Intravenous electrical vagal nerve stimulation prior to coronary reperfusion in a canine ischemia-reperfusion model markedly reduces infarct size and prevents subsequent heart failure

INTERNATIONAL JOURNAL OF CARDIOLOGY

卷:227

Article

Arimura, Takahiro¹  Saku, Keita²  Kakino, Takamori¹  Nishikawa, Takuya¹  Tohyama, Takeshi¹  Sakamoto, Takafumi¹  Sakamoto, Kazuo¹  Kishi, Takuya³  Ide, Tomomi¹  Sunagawa, Kenji² 

[1] Grad Sch Med Sci, Dept Cardiovasc Med, Higashi Ku, 1-1-3 Maidashi, Fukuoka 8128582, Japan

[2] Ctr Disrupt Cardiovasc Med, Dept Therapeut Regulat Cardiovasc Homeostasis, Higashi Ku, 1-1-3 Maidashi, Fukuoka 8128582, Japan

[3] Kyushu Univ, Ctr Disrupt Cardiovasc Med, Collaborat Res Inst Innovat Therapeut Cardiovasc, Higashi Ku, 1-1-3 Maidashi, Fukuoka 8128582, Japan

关键词: Vagal nerve stimulation;    Acute myocardial infarction;    Chronic heart failure;    Autonomic nervous system;    Infarct size;   

DOI  :  10.1016/j.ijcard.2016.10.074

来源: Elsevier

【 摘 要 】

Background: Reducing myocardial damage is a prerequisite to prevent chronic heart failure after acute myocardial infarction (AMI). Although vagal nerve stimulation (VNS) has been repeatedly demonstrated to have potent anti-infarct effect, technical difficulties have precluded its clinical application. We developed a novel therapeutic strategy of intravenous VNS (iVNS) and examined whether iVNS administered prior to coronary reperfusion in a canine AMI model reduces infarct size and prevents heart failure. Methods and results: In 35 mongrel dogs, we induced ischemia by ligating the left anterior descending coronary artery and then reperfused 3 h later (I/R) We transvenously placed a catheter electrode in the superior vena cava and adjusted the stimulation intensity to a level that induced bradycardia but maintained stable hemodynamics (continuous, 5.1 +/- 2.1 V. 10 Hz). We administered iVNS from onset (iVNS-0, n = 7) Of 90 min after onset (iVNS-90, n 7) of ischemia until one hour after reperfusion. Four weeks after ischemia-reperfusion, iVNS markedly reduced infarct size (iVNS-0: 24 +/- 2.1%, p < 0.05 and iVNS-90: 4.5 +/- 4.5%, p < 0.05) compared with I/R control (I/R: 13.3 +/- 2.5%), and improved cardiac performance and hemodynamics. Atrial pacing (n 7) to abolish iVNS-induced bradycardia significantly attenuated the beneficial effects of iVNS. Conclusions: Short-term iVNS delivered prior to coronary reperfusion markedly reduced infarct size and preserved cardiac function one month after AMI. The bradycardic effect plays an important role in the beneficial effect of iVNS. How other mechanisms contribute to the reduction of infarct size remains to be studied. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

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