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Heart Rhythm. 2013 Oct;10(10):1525-30. doi: 10.1016/j.hrthm.2013.07.015. Epub 2013 Jul 11.

Renal denervation suppresses ventricular arrhythmias during acute ventricular ischemia in pigs.

Author information

1
Klinik für Innere Medizin III, Universitätsklinikum des Saarlandes, Homburg/Saar, Germany. Electronic address: Dominik.Linz@uks.eu.

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.

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

PMID:
23851058
DOI:
10.1016/j.hrthm.2013.07.015
[Indexed for MEDLINE]
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