Browsing by Author "Al-Shehri, Abdullah"
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Item Prevalence and pattern of lipid disorders in Saudi patients with angiographically documented coronary artery disease(2014) Al-Shehri, AbdullahObjective: The aim of the study was to assess the prevalence and patterns of dyslipidemia in Saudi patients with angiographically documented coronary artery disease (CAD). Materials and Methods: This is a cross-sectional, hospital-based study, which was conducted on all Saudi patients who underwent coronary angiography under the author's personal care and were found to have > 50% coronary stenosis. Fasting lipid profile was measured in all patients during the admission for the coronary angiography. Results: Two hundred and ninety-five patients were included in the study. The mean age (±Standard deviation) was 55.1 ± 11, ranging from 17 to 86 years. The majority of patients were males: 229 (77.6%). Mean total cholesterol was 175.6 ± 47.6 mg/dl, mean low-density lipoprotein cholesterol (LDL-C) was 111.3 ± 40.3 mg/dl, mean high density lipoprotein cholesterol (HDL-C) was 38.27 ± 9.5 mg/dl and mean triglyceride level was 141.8 ± 74.8 mg/dl. 21 (7.1%) patients had normal coronary arteries, 107 (36.3%) had one vessel disease, 78 (26.4%) had two vessel disease and 89 (30.2%) had three vessel disease. There was a significant correlation between the extent of CAD and age (P = 0.003), sex (P = 0.0002), total cholesterol (P = 0.02) and low HDL-C (P < 0.001. 21 (7.1%) patients were asymptomatic, 110 (37.3%) had stable angina, 127 (43.1%) had none ST elevation acute coronary syndrome, 20 (6.8%) had ST elevation myocardial infarction and 17 (5.7%) had heart failure. There was also a significant correlation between age (P = 0.03), sex (P < 0.001), LDL-C (P = 0.005) and low HDL-C (P < 0.001) and the severity of CAD. Conclusion: Dyslipidemia is a very prevalent risk factor in Saudi patients with CAD. Low HDL-C was the most frequent lipid abnormality, which significantly impacts on the extent of the CAD.Item β 2 adrenergic receptor gene polymorphisms in normal and in patients with myocardial infarction in the eastern province of Saudi Arabia(2013) Al-Rubaish, Abdullah; Al-Shehri, Abdullah; Al-Ali, Abdullah; Al-Ali, Amein; Al-Nafaie, Awatif; Larbi, Emmanuel; Al-Muhanna, Fahd; Asselberg, Folkert; Al-Faraidy, KhalidShakil, MohammedSingle nucleotide polymorphisms (SNPs) of the ?2 -adrenergic receptor (?2 -AR) gene have been implicated in the pathogenesis of cardiovascular diseases. This study evaluated two ?2 -AR SNPs in association with myocardial infarction (MI), namely arginine-glycine (G16R) substitution at codon 16 and glutamine-glutamic (Q27E) substitution at condon 27. bjectives: Therefore, our main objective was to determine the association of these two SNPs among patients with MI with and without type 2 diabetes (T2D). Materials and Methods: Blood samples were collected from 201 MI patients with and without diabetes and from 115 controls and the ?2 -AR gene polymorphisms at codon 16 and codon 27 were assessed by restriction fragment length polymorphism. The ?2 test was used to compare differences between groups. Results: The SNPs did not deviate significantly from Hardy-Weinberg equilibrium in the control population. The allele and genotype frequencies of the ?2 -AR gene polymorphism at codon 16 (G16R) was significantly different between MI cases and controls (?2 = 10.495, P < 0.05 and ?2 = 8.849, P < 0.05, respectively). No significant difference in genotype and allele frequencies at codon 27 was shown between these two groups (?2 = 2.661, P ? 0.05 and ?2 = 1.587, P ? 0.05, respectively). When the MI patients with and without T2D were pooled together, genotype distribution was different between cases and controls at codon 16 (?2 = 4.631, P = 0.099) and codon 27 (?2 = 7.247, P = 0.027). However, no significant differences were found in allele frequencies for codon 16 and codon 27 between the two groups (?2 = 0.628, P = 0.428; ?2 = 0.33, P = 0.565, respectively). Conclusion: Our findings indicate a moderate association of the ?2 -AR G16R gene polymorphism with MI suggesting that this gene plays a universal role in the development of MI across ethnicities. However, there was no association of ?2 -AR G16R gene polymorphism with diabetic patients with MI.
