevertheless, there are patients without any above mentioned risk factors who develop atherosclerosis. In addition to that, there are also patients with several risk factors who do not develop severe coronary artery disease.
According to research studies high blood levels of some substances in the blood (biochemical markers) as well as some genes in the DNA of our cells may be associated with an increased risk of developing CAD and faster progression of the disease.
The purpose of this study is to find a correlation between certain blood markers and growth of the plaques, regardless of the presence of the classic risk factors for atherosclerosis. If we prove our hypothesis we will be one step closer to predicting the extent of atherosclerosis by performing certain blood tests.
Coronary Artery Disease
|Study Design:||Observational Model: Case Control
Time Perspective: Prospective
|Official Title:||Multi-Analyte, Genetic, and Thrombogenic Markers of Atherosclerosis (The MAGMA STUDY)|
- severity of angiographically-defined coronary lesions as determined by comprehensive biomarker risk profile [ Time Frame: 1.5 years ]To develop a comprehensive biomarker risk profile that will correlate with the severity of angiographically-defined coronary lesions, independently of the classic risk factors for atherosclerosis.
- Genetic Components [ Time Frame: 5 years ]To evaluate the contribution of genetic components to the presence of coronary artery disease in association with environmental factors. Of interest is to see whether certain genes might accelerate atherosclerosis in subgroups like smokers, diabetics, obese subjects, or various ethnic groups
- Biomarker Profile [ Time Frame: 1.5 years ]To determine the difference in the biomarker profile between CAD patients, patients with no known angiographically identified disease and healthy volunteers.
- Drug treatment strategies [ Time Frame: 1.5 years ]To determine the effect of different drug treatment strategies on biomarker profile.
- Prediction Model [ Time Frame: 1.5 years ]To create prediction model for major CV events based on genetic and other nongenetic biomarkers.
- Verigene [ Time Frame: 1.5 years ]To demonstrate the utility of the Point-of-Care Verigene 2C19/CBS Nucleic Acid Assay for detecting CYP2C19 variants.
- Urinary 11-dehydro thromboxane B2 [ Time Frame: 1.5 years ]To determine an association between urinary 11-dehydro thromboxane B2 concentrations with the severity of angiographically-defined coronary lesions.
- Lp-PLA2 [ Time Frame: 1.5 years ]To determine the association between Lp-PLA2 and angiographically-defined coronary lesions.
- Association of low-density lipoproteins/β2-glycoprotein I (β2GPI) [ Time Frame: 1.5 years ]To determine the association between oxidized low-density lipoprotein (oxLDL)/ β2-glycoprotein I (β2GPI) complexes and angiographically-defined coronary lesions.
Biospecimen Retention: Samples With DNA
|Study Start Date:||June 2010|
|Estimated Study Completion Date:||December 2014|
|Estimated Primary Completion Date:||June 2014 (Final data collection date for primary outcome measure)|
300 healthy controls free from any pharmacologic therapy
Suspected CAD - Cardiac Cathetrization
subject's ≥18 years undergoing coronary angiography (inpatient cohort)or who have undergone coronary angiography within 5 years
Show Detailed Description
Please refer to this study by its ClinicalTrials.gov identifier: NCT01276678
|Contact: Kevin P Bliden, B.S. MBAfirstname.lastname@example.org|
|Contact: Tania B Gesheff, MSNemail@example.com|
|United States, Maryland|
|Sinai Center for Thrombosis Research||Recruiting|
|Baltimore, Maryland, United States, 21215|
|Contact: Kevin P Bliden, B.S. MBA 410-601-4795 firstname.lastname@example.org|
|Contact: Tania B Gesheff, MSN 4106014795 email@example.com|
|Principal Investigator:||Paul A Gurbel, M.D., FACC||Sinai Center for Thrombosis Research|