Efficacy of esmolol as a myocardial protective agent during continuous retrograde blood cardioplegia.
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 To do so, blood samples were simultaneously withdrawn upstream (in the cardioplegia line) and downstream of the myocardium (in the left coronary ostium) 10 and 30 minutes after aortic crossclamping.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.


CONCLUSIONS
Esmolol provides potent myocardial protection in hypertrophied hearts, at least in part, by reducing myocardial oxygen metabolism.
Scorsin
Marcio
M
Service de Chirurgie Cardiaque, Centre Cardiologique du Nord, Saint-Denis, France. mscorsin@hotmail.com
Mebazaa
Alexandre
A
Al Attar
Nawwar
N
Medini
Betta
B
Callebert
Jacques
J
Raffoul
Richard
R
Ramadan
Ramzi
R
Maillet
Jean Michel
JM
Ruffenach
Alain
A
Simoneau
François
F
Nataf
Patrick
P
Payen
Didier
D
Lessana
Arrigo
A
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D000368:Aged; D001024:Aortic Valve Stenosis / Q000150:complications / Q000601:surgery*; D002314:Cardioplegic Solutions / Q000009:adverse effects; D002315:Cardiopulmonary Bypass; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000150:complications; D019344:Lactic Acid / Q000097:blood; D007902:Length of Stay; D008875:Middle Aged; D009200:Myocardial Contraction / Q000187:drug effects; D017202:Myocardial Ischemia / Q000209:etiology / Q000517:prevention & control*; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium / Q000494:pharmacology / Q000627:therapeutic use*; D011412:Propanolamines / Q000494:pharmacology / Q000627:therapeutic use*; D016896:Treatment Outcome; D014336:Troponin / Q000097:blood
D000319:Adrenergic beta-Antagonists; D002314:Cardioplegic Solutions; D011412:Propanolamines; D014336:Troponin; D019344:Lactic Acid; C036604:esmolol; D011188:Potassium