title: Renal denervation suppresses ventricular arrhythmias during acute ventricular ischemia in pigs.
abstract: BACKGROUND
  Increased sympathetic activation during acute ventricular ischemia is involved in the occurrence of life-threatening arrhythmias.
  
  
  OBJECTIVE
  To test the effect of sympathetic inhibition by renal denervation (RDN) on ventricular ischemia/reperfusion arrhythmias.
  
  
  METHODS
  Anesthetized pigs, randomized to RDN or SHAM treatment, were subjected to 20 minutes of left anterior descending coronary artery (LAD) occlusion followed by reperfusion. Infarct size, hemodynamics, premature ventricular contractions, and spontaneous ventricular tachyarrhythmias were analyzed. Monophasic action potentials were recorded with an epicardial probe at the ischemic area.
  
  
  RESULTS
  Ventricular ischemia resulted in an acute reduction of blood pressure (-29%) and peak left ventricular pressure rise (-40%), which were not significantly affected by RDN. However, elevation of left ventricular end-diastolic pressure (LVEDP) during LAD ligation was attenuated by RDN (ΔLVEDP: +1.8 ± 0.6 mm Hg vs +9.7 ± 1 mm Hg in the SHAM group; P = .046). Infarct size was not affected by RDN compared to SHAM. RDN significantly reduced spontaneous ventricular extrabeats (160 ± 15/10 min in the RDN group vs 422 ± 36/10 min in the SHAM group; P = .021) without affecting coupling intervals. In 5 of 6 SHAM-treated animals, ventricular fibrillation (VF) occurred during LAD occlusion. By contrast, only 1 of 7 RDN-treated animals experienced VF (P = .029). Beta-receptor blockade by atenolol showed comparable effects. Neither VF nor transient shortening of monophasic action potential duration during reperfusion was inhibited by RDN.
  
  
  CONCLUSIONS
  RDN reduced the occurrence of ventricular arrhythmias/fibrillation and attenuated the rise in LVEDP during left ventricular ischemia without affecting infarct size, changes in ventricular contractility, blood pressure, and reperfusion arrhythmias. Therefore, RDN may protect from ventricular arrhythmias during ischemic events.
authors.affiliation: Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg/Saar, Germany. Electronic address: Dominik.Linz@uks.eu.
authors.forename: Dominik
authors.initials: D
authors.lastname: Linz
authors.forename: Klaus
authors.initials: K
authors.lastname: Wirth
authors.forename: Christian
authors.initials: C
authors.lastname: Ukena
authors.forename: Felix
authors.initials: F
authors.lastname: Mahfoud
authors.forename: Janine
authors.initials: J
authors.lastname: Pöss
authors.forename: Benedikt
authors.initials: B
authors.lastname: Linz
authors.forename: Michael
authors.initials: M
authors.lastname: Böhm
authors.forename: Hans-Ruprecht
authors.initials: HR
authors.lastname: Neuberger
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001262:Atenolol / Q000627:therapeutic use; D004195:Disease Models, Animal; D007668:Kidney / Q000294:innervation*; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000150:complications*; D013552:Swine; D013562:Sympathectomy; D017180:Tachycardia, Ventricular / Q000209:etiology / Q000517:prevention & control*; D014693:Ventricular Fibrillation / Q000209:etiology / Q000517:prevention & control*; D018879:Ventricular Premature Complexes / Q000209:etiology / Q000517:prevention & control*
chemical_list: D000889:Anti-Arrhythmia Agents; D001262:Atenolol
keywords: +dP/dt; AF; BP; DAD; ECG; LAD; LVEDP; LVESP; MAP; MAPD(50); Myocardial infarction; PVC; RDN; Renal denervation; Sympathetic nervous system; VF; Ventricular fibrillation; atrial fibrillation; blood pressure; delayed afterdepolarization; electrocardiogram; left anterior descending coronary artery; left ventricular end-diastolic pressure; left ventricular end-systolic pressure; monophasic action potential; monophasic action potential duration at 50% repolarization; peak left ventricular pressure decay; peak left ventricular pressure rise; premature ventricular contraction; renal denervation; ventricular fibrillation; −dP/dt