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The relationship between diastolic blood pressure and coronary artery calcification is dependent on single nucleotide

Daniel S Kim, Jennifer A Smith, Lawrence F Bielak

  • 1Department of Epidemiology, University of Michigan School of Public Health, 1415 Washington Heights, Ann Arbor 48109, MI, USA. skardia@umich.edu.

BMC Medical Genetics
|September 5, 2014
PubMed

Insights

Genetic variations in the 9p21.3 region influence coronary heart disease (CHD) risk by modifying the link between diastolic blood pressure (DBP) and coronary artery calcification (CAC) quantity.

Area of Science:

  • Genetics
  • Cardiovascular Disease
  • Genomic Epidemiology

Background:

  • Single nucleotide polymorphisms (SNPs) in the 9p21.3 region are linked to coronary heart disease (CHD), myocardial infarction, and coronary artery calcification (CAC).
  • Previous research shows a connection between blood pressure and CAC.
  • The 9p21.3 region's role in CHD risk requires further investigation into its interaction with blood pressure.

Purpose of the Study:

  • To investigate if SNPs in the 9p21.3 region modify the association between blood pressure and CAC quantity.
  • To explore potential mechanisms linking 9p21.3 genetic variants to CHD risk.

Main Methods:

  • Utilized data from 974 participants in the Genetic Epidemiology Network of Arteriopathy (GENOA) Study, measuring CAC via computed tomography (CT).
  • Employed linear mixed effects models to test for interactions between seven 9p21.3 SNPs and blood pressure levels concerning CAC quantity.
  • Replicated significant SNP-DBP interactions in the Framingham Heart Study Offspring Cohort (N=1,140).

Main Results:

  • One SNP, rs2069416 in CDKN2B-AS1, significantly modified the association between diastolic blood pressure (DBP) and CAC quantity (combined P=0.0065).
  • This interaction remained significant after Bonferroni correction (P=0.0455).

Conclusions:

  • The relationship between DBP and CAC is influenced by genetic variation within the 9p21.3 region.
  • 9p21.3 variants may act as independent CHD risk factors and modulate the impact of DBP on subclinical coronary atherosclerosis.
Abstract

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