RESUMO
Studies have shown association of lipoprotein lipase (LPL) polymorphisms with coronary artery disease (CAD); however, limited studies on the genetics of CAD have been done in the Philippines. Because of their effects on high-density lipoprotein and triglyceride metabolism, the G-allele of the Ser447X variant of LPL gene has been shown to be atheroprotective, while HindIII polymorphism has been shown to be pro-atherogenic. We assessed 1301 patients undergoing coronary angiography to determine the prevalence of HindIII and Ser447X polymorphisms and their association with angiographically significant CAD. Genotyping for HindIII and Ser447X variants were analyzed by real-time PCR. Multivariate analyses were performed to determine the interaction between LPL polymorphisms and risk factors of CAD. CAD+ group (72%) was predominantly male (76%) with a mean age of 60.17 ± 11.01 with hypertension (89%), dyslipidemia (84%) and smoking (54%) as the most common risk factors. HindIII carriage frequency among the CAD+ group was 20.3% with a genotypic distribution of 78.71% (T/T), 19.83% (T/G) and 1.46% (G/G). Ser447X carriage frequency among the CAD+ group was 8.0% with a genotypic distribution of 91.39% (C/C), 8.38% (C/G) and 0.23% (G/G). HindIII and Ser447X polymorphisms were both not significantly associated with CAD. LPL polymorphic allele HindIII was common, while Ser447X was rare. Present study did not show association of LPL polymorphisms with the development of CAD. However, among patients with dyslipidemia, presence of Ser447X allele is associated with an increased risk (OR 2.6; 95% CI 2.1-3.7; p value < 0.001) of developing CAD than those without LPL polymorphisms.
RESUMO
BACKGROUND: To determine predictive variables for permanent pacemaker (PPM) insertion after transcatheter aortic valve replacement (TAVR) with the CoreValve Revalving System (CRS). METHODS AND RESULTS: A total of 121 patients with severe aortic stenosis (AS) were recruited from six Asian medical centers between March 2010 and May 2013. Four patients with preexisting PPM were excluded. The mean age of the remaining 117 patients was 81.2 ± 5.1 years. Twenty-three patients (19.7%) required post-TAVR PPM, with a median time-to-insertion of 7 days (interquartile range, 5-13 days). Two variables were identified as independent predictors of PPM: (1) device depth from the non-coronary cusp (NCC) (odds ratio [OR], 1.263; P=.02) determined by aortic root angiography; and (2) the perimeter stretching index (OR, 1.584; P<.001) determined by computed tomography. The predictive cut-off values were as follows: a perimeter stretching index >1.13 (P<.001) and a device depth from the NCC >7.8 mm (P<.001). The diagnostic accuracy of these variables was 93.2% and 71%, respectively. CONCLUSION: Depth of the device from the NCC and the perimeter stretching index are independent predictors of PPM insertion after CRS-TAVR.