HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Joel S. Corvera Faraz Kerendi Michael E. Halkos Zhi-Qing Zhao Robert A. Guyton Jakob Vinten-Johansen Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Corvera, J. S. Articles by Vinten-Johansen, J. Search for Related Content PubMed PubMed Citation Articles by Corvera, J. S. Articles by Vinten-Johansen, J. Related Collections Cardiac - pharmacology Myocardial protection

J Thorac Cardiovasc Surg 2005;129:599-606
© 2005 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Polarized arrest with warm or cold adenosine/lidocaine blood cardioplegia is equivalent to hypothermic potassium blood cardioplegia

^a Cardiothoracic Research Laboratory and Carlyle Fraser Heart Center, Emory University School of Medicine, Atlanta, Ga, USA,
^b Department of Physiology and Pharmacology, James Cook University, Townsville, Queensland, Australia

Received for publication August 3, 2003; revisions received June 21, 2004; accepted for publication July 9, 2004.

^* Address for reprints: Jakob Vinten-Johansen, PhD, Cardiothoracic Research Laboratory, Emory University School of Medicine, 550 Peachtree St, NE, Atlanta, GA 30308 (E-mail: jvinten{at}emory.edu).

BACKGROUND: Hypothermic depolarizing hyperkalemic (K⁺ 20 mEq/L) blood cardioplegia is the "gold standard" in cardiac surgery. K⁺ has been associated with deleterious consequences, eg, intracellular calcium overload. This study tested the hypothesis that elective arrest in a polarized state with adenosine (400 µmol/L via adenosine triphosphate–sensitive potassium channel opening) and the Na⁺ channel blocker lidocaine (750 µmol/L) as the arresting agents in blood cardioplegia provides cardioprotection comparable to standard hypothermic K⁺-blood cardioplegia.

METHODS: Anesthetized dogs were placed on cardiopulmonary bypass and assigned to 1 of 3 groups receiving antegrade cardioplegia delivered every 20 minutes for 1 hour of arrest: cold (10°C) K⁺-blood cardioplegia (n = 6), cold (10°C) adenosine/lidocaine blood cardioplegia (n = 6), or warm (37°C) adenosine/lidocaine blood cardioplegia (n = 6). After an hour of arrest, cardiopulmonary bypass was discontinued, and reperfusion was continued for 120 minutes.

RESULTS: Time to arrest was longer with cold and warm adenosine/lidocaine blood cardioplegia (175 ± 19 seconds and 143 ± 19 seconds, respectively) compared with K⁺-blood cardioplegia (27 ± 2 seconds; P < .001). Postcardioplegia left ventricular systolic function (slope of the end-systolic pressure/dimension relationship) was comparable among the 3 groups (K⁺-blood cardioplegia, 15.2 ± 2.1 mm Hg/mm; cold adenosine/lidocaine blood cardioplegia, 15.9 ± 3.4 mm Hg/mm; warm adenosine/lidocaine blood cardioplegia, 14.1 ± 2.8 mm Hg/mm; P = .90). Plasma creatine kinase activity in cold and warm adenosine/lidocaine blood cardioplegia was similar to that in K⁺-blood cardioplegia at 120 minutes of reperfusion (cold adenosine/lidocaine blood cardioplegia, 11.5 ± 2.1 IU/g protein; warm adenosine/lidocaine blood cardioplegia, 10.1 ± 0.9 IU/g protein; K⁺-blood cardioplegia, 7.6 ± 0.8 IU/g protein; P = .17). Postcardioplegia coronary artery endothelial function was preserved in all groups.

CONCLUSIONS: Intermittent polarized arrest with warm or cold adenosine/lidocaine blood cardioplegia provided the same degree of myocardial protection as intermittent hypothermic K⁺-blood cardioplegia in normal hearts.

This article has been cited by other articles:

				O. Jakobsen, T. A. Stenberg, O. Losvik, S. Ekse, D. G. Sorlie, and L. M. Ytrebo Adenosine instead of supranormal potassium in cardioplegic solution preserves endothelium-derived hyperpolarization factor-dependent vasodilation Eur. J. Cardiothorac. Surg., January 1, 2008; 33(1): 18 - 24. [Abstract] [Full Text] [PDF]

				O. Jakobsen, S. Muller, E. Aarsaether, T. Steensrud, and D. G. Sorlie Adenosine instead of supranormal potassium in cardioplegic solution improves cardioprotection Eur. J. Cardiothorac. Surg., September 1, 2007; 32(3): 493 - 500. [Abstract] [Full Text] [PDF]

				K. L. Sloots, J. Vinten-Johansen, and G. P. Dobson Warm nondepolarizing adenosine and lidocaine cardioplegia: Continuous versus intermittent delivery J. Thorac. Cardiovasc. Surg., May 1, 2007; 133(5): 1171 - 1178. [Abstract] [Full Text] [PDF]

				H. B. Fallouh and D. J. Chambers ICVTS on-line discussion A The safety of using millimolar doses of lidocaine as cardioplegia Interactive CardioVascular and Thoracic Surgery, April 1, 2007; 6(2): 176 - 176. [Full Text] [PDF]

				S. Yamaguchi, G. Watanabe, S. Tomita, and S. Tabata Lidocaine-magnesium blood cardioplegia was equivalent to potassium blood cardioplegia in left ventricular function of canine heart Interactive CardioVascular and Thoracic Surgery, April 1, 2007; 6(2): 172 - 176. [Abstract] [Full Text] [PDF]