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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.

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