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Clinical Trial
. 2003 May;125(5):1022-9.
doi: 10.1067/mtc.2003.175.

Efficacy of esmolol as a myocardial protective agent during continuous retrograde blood cardioplegia

Marcio Scorsin  1 , Alexandre Mebazaa, Nawwar Al Attar, Betta Medini, Jacques Callebert, Richard Raffoul, Ramzi Ramadan, Jean Michel Maillet, Alain Ruffenach, François Simoneau, Patrick Nataf, Didier Payen, Arrigo Lessana
Affiliations
Free article
Clinical Trial

Efficacy of esmolol as a myocardial protective agent during continuous retrograde blood cardioplegia

Marcio Scorsin et al. J Thorac Cardiovasc Surg. 2003 May.
Free article

Abstract

Objective: Esmolol, an ultra-short-acting beta-blocker, is known to attenuate myocardial ischemia-reperfusion injury. The aim of this study was to compare the effects of esmolol and potassium on myocardial metabolism during continuous normothermic retrograde blood cardioplegia.

Methods: Forty-one patients operated on for isolated aortic valve stenosis were randomly assigned to continuous coronary infusion with either potassium or esmolol during cardiopulmonary bypass. Myocardial metabolism was assessed by measuring the transmyocardial gradient of oxygen content indexed to left ventricular mass of glucose, lactate, and nitric oxide. To do so, blood samples were simultaneously withdrawn upstream (in the cardioplegia line) and downstream of the myocardium (in the left coronary ostium) 10 and 30 minutes after aortic crossclamping.

Results: Although the cardioplegia flow rate and pressure were similar, esmolol markedly reduced the transmyocardial gradient of oxygen content indexed to left ventricular mass compared with potassium: 13 +/- 6 vs 20 +/- 6 mL of oxygen per liter of blood per 100 g of myocardium, respectively, at 10 minutes and 16 +/- 8 vs 24 +/- 8 mL of oxygen per liter of blood per 100 g of myocardium, respectively, at 30 minutes (P =.009). Coronary glucose and lactate transmyocardial gradients were similar in both groups, indicating adequate myocardial perfusion in all patients at all times. In addition, during retrograde cardioplegia, esmolol showed a lower nitric oxide release compared with that caused by potassium (39 +/- 49 micro mol x L(-1) for potassium vs 14 +/- 8 micro mol x L(-1) for esmolol at 10 minutes and 39 +/- 47 micro mol x L(-1) for potassium vs 6 +/- 8 micro mol x L(-1) for esmolol at 30 minutes, P =.05). However, hemodynamic parameters and plasma troponin I levels remained unchanged postoperatively between the 2 types of cardioplegia.

Conclusion: Esmolol provides potent myocardial protection in hypertrophied hearts, at least in part, by reducing myocardial oxygen metabolism.

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