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Published online by Cambridge University Press:  01 January 2008

N. K. Chinnan*
Affiliation:
The Canberra Hospital Woden, ACT, Australia
G. D. Puri
Affiliation:
Department of Anaesthesia and Intensive CarePost Graduate Institute of Medical Education and Research (PGIMER)Chandigarh, India
S. K. S. Thingnam
Affiliation:
Department of Cardiothoracic and Vascular SurgeryPost Graduate Institute of Medical Education and Research (PGIMER)Chandigarh, India
*
Correspondence to: Nevin Kollannoor Chinnan, The Canberra Hospital, PO Box-11, Woden, ACT, Australia. E-mail: [email protected]; Tel: +61 424486052; Fax: +61 262443300

Abstract

Type
Correspondence
Copyright
Copyright © European Society of Anaesthesiology 2007

EDITOR:

We thank Kiss and colleagues for their valuable comments. The faster onset of electromechanical arrest after administration of cardioplegia is very likely due to the coronary vasodilating properties of nicorandil [Reference Chinnan, Puri and Thingnam1]. Coronary vasodilatation could have also resulted in better distribution of the cardioplegic solution and improved myocardial preservation and, hence, fewer arrhythmias while coming off cardiopulmonary bypass (CPB) and less risk of postoperative myocardial infarction. The increased incidence of myocardial infarction in the nicorandil group coronary artery bypass grafting (CABG) patients could be multifactorial. However, it is interesting to note that three out of four patients who had a postoperative myocardial infarction in the nicorandil group, CABG patients were diabetics. Our study did not look into coronary artery spasms in the postoperative period. In this context, we would like to refer to a case report where nicorandil infusion was used to manage distal micro-vascular spasm characterized by ST segment elevation in the electrocardiogram, serially elevated cardiac enzymes (creatine kinase and creatine phosphokinase-MB) and new onset regional wall motion abnormalities in the absence of fixed or vasospastic occlusion of coronary vessels on angiography [Reference Mizogami, Shimo, Taguchi and Horita2]. With regard to reperfusion injuries and arrhythmias, intravenous and intracoronary nicorandil have been shown to be of benefit after percutaneous coronary interventions for acute myocardial infarctions [Reference Takarabe, Okazaki, Higuchi, Murayama, Natsuaki and Itoh3,Reference Ota, Nishikawa and Takeuchi4]. After prolonged cardioplegic arrest (4 h) in an isolated rabbit heart model, nicorandil was found to attenuate ischaemia–reperfusion injury of the myocardium and coronary endothelium, and ameliorate leukocyte activation [Reference Hara, Horinaka and Yabe5]. These findings by other researchers are in accordance with our observations. We would also like to clarify that we used a terminal infusion of warm blood cardiolplegia (hot shots) before coming off CPB as it is the present day standard of care and apologize for not making that clear in our study protocol. We fully agree with Kiss and colleagues that a larger multicentre randomized controlled trial is required to determine the efficacy and the role of nicorandil in certain subclasses of patients like those developing coronary artery spasms in the postoperative period, and diabetics undergoing cardiac surgery.

References

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