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Articles by R Gobin
Total Records ( 2 ) for R Gobin
  E Di Angelantonio , R Chowdhury , N Sarwar , K. K Ray , R Gobin , D Saleheen , A Thompson , V Gudnason , N Sattar and J. Danesh
 

Background— Measurement of B-type natriuretic peptide (BNP) concentration or its precursor (N-terminal fragment [NT-proBNP]) is recommended in patients with symptoms of left ventricular dysfunction and in other settings, but the relevance of these peptides to cardiovascular disease (CVD) in general populations or in patients with stable vascular disease is uncertain.

Methods and Results— Data were collated from 40 long-term prospective studies involving a total of 87 474 participants and 10 625 incident CVD outcomes. In a comparison of individuals in the top third with those in the bottom third of baseline values of natriuretic peptides, the combined risk ratio (RR), adjusted for several conventional risk factors, was 2.82 (95% confidence interval [CI], 2.40 to 3.33) for CVD. Analysis of the 6 studies with at least 250 CVD outcomes (which should be less prone to selective reporting than are smaller studies) yielded an adjusted RR of 1.94 (95% CI, 1.57 to 2.39). RRs were broadly similar with BNP or NT-proBNP (RR, 2.89 [95% CI, 1.91 to 4.38] and 2.82 [95% CI, 2.35 to 3.38], respectively) and by different baseline vascular risk (RR, 2.68 [95% CI, 2.07 to 3.47] in approximately general populations; RR, 3.35 [95% CI, 2.38 to 4.72] in people with elevated vascular risk factors; RR, 2.60 [95% CI, 1.99 to 3.38] in patients with stable CVD). Assay of BNP or NT-proBNP in addition to measurement of conventional CVD risk factors yielded generally modest improvements in risk discrimination.

Conclusions— Available prospective studies indicate strong associations between circulating concentration of natriuretic peptides and CVD risk under a range of different circumstances. Further investigation is warranted, particularly in large general population studies, to clarify any predictive utility of these markers and to better control for publication bias.

  D Saleheen , N Soranzo , A Rasheed , H Scharnagl , R Gwilliam , M Alexander , M Inouye , M Zaidi , S Potter , P Haycock , S Bumpstead , S Kaptoge , E Di Angelantonio , N Sarwar , S. E Hunt , N Sheikh , N Shah , M Samuel , S. R Haider , M Murtaza , A Thompson , R Gobin , A Butterworth , U Ahmad , A Hakeem , K. S Zaman , A Kundi , Z Yaqoob , L. A Cheema , N Qamar , A Faruqui , N. H Mallick , M Azhar , A Samad , M Ishaq , S. Z Rasheed , R Jooma , J. H Niazi , A. R Gardezi , N. A Memon , A Ghaffar , F. u Rehman , M. M Hoffmann , W Renner , M. E Kleber , T. B Grammer , J Stephens , A Attwood , K Koch , M Hussain , K Kumar , A Saleem , M. S Daood , A. A Gul , S Abbas , J Zafar , F Shahid , S. M Bhatti , S. S Ali , F Muhammad , G Sagoo , S Bray , R McGinnis , F Dudbridge , B. R Winkelmann , B Boehm , S Thompson , W Ouwehand , W Marz , P Frossard , J Danesh and P. Deloukas
  Background—

Evidence is sparse about the genetic determinants of major lipids in Pakistanis.

Methods and Results—

Variants (n=45 000) across 2000 genes were assessed in 3200 Pakistanis and compared with 2450 Germans using the same gene array and similar lipid assays. We also did a meta-analysis of selected lipid-related variants in Europeans. Pakistani genetic architecture was distinct from that of several ethnic groups represented in international reference samples. Forty-one variants at 14 loci were significantly associated with levels of HDL-C, triglyceride, or LDL-C. The most significant lipid-related variants identified among Pakistanis corresponded to genes previously shown to be relevant to Europeans, such as CETP associated with HDL-C levels (rs711752; P<10–13), APOA5/ZNF259 (rs651821; P<10–13) and GCKR (rs1260326; P<10–13) with triglyceride levels; and CELSR2 variants with LDL-C levels (rs646776; P<10–9). For Pakistanis, these 41 variants explained 6.2%, 7.1%, and 0.9% of the variation in HDL-C, triglyceride, and LDL-C, respectively. Compared with Europeans, the allele frequency of rs662799 in APOA5 among Pakistanis was higher and its impact on triglyceride concentration was greater (P-value for difference <10–4).

Conclusions—

Several lipid-related genetic variants are common to Pakistanis and Europeans, though they explain only a modest proportion of population variation in lipid concentration. Allelic frequencies and effect sizes of lipid-related variants can differ between Pakistanis and Europeans.

 
 
 
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