Right ventricular infarction causes heterogeneous autonomic denervation of the viable peri-infarct area

Arif Elvan, Douglas P. Zipes

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Background-Because efferent autonomic pathways to the right ventricle (RV) differ from the efferent autonomic projections to the left ventricle (LV), we assessed the effects of RV infarction on this innervation. Methods and Results-We measured the ventricular effective refractory period (ERP) shortening in response to bilateral ansae subclaviae stimulation and ERP lengthening induced by bilateral vagal stimulation as markers of autonomic innervation before and after RV myocardial infarction (RVMI) produced by coronary ligation (n=28 dogs) or intracoronary latex injection (n= 18 dogs) into a marginal branch of the right coronary artery in open-chest anesthetized dogs. In each dog, ERPs measured in viable peri-infarct area at two RV outflow tract (RVOT) sites and two septal and four lateral sites at the RV free wall after RVMI showed reduced or absent ERP shortening during bilateral ansae subclaviae stimulation laterally, septally, and at RVOT sites 3 hours after RVMI. ERP shortening in response to infused norepinephrine was still present. Bilateral vagal stimulation during background norepinephrine infusion (0.10 to 0.25 μg/kg per minute) lengthened the ERP at all test sites before latex injection. After transmural RVMI, vagally induced ERP prolongation was attenuated or lost at lateral, septal, and RVOT test sites. Conclusions-RVMI causes sympathetic and vagal denervation at viable sites at the RVOT, lateral, and, to a lesser extent, septal sides of the viable peri- infarct area. Autonomic denervation in the RVOT might contribute to the development of ventricular tachyarrhythmias after the acute stage of myocardial infarction involving the R.V.

Original languageEnglish
Pages (from-to)484-492
Number of pages9
JournalCirculation
Volume97
Issue number5
StatePublished - Feb 10 1998

Fingerprint

Autonomic Denervation
Infarction
Heart Ventricles
Myocardial Infarction
Dogs
Latex
Norepinephrine
Efferent Pathways
Autonomic Pathways
Injections
Sympathectomy
Tachycardia
Ligation
Coronary Vessels
Thorax

Keywords

  • Infarction
  • Innervation
  • Ventricles

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Right ventricular infarction causes heterogeneous autonomic denervation of the viable peri-infarct area. / Elvan, Arif; Zipes, Douglas P.

In: Circulation, Vol. 97, No. 5, 10.02.1998, p. 484-492.

Research output: Contribution to journalArticle

Elvan, Arif ; Zipes, Douglas P. / Right ventricular infarction causes heterogeneous autonomic denervation of the viable peri-infarct area. In: Circulation. 1998 ; Vol. 97, No. 5. pp. 484-492.
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abstract = "Background-Because efferent autonomic pathways to the right ventricle (RV) differ from the efferent autonomic projections to the left ventricle (LV), we assessed the effects of RV infarction on this innervation. Methods and Results-We measured the ventricular effective refractory period (ERP) shortening in response to bilateral ansae subclaviae stimulation and ERP lengthening induced by bilateral vagal stimulation as markers of autonomic innervation before and after RV myocardial infarction (RVMI) produced by coronary ligation (n=28 dogs) or intracoronary latex injection (n= 18 dogs) into a marginal branch of the right coronary artery in open-chest anesthetized dogs. In each dog, ERPs measured in viable peri-infarct area at two RV outflow tract (RVOT) sites and two septal and four lateral sites at the RV free wall after RVMI showed reduced or absent ERP shortening during bilateral ansae subclaviae stimulation laterally, septally, and at RVOT sites 3 hours after RVMI. ERP shortening in response to infused norepinephrine was still present. Bilateral vagal stimulation during background norepinephrine infusion (0.10 to 0.25 μg/kg per minute) lengthened the ERP at all test sites before latex injection. After transmural RVMI, vagally induced ERP prolongation was attenuated or lost at lateral, septal, and RVOT test sites. Conclusions-RVMI causes sympathetic and vagal denervation at viable sites at the RVOT, lateral, and, to a lesser extent, septal sides of the viable peri- infarct area. Autonomic denervation in the RVOT might contribute to the development of ventricular tachyarrhythmias after the acute stage of myocardial infarction involving the R.V.",
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