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Articles by A. D. Hingorani
Total Records ( 2 ) for A. D. Hingorani
  T Shah , P Newcombe , L Smeeth , J Addo , J. P Casas , J Whittaker , M. A Miller , L Tinworth , S Jeffery , P Strazzullo , F. P Cappuccio and A. D. Hingorani
  Background—

Eligibility for rosuvastatin treatment for cardiovascular disease prevention includes a C-reactive protein (CRP) concentration >2 mg/L. Most observational studies of CRP and cardiovascular disease have been in Europeans. We evaluated the influence of ancestry on population CRP concentration to assess the implications for statin targeting in non-Europeans.

Methods and Results—

In a systematic review and meta-analysis among 221 287 people from 89 studies, geometric mean CRP was 2.6 mg/L (95% credible interval, 2.27 to 2.96) in blacks resident in the United States (n=18 585); 2.51 mg/L (95% CI, 1.18 to 2.86) in Hispanics (n=5049); 2.34 mg/L (95% CI, 1.99 to 2.8) in South Asians (n=1053); 2.03 mg/L (95% CI, 1.77 to 2.3) in whites (n=104 949); and 1.01 mg/L (95% CI, 0.88 to 1.18) in East Asians (n=39 521). Differences were not explained by study design or CRP assay and were preserved after adjustment for age and body mass index. At age 60 years, fewer than half of East Asians but more than two thirds of Hispanics were estimated to have CRP values exceeding 2 mg/L. HapMap frequencies of CRP polymorphisms known to associate with CRP concentration but not coronary heart disease events differed by ancestry. In participant data from the Wandsworth Heart and Stroke Study including European, South Asian and African, and Caribbean-descent subjects, body mass index, systolic blood pressure, and smoking contributed to between-group differences in CRP, but the majority of the difference in CRP was unexplained.

Conclusions—

Differences in CRP concentration in populations of diverse ancestry are sufficiently large to affect statin eligibility, based on a single CRP threshold of 2 mg/L, and only partially influenced by differences in variables related to cardiovascular risk. A single threshold value of CRP for cardiovascular risk prediction could lead to inequalities in statin eligibility that may not accurately reflect underlying levels of cardiovascular risk.

  F Drenos , P. J Talmud , J. P Casas , L Smeeth , J Palmen , S. E Humphries and A. D. Hingorani
 

Individuals at risk of coronary heart disease (CHD) show multiple correlations across blood biomarkers. Single nucleotide polymorphisms (SNPs) indexing biomarker differences could help distinguish causal from confounded associations because of their random allocation prior to disease. We examined the association of 948 SNPs in 122 candidate genes with 12 CHD-associated phenotypes in 2775 middle aged men (a genic scan). Of these, 140 SNPs indexed differences in HDL- and LDL-cholesterol, triglycerides, C-reactive protein, fibrinogen, factor VII, apolipoproteins AI and B, lipoprotein-associated phospholipase A2, homocysteine or folate, some with large effect sizes and highly significant P-values (e.g. 2.15 standard deviations at P = 9.2 x 10–140 for F7 rs6046 and FVII levels). Top ranking SNPs were then tested for association with additional biomarkers correlated with the index phenotype (phenome scan). Several SNPs (e.g. in APOE, CETP, LPL, APOB and LDLR) influenced multiple phenotypes, while others (e.g. in F7, CRP and FBB) showed restricted association to the index marker. SNPs influencing six blood proteins were used to evaluate the nature of the associations between correlated blood proteins utilizing Mendelian randomization. Multiple SNPs were associated with CHD-related quantitative traits, with some associations restricted to a single marker and others exerting a wider genetic ‘footprint’. SNPs indexing biomarkers provide new tools for investigating biological relationships and causal links with disease. Broader and deeper integrated analyses, linking genomic with transcriptomic, proteomic and metabolomic analysis, as well as clinical events could, in principle, better delineate CHD causing pathways amenable to treatment.

 
 
 
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