The Pattern of Vascular Risk Genes in Middle Age Patients with Acute Coronary Syndrome,MAHMOUD MAHFOUZ and SHEREEN MAHMOUD
Abstract
In the general population, cardiovascular risk is thought to be determined, at least in part, genetically. Ethnic differences were reported in many of the gene abnormalities such as factor V Leiden and PAI-1 4G/5G. PAI is reported to play central role in ventricular remodeling after MI.
Aim of Work: The aim of this descriptive study is to study the pattern of vascular risk genes in patients with ischemic heart disease and its relation to severity & prognosis and to study if ischemic heart failure can be genetically predicted.
Subjects and Methods: The study was conducted on 30 patients with acute ischemic chest pain admitted in the ER of one tertiary care Hospitals in Cairo. Complete history taking, with special concern to the duration of chest pain, history of smoking, diabetes, hypertension and previous ischemic attacks. Thorough physical examination was done mainly to identify an alternative cause of chest pain and for risk stratification. Laboratory investigations were done including the biochemical markers (CPK, LDP, troponin). Electrocardiography and echocardiography were done for all patients. Blood samples were examined for vascular risk genes using conventional PCR. Test for 12 mutations/polymorphism CVD strip assay is based on reverse hybridization of biotinylated PCR product to a parallel array of allele-specific oligonucleotides immobi-lized on membrane test strips. The strip assay provides ready-to-use reagents for completion in four steps. The following genes were examined: Factor V leiden G1691A, factor V Leiden H1299R (R2), Prothrombin G20210A, factor XIII v34L, B-firbinogen 455G7A, PAI-1 4G/5G, HPA-1 a/b, 5,10- Methylenetetrahydrofolate reductase (MTHFR, C677T, MTFR A1298C), Angiotensin-converting enzyme (ACE), I/D, Apo-lipoproteins (Apo B R3500Q and Apo E 1,2,3,4).
Results: Showed that ACE I/D and PAI 4G 5G were the most encountered gene abnormalities in our cases whereas no single mutation had been reported in Apo B R3500Q and prothrombin G20210A genes. Heterozygous mutations were detected in factor V Leiden G1691A, H1299R factor XIII V34L and HPAI. Twenty nine patients had 2 or more abnormal alleles Five patients (16.7%) had six abnormal alleles, 6 patients (20%) had 5 abnormal alleles, 8 patients (26.7%) had three abnormal alleles, 5 patients (16.7%) had two abnormal alleles and only one patient (3.3%) had one abnormal allele.
There were no statistically significant correlation between genotypes of the risk genes and any of clinical, laboratory, echocardiographic and ECG findings among the study group.
Conclusion: ACE I/D and PAI 4G/5G were the most encountered gene abnormalities, in a small random sample of Egyptian patients with ischemic heart disease. A larger study may be of value to determine which of the patients may be vulnerable to heart failure post MI which may represent potential new pharmacological targets leading to better clinical outcome.