Genetic Predisposition of Coronary Artery Disease -- The COROGENE-Study
Recruitment status was Recruiting
The aim of this study is to identify genetic loci,or gene variations contributing to inflammation and to the development of CHD. We will compare coronary angiogram results to genetic findings within coronary artery disease patients and in patients with normal coronaries.
|Study Design:||Observational Model: Defined Population
Time Perspective: Longitudinal
|Official Title:||Genetic Predisposition of Coronary Artery Disease in Patients Verified With Coronary Angiogram The COROGENE-Study|
|Study Start Date:||June 2006|
|Estimated Study Completion Date:||December 2009|
Coronary artery disease (CAD) is a chronic inflammatory disease, progression of which may be accelerated by immunological mechanisms. Genes involved in regulation of inflammation and protection against infectious agents may affect picture of the disease . Major Histocompatibility Complex (MHC) region carries genes involved in innate and adaptive immunity and inflammation. We have for the first time, identified genetic factors located in HLA region, showing several fold risk for disease predisposition likely forming an important component to explain the high incidence of coronary heart disease in the Finnish population.
The aim of this study is to rerun our preliminary results, and further identify genetic loci, or gene variations contributing to the development of CHD. The strategy is to collect altogether 5000 patients assigned to coronary angiogram in Helsinki University Central Hospital. We will compare the angiogram results to genetic findings first in patients with normal coronaries, and in patients with different stages of CHD. Secondly we will compare phenotypic changes in inflammation and try to find out if the phenotype differs in different genotypes. Thirdly we will collect patients from hospital discharge registry, and compare mortality and morbidity results in different gene groups.
Finally, we aim to record echocardiograms of the aortic valves in altogether 3500 consecutive patients undergoing coronary angiography. We try to identify genetic loci and gene variations contributing to the fibrosis and calcification of the aortic valve.
The results of the study provide a possibility to develop a gene test to recognize patients at risk at its early stage, and needing for preventive medicine.
Please refer to this study by its ClinicalTrials.gov identifier: NCT00417534
|Contact: Juha P Sinisalo, MD, PhDemail@example.com|
|Helsinki University Central Hospital, Division of Cardiology||Recruiting|
|Helsinki, Finland, 00290|
|Contact: Juha P Sinisalo, MD, PhD +35894711 firstname.lastname@example.org|
|Principal Investigator: Juha P Sinisalo, MD, PhD|
|Principal Investigator:||Juha P Sinisalo, MD, PhD||Helsinki University Central Hospital, Division of Cardiology|