Association of 25 bp Deletion in MYBPC3 Gene with Left Ventricle Dysfunction in Coronary Artery Disease Patients 英文参考文献.docVIP
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Association of 25 bp Deletion in MYBPC3 Gene with Left Ventricle Dysfunction in Coronary Artery Disease Patients 英文参考文献
Associationof25bpDeletioninMYBPC3GenewithLeft
VentricleDysfunctioninCoronaryArteryDisease
Patients
AnshikaSrivastava1,NaveenGarg2,TulikaMittal1,RoopaliKhanna2,ShipraGupta3,PrahladKishore
Seth3,BalrajMittal1*
1Department ofGenetics,SanjayGandhi PostGraduate InstituteofMedicalSciencesLucknow(UP),Lucknow, India,2DepartmentofCardiology,SanjayGandhiPost
GraduateInstituteofMedicalSciencesLucknow(UP),Lucknow,India,3BioinformaticCenter,BiotechParkLucknow(UP),Lucknow,India
Abstract
Rationale: Mutations in MYBPC3 encoding cardiac myosin binding protein C are common genetic cause of hereditary
cardiacmyopathies.Anintronic25-bpdeletioninMYBPC3at39regionisassociatedwithdilated(DCM)andhypertrophic
(HCM) cardiomyopathies in Southeast Asia. However, the frequency of MYBPC3 25bp deletion and associated clinical
presentationhasnotbeenestablishedinanunrelatedcohortofleftventriculardysfunction(LVD)secondarytocoronary
arterydisease(CAD)patients.
Objective:WesoughttodeterminetheroleofMYBPC325bppolymorphismonLVDintwocohortsofCADpatients.
MethodsandResults:Thestudyincluded265consecutivepatientswithangiographicallyconfirmedCADand220controls.
MYBPC3 25bp polymorphism was determined by polymerase chain reaction. Our results showed that carrier status of
MYBPC3 25bp deletion was associated with significant compromised left ventricle ejection fraction (LVEF #45) in CAD
patients(pvalue = ,0.001;OR=4.49).Tovalidateourresults,weperformedareplicationstudyinadditional140caseswith
similarclinicalcharacteristicsandresultsagainconfirmedconsistentfindings(p=0.029;OR=3.3).Also,presenceofthegene
deletiondidnothavesignificantassociationinCADpatientswithpreservedejectionfraction(LVEF.45)(pvalue =0.1;OR
=2.3).
Conclusion: The frequency of MYBPC3 DW genotypeand Dallele was associated with compromisedLVEF implyingthat
geneticvariantsofMYBPC3encodingmutantstructuralsarcomereproteincouldincreasesusceptibilitytoleftventricular
dysfunction.Therefore,25bpdeletioninMYBPC3mayrepresentageneticmarkerforcar
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