Submitted: 31 Aug 2020
Accepted: 25 Dec 2020
ePublished: 24 Jan 2021
EndNote EndNote

(Enw Format - Win & Mac)

BibTeX BibTeX

(Bib Format - Win & Mac)

Bookends Bookends

(Ris Format - Mac only)

EasyBib EasyBib

(Ris Format - Win & Mac)

Medlars Medlars

(Txt Format - Win & Mac)

Mendeley Web Mendeley Web
Mendeley Mendeley

(Ris Format - Win & Mac)

Papers Papers

(Ris Format - Win & Mac)

ProCite ProCite

(Ris Format - Win & Mac)

Reference Manager Reference Manager

(Ris Format - Win only)

Refworks Refworks

(Refworks Format - Win & Mac)

Zotero Zotero

(Ris Format - Firefox Plugin)

J Cardiovasc Thorac Res. 2021;13(2): 109-115.
doi: 10.34172/jcvtr.2021.09

Scopus ID: 85106495484
  Abstract View: 151
  PDF Download: 154

Original Article

Association of APOA1-75G/A and +83C/T polymorphic variation with acute coronary syndrome patients in Kashmir (India)

Arshad A. Pandith 1* ORCID logo, Irfan Ahmad Bhat 2, Iqra Niyaz 3*, Iqbal Qasim 1, Ina A. Bhat 1, Usma Manzoor 1, Aabid M. Koul 1

1 Advanced Center for Human Genetics, SK Institute of Medical Sciences (SKIMS), Srinagar, J & K 190011, India
2 Department of Medicine, Government Medical College, 190010, Srinagar, J & K, India
3 Department of Clinical Biochemistry, University of Kashmir, J & K-190011, India


Introduction: Acute coronary syndrome (ACS) comes under the ambit of cardiovascular disease.APOA-1 gene plays a vital role in lipid metabolism and has been observed to have plausible role in ACS. This cross sectional case-control study was conducted to evaluate association between APOA1-75G/A(rs1799837), +83C/T (rs5069) genotypes and risk for ACS.
Methods: The current case-control study that included confirmed 90 ACS cases and 150 healthy controls were genotyped for APOA1-75 G/A and +83 C/T by Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLF) method.
Results: APOA1-75G/A distribution of genotypes/alleles among cases and controls was seen proportionally same with no association to ACS (P = 0.5).

APOA1+83 C/T variants showed protective effect with ACS where variant TT genotype presented more in controls (12%) than cases (1.6%) (P = 0.004) and likewise variant ‘T’ allele was found more in controls than ACS cases (9.4% vs.28.5% respectively: P < 0.05). Further, significantly high difference of CT genotype was seen among cases and controls 15% vs. 33% respectively (P = 0.002). The overall distribution of different haplotypes showed a marked difference in GT when compared with GC between cases and controls (P = 0.0001).
Conclusion: The study shows that TT genotype and variant T allele of APOA1 +83 C/T depicted a protective role with respect to ACS whereas APOA1-75G>A showed no relation. Haplotype GT was observed to significantly over-represent in controls with its protective effect in ACS as against wild type haplotype GC.

Keywords: Acute Coronary Syndrome, Cardiovascular Disease, APOA1 Gene, Polymorphism, Haplotype, Kashmir
First Name
Last Name
Email Address
Security code

Abstract View: 152

Your browser does not support the canvas element.

PDF Download: 154

Your browser does not support the canvas element.