Interact CardioVasc Thorac Surg 2008;7:1162-1163. doi:10.1510/icvts.2008.186494
© 2008 European Association of Cardio-Thoracic Surgery
Brief communication - Cardiac general |
Is blood versus crystalloid cardioplegia relevant? Significantly improved protection may require new cardioplegic concepts!
Hazem B. Fallouh* and
David J. Chambers
Cardiac Surgical Research/Cardiothoracic Surgery, The Rayne Institute (King's College London), Guy's and St. Thomas' NHS Foundation Trust, St. Thomas' Hospital, London SE1 7EH, UK
Received 24 June 2008;
accepted 22 August 2008
Corresponding author. Tel.: +44 207 1880957; fax: +44 207 1880970.
E-mail address: hazem.fallouh{at}kcl.ac.uk (H.B. Fallouh).
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Abstract
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The predominant method of myocardial protection during cardiac surgery is hyperkalaemic cardioplegia, inducing depolarised arrest. Since its development in the 1970s, the only real change has been to alter the vehicle to blood. Although blood cardioplegia was shown to be ‘superior’ to crystalloid cardioplegia, this advantage is marginal and might explain the continuous use of crystalloid cardioplegia by some surgeons. To achieve significant improvements in cardioplegic protection, more radical and conceptual changes in the solution, such as those potentially achieved by ‘polarised’ arrest, should be explored.
Key Words: Myocardial protection; Crystalloid; Blood; Cardioplegia
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1. Introduction
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The introduction, in the 1970s, of cardioplegic solutions based on an ‘extracellular-type’ formulation with moderate hyperkalaemia, together with the general acceptance and uptake by cardiac surgeons of this technique, has revolutionised cardiac surgery. Hyperkalaemic cardioplegia offered significant improvement in outcome over ischaemic hypothermic arrest, and it has become the gold standard for myocardial protection of the elective global ischaemia required for optimal cardiac surgery. Subsequently, innumerable experimental and clinical studies have been conducted with the aim of improving the basic hyperkalaemic protection (by a variety of outcomes) using techniques such as addition of substrates or various classes of drug, scavenging of reactive oxygen species or preconditioning. Interestingly, however, most studies have failed to translate into the clinical arena, with the exception being the increased use of blood as the vehicle solution for the hyperkalaemic cardioplegia [1, 2]. This was derived from many comparative studies showing a protective benefit with blood cardioplegia, and despite many early studies that may have used conditions biased in favour of blood usage (such as higher temperatures, substrate additions, etc.), a recent ‘best evidence’ review by Jacobs and colleagues [3] has shown the benefit from blood cardioplegia to be scant. There was no clear-cut conclusion, which might explain why some surgeons continue to use, and favour the simplicity of, crystalloid hyperkalaemic cardioplegia. Herein lies the difficulty of translating experimental (animal-based) studies; clear differences that can be determined due to the controlled conditions and reproducibility of these experimental studies with direct and easily measured endpoints fail to manifest in clinical studies. This is probably due to the disease complexity and manifold factors associated with the importance of minimising the injury to the patient during clinical studies, which makes any expected outcome differences small.
Both the crystalloid and blood cardioplegic techniques described in this review [3] have invariably been based on the concept of hyperkalaemia, with arrest due to the consequent membrane potential depolarisation [4]. Although ‘extracellular-type’ hyperkalaemic cardioplegia is by far the most commonly used cardioplegic solution worldwide, an alternative ‘intracellular-type’ crystalloid solution is available. The HTK solution, originally developed by Bretschneider [5] in the 1960s, has been commonly used in Germany since that time and has been shown to have comparative safety and efficacy characteristics to hyperkalaemic solutions [6]. Although HTK solution contains elevated potassium (10 mmol/l), the membrane potential at arrest is slightly less ‘depolarised' than conventional hyperkalaemic solutions [7]. This is due to its ‘intracellular-type’ formulation that is based on low sodium and low calcium. As a consequence, a blood-based HTK solution is impossible as this would invalidate the concept on which it is based. The concept of inducing arrest at a membrane potential that is close to that of the resting membrane potential [4], commonly termed ‘polarised’ arrest, is one that has been increasingly proposed over recent years as a means of achieving improved myocardial protection. Hence, experimental studies that use polarising cardioplegic solutions have been shown to provide a beneficial alternative to conventional hyperkalaemic depolarising solutions. Mechanisms of inducing effective polarised arrest have been demonstrated experimentally and include sodium channel blockers [8, 9] and potassium channel openers [10]. Potentially, this concept could be used in blood-based solutions, which might offer the combined benefit of possible superior protection of blood-based solutions with that of polarised arrest leading to improvements in current clinically used myocardial protection strategies. The experimental challenge is to determine the efficacy of drugs that may be useful in this context but that are devoid of the adverse effects.
Jacob and colleagues [3] have demonstrated that blood as a vehicle may add to the protection offered by hyperkalaemia; however, its advantage over crystalloid cardioplegia is relatively marginal, and may explain why crystalloid cardioplegia is still in use. We believe that new concepts of cardioplegic arrest (such as polarised arrest) should be explored and studied clinically. This is especially important with the current population of cardiac surgery patients, who are sicker, more elderly and have more severe disease requiring more complicated and longer operative procedures.
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References
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Abstract
1. Introduction