PMID- 26972302
OWN - NLM
STAT- MEDLINE
DCOM- 20161213
LR  - 20161230
IS  - 1559-0283 (Electronic)
IS  - 1085-9195 (Linking)
VI  - 74
IP  - 1
DP  - 2016 Mar
TI  - Hyperhomocysteinemia Alters Sinoatrial and Atrioventricular Nodal Function: Role 
      of Magnesium in Attenuating These Effects.
PG  - 59-65
LID - 10.1007/s12013-015-0711-8 [doi]
AB  - Patients with hyperhomocysteinemia (HHcy), or elevated plasma homocysteine (Hcy), 
      are at higher risk of developing arrhythmias and sudden cardiac death; however, 
      the mechanisms are unknown. In this study, the effects of HHcy on sinus node 
      function, atrioventricular conduction, and ventricular vulnerability were 
      investigated by electrophysiological (EP) analysis, and the role of magnesium 
      (Mg(2+)), an endogenous N-methyl-D-aspartate (NMDA) receptor antagonist, in 
      attenuating EP changes due to HHcy was explored. Wild-type mice (WT) and mice 
      receiving Hcy in the drinking water for 12 weeks (DW) were subjected to 
      electrocardiographic and EP studies. DW compared to WT had significantly shorter 
      RR, PR, QT, and HV intervals, corrected sinus node recovery times (CSNRT), 
      Wenckebach periodicity (WP), atrioventricular nodal effective refractory periods 
      (AVNERP), and right ventricular effective refractory periods (RVERP). To examine 
      the role of Mg(2+) in mitigating conduction changes in HHcy, WT, DW, and 
      heterozygous cystathionine-beta-synthase knockout mice (CBS (+/-) ) were subjected 
      to repeat EP studies before and after administration of low-dose magnesium 
      sulfate (20 mg/kg). Mg(2+) had no effect on EP variables in WT, but significantly 
      slowed CSNRT, WP, and AVNERP in DW, as well as WP and AVNERP in CBS (+/-) . These 
      findings suggest that ionic channels modulated by Mg(2+) may contribute to 
      HHcy-induced conduction abnormalities.
FAU - Soni, Chirag V
AU  - Soni CV
AD  - Department of Physiology and Biophysics, University of Louisville School of 
      Medicine, Louisville, KY, 40202, USA. cvsoni01@louisville.edu.
FAU - Tyagi, Suresh C
AU  - Tyagi SC
AD  - Department of Physiology and Biophysics, University of Louisville School of 
      Medicine, Louisville, KY, 40202, USA.
FAU - Todnem, Nathan D
AU  - Todnem ND
AD  - Department of Physiology and Biophysics, University of Louisville School of 
      Medicine, Louisville, KY, 40202, USA.
FAU - Givvimani, Srikanth
AU  - Givvimani S
AD  - Department of Physiology and Biophysics, University of Louisville School of 
      Medicine, Louisville, KY, 40202, USA.
FAU - Pushpakumar, Sathnur B
AU  - Pushpakumar SB
AD  - Department of Physiology and Biophysics, University of Louisville School of 
      Medicine, Louisville, KY, 40202, USA.
FAU - Villafane, Juan
AU  - Villafane J
AD  - Department of Pediatrics, University of Kentucky College of Medicine, Lexington, 
      KY, 40506, USA.
FAU - Maldonado, Claudio
AU  - Maldonado C
AD  - Department of Physiology and Biophysics, University of Louisville School of 
      Medicine, Louisville, KY, 40202, USA.
AD  - Department of Surgery, University of Louisville School of Medicine, Louisville, 
      KY, 40202, USA.
LA  - eng
GR  - HL-71010/HL/NHLBI NIH HHS/United States
GR  - HL-74185/HL/NHLBI NIH HHS/United States
GR  - HL-88012/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Cell Biochem Biophys
JT  - Cell biochemistry and biophysics
JID - 9701934
RN  - EC 4.2.1.22 (Cystathionine beta-Synthase)
RN  - I38ZP9992A (Magnesium)
SB  - IM
MH  - Action Potentials
MH  - Animals
MH  - Cystathionine beta-Synthase/genetics/metabolism
MH  - Hyperhomocysteinemia/metabolism/*physiopathology
MH  - Magnesium/*metabolism
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Refractory Period, Electrophysiological
MH  - Sinoatrial Node/metabolism/*physiopathology
OTO - NOTNLM
OT  - Arrhythmia
OT  - Atrioventricular node
OT  - Cardiac N-methyl-D-aspartate receptor
OT  - Electrophysiological studies
OT  - Homocysteine
OT  - Sinoatrial node
OT  - Sudden cardiac death
EDAT- 2016/03/15 06:00
MHDA- 2016/12/15 06:00
CRDT- 2016/03/15 06:00
PHST- 2016/03/15 06:00 [entrez]
PHST- 2016/03/15 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
AID - 10.1007/s12013-015-0711-8 [pii]
AID - 10.1007/s12013-015-0711-8 [doi]
PST - ppublish
SO  - Cell Biochem Biophys. 2016 Mar;74(1):59-65. doi: 10.1007/s12013-015-0711-8.