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Abstract: Background: Polymorphisms in cholesteryl ester protein gene have been linked to risk of coronary heart disease (CHD) in many world populations through their effect on reverse cholesterol transport. Methods: Five hundred four (504) unrelated electrocardiograph confirmed cases of CHD and 338 population based controls, matched by age and gender, belonging to the Tamilian population of south India were genotyped for polymorphisms in CETP gene using PCR RFLP methods. Results: The multivariate logistic regression analyses demonstrated that CETP B1B1 and CA genotypes of TaqIB and −629C>A were significantly associated with increased risk for CHD (odds ratio (OR) 2.7; 95% confidence intervals (CI) (1.5–3.3); OR 1.5 (1.1–2.4)) respectively. Combined wild genotypes of CETP gene showed an association with CHD (OR–1.7 (1.0–2.9) as well as the combined heterozygous mutants (OR 1.5 (1.0–2.3); p–0.03). Subgroup analysis based on gender revealed that men harboring CETP B1B1 and CA genotypes have a significant risk for CHD B1B1- 2.7 (1.7–4.3), CA-1.8 (1.3–2.6). There was no link between CETP I450V polymorphism and CHD. Analysis based on hypertensive status showed a significant association between these polymorphisms and non hypertensive CHD patients. Conclusions: The risk in non hypertensive and male CHD patients is higher in the presence of CETP B1B1 and CA genotypes. [Copyright &y& Elsevier]

Abstract: Introduction: Thrombospondin 1 and 2 are multidomain calcium-binding extracellular glycoproteins and they play a role in platelet aggregation, inflammatory response and assembly of connective tissue extracellular matrix. The association of thrombospondins (TSP) in the pathogenesis of coronary artery disease (CAD) and myocardial infarction (MI) is well established. The association of the TSP-1 (Asn700Ser, 2210A→G, rs2228262) and TSP-2 un-translated region (UTR) (3949T→G, rs8089) gene variations among South Indian CAD and MI patients has been examined in the present study. Materials and Methods: We analyzed the thrombospondin polymorphisms in unrelated CAD patients (n=511) and a subgroup with an event of MI (n=173) compared with controls (n=522). The polymorphisms were assessed using polymerase chain reaction, restriction fragment length analysis and the circulating TSP concentration were measured using enzyme linked immune-sorbent assay. Results: The prevalence of TSP-1 and TSP-2 alleles did not show any significant difference statistically, when compared controls against CAD/MI patients. The rare GG genotype of the N700S polymorphism was not observed among the studied population. Further, multiple regression analysis revealed that there was no significant risk for CAD (OR=1.68; 95% CI 0.927 - 3.055; p=0.087) or MI (OR=1.84; 95% CI 0.846 - 4.007; p=0.124) for the GA genotype. The GA genotype showed no impact on clinical characteristics of the CAD patients and their circulating TSP-1 levels. A similar non-association was observed for the TSP-2 in 3949T→G polymorphism (GG genotype) for CAD (OR=0.64; 95% CI 0.278 - 1.455; p=0.636) and MI (OR=0.53; 95% CI 0.166 - 1.675; p=0.278). Conclusions: Our data suggests that the presence of thrombospondin-1 (rs2228262) and thrombospondin-2 (rs8089) variants need not be considered a risk for coronary artery disease or myocardial infarction among South Indians. [Copyright &y& Elsevier]