Browsing by Subject "Myocardial infarction"

Coronary artery disease is a leading cause of death and disability globally. The complement system has an important role in vascular health by defending against pathogens and regulating inflammation. Dysregulation of complement activation can lead to inflammation and the weakening of the vascular wall. The study investigated polymorphisms in the complement factor H (CFH) - complement factor H related (CFHR) genes region, which can predispose to inflammation and thus lead to coronary artery diseases. This study specifically focused on the CFHR 1 gene region because it competes with complement factor H, which plays a protective role. The protein structure of CFH and CFHR1 is similar. CFH protects the complement attacks, and on the other hand, CFHR1 does not prevent complement activation. 225 samples were selected for this study to evaluate the CFH-CFHR gene region in different patient groups from the COROGENE Cohort. Patients were assigned for coronary angiograms at the Helsinki University Central Hospital, and samples were collected every 5 years within 12 months to study trends in heart disease and coronary risk factors. Samples were analysed by SALSA MLPA (Multiplex Ligation-dependent Probe Amplification) to detect the presence of copy number variations (CNVs) in the CFH-CFHR gene region. The results of analysis indicate that the mortality rate was higher in this follow-up among males with CFHR 1 deletion compared to males with a normal genotype (p= 0.013). Furthermore, males with myocardial infarction (MI) and CFHR 1 deletion have a higher mortality rate than males with a normal genotype (p = 0.032). The results of logistic regression analysis indicate that CFHR 1 deletion, combined with other risk factors, is more likely to lead to non-ST elevated myocardial infarction (NSTEMI), than ST elevated myocardial infarction (STEMI). NSTEMI is more difficult to detect on an ECG compared to STEMI. A limitation of this study was the small sample size in each group. This study adds to the understanding that STEMI and NSTEMI have different risk factors. These differences should perhaps be considered in diagnostics and treatment once we understand them.