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Myocardial β-Blockade as an Alternative to Cardioplegic Arrest during Coronary Artery Surgery

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The authors' recent experimental work has demonstrated that myocardial protection using continuous coronary perfusion with warm β-blocker-enriched blood avoids myocardial ischaemia and minimizes myocardial oedema formation, thus completely preserving left ventricle function. The purpose of this clinical study was to compare this alternative technique in terms of structural and functional myocardial protection with the routinely used crystalloid Bretschneider cardioplegia. Sixty coronary artery surgery patients were randomized to receive either crystalloid cardioplegia or continuous coronary perfusion with warm blood enriched with the ultra-short acting β-blocker esmolol. Cardiac function was evaluated using transoesophageal echocardiography (fractional area of contraction) and cardiac metabolism using arterial-coronary sinus lactate concentration difference (a — CSDLAC). From left ventricular biopsies, the authors determined myocardial oedema, heat-shock-protein-70. intercellular-adhesion-molecule and actin pattern. Patients with crystalloid cardioplegia received 3.6 ± 0.8 grafts during 64 ± 20 min cross-clamp time (β-blocker: 3.5 ± 0.9 grafts during 68 ± 22 min; NS). Following cross-clamp removal crystalloid cardioplegia hearts released significant lactate amounts (a −CSDLAC − 1.0 ± 0.6 versus − 0.1 ± 0.2 mmol/litre in β-blocker hearts; P < 0.05). In crystalloid cardioplegia hearts, myocardial water content increased from 82.1 ± 2.1% pre-cardiopulmonary bypass to 83.2 ± 1.7% at the end of cardiopulmonary bypass ( P < 0.05); in β blocker hearts myocardial water content remained unchanged (pre-cardiopulmonary bypass: 82.3 ± 1.9%; end of cardiopulmonary bypass: 82.4 ± 1.7%; NS). At the end of cardiopulmonary bypass, left ventricular biopsies of β-blocker hearts showed less structural damage as determined by heat shock protein-70. intercellular adhesion molecule-I and deranged actin cross-striation pattern as compared with crystalloid cardioplegia hearts ( P < 0.05). The postcardiopulmonary bypass fractional area of contraction was similar in both groups (β-blocker: 65 ± 14%; crystalloid cardioplegia: 62 ± 16%); however, β-blocker patients required less inotropic stimulation (dopamine: β-blocker: 2.9 ± 2.5 versus crystalloid cardioplegia: 5.0 ± 2.3 μg/kg per min: P < 0.05). The data suggest that continuous coronary perfusion with warm esmolol-enriched blood results in better myocardial protection compared with crystalloid cardioplegia. It is concluded that the concept of β-blocker-induced cardiac surgical conditions may be a useful alternative for myocardial protection during coronary artery surgery.
Title: Myocardial β-Blockade as an Alternative to Cardioplegic Arrest during Coronary Artery Surgery
Description:
The authors' recent experimental work has demonstrated that myocardial protection using continuous coronary perfusion with warm β-blocker-enriched blood avoids myocardial ischaemia and minimizes myocardial oedema formation, thus completely preserving left ventricle function.
The purpose of this clinical study was to compare this alternative technique in terms of structural and functional myocardial protection with the routinely used crystalloid Bretschneider cardioplegia.
Sixty coronary artery surgery patients were randomized to receive either crystalloid cardioplegia or continuous coronary perfusion with warm blood enriched with the ultra-short acting β-blocker esmolol.
Cardiac function was evaluated using transoesophageal echocardiography (fractional area of contraction) and cardiac metabolism using arterial-coronary sinus lactate concentration difference (a — CSDLAC).
From left ventricular biopsies, the authors determined myocardial oedema, heat-shock-protein-70.
intercellular-adhesion-molecule and actin pattern.
Patients with crystalloid cardioplegia received 3.
6 ± 0.
8 grafts during 64 ± 20 min cross-clamp time (β-blocker: 3.
5 ± 0.
9 grafts during 68 ± 22 min; NS).
Following cross-clamp removal crystalloid cardioplegia hearts released significant lactate amounts (a −CSDLAC − 1.
0 ± 0.
6 versus − 0.
1 ± 0.
2 mmol/litre in β-blocker hearts; P < 0.
05).
In crystalloid cardioplegia hearts, myocardial water content increased from 82.
1 ± 2.
1% pre-cardiopulmonary bypass to 83.
2 ± 1.
7% at the end of cardiopulmonary bypass ( P < 0.
05); in β blocker hearts myocardial water content remained unchanged (pre-cardiopulmonary bypass: 82.
3 ± 1.
9%; end of cardiopulmonary bypass: 82.
4 ± 1.
7%; NS).
At the end of cardiopulmonary bypass, left ventricular biopsies of β-blocker hearts showed less structural damage as determined by heat shock protein-70.
intercellular adhesion molecule-I and deranged actin cross-striation pattern as compared with crystalloid cardioplegia hearts ( P < 0.
05).
The postcardiopulmonary bypass fractional area of contraction was similar in both groups (β-blocker: 65 ± 14%; crystalloid cardioplegia: 62 ± 16%); however, β-blocker patients required less inotropic stimulation (dopamine: β-blocker: 2.
9 ± 2.
5 versus crystalloid cardioplegia: 5.
0 ± 2.
3 μg/kg per min: P < 0.
05).
The data suggest that continuous coronary perfusion with warm esmolol-enriched blood results in better myocardial protection compared with crystalloid cardioplegia.
It is concluded that the concept of β-blocker-induced cardiac surgical conditions may be a useful alternative for myocardial protection during coronary artery surgery.

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