Myocardial protection: the forgotten ‘polarized’ modality

We read with interest the review by Allen [1] highlighting the importance of myocardial protection, and we agree that it is time to bring the topic back on the agendas of major societies and meetings. We also agree that successful myocardial protection is associated with low perioperative enzymatic leakage and preservation of interventricular septal kinesis, 2 areas that should be routinely assessed. However, creatin-phosphokinase-MB (CPK-MB) has low sensitivity and specificity for the diagnosis of myocardial damage and we strongly recommend the use of troponin assays as per the guidelines supporting a universal definition of myocardial infarction. However, inadequate intraoperative myocardial protection is also supported by mid-to-high postoperative inotropic support and/or intra-aortic balloon pump (IABP). Indeed, the vasoactive-inotropic score predicts myocardial infarction and mortality after cardiac surgery [2] and IABP indicates a higher degree of myocardial damage requiring mechanical ventricular support. Another area of concern raised at the 2019 European Association for Cardio-Thoracic Surgery/European Association of Cardiothoracic Anesthesiology/European Board of Cardiovascular Perfusion (EACTS/EACTA/EBCP) guidelines on cardiopulmonary bypass [3] is that we still do not know the best available cardioplegic solution. After a brief discussion on the major depolarizing solutions, Allen mentioned an alternative ‘polarized’ modality using adenosine, lidocaine and magnesium (ALM). We have been using the ALM ‘polarized’ concept for 8 years and conducted a prospective randomized trial in all-comers patients [4]. We compared the ‘polarized’ Verona ALM cardioplegia to the Buckberg solution and found lower postoperative troponin release and improved left ventricular function in the patients receiving ALM cardioplegia [4]. It is clear that high-potassium solutions present some level of myocardial toxicity, which has been partly addressed by keeping the heart cold, intermittent dosing and reduced ‘on-pump’ times. The suggested ‘integrated strategy’ moving forward still focuses on hyperkalemic blood cardioplegia and subjects the heart to prolonged depolarization times. A prolonged ‘depolarized’ membrane leads to calcium overload, mitochondrial dysfunction and atrial and ventricular potassium heterogeneities, which can ultimately lead to arrhythmias, ischaemia–reperfusion injury and low output [5]. For that reason, we support a ‘polarized cardiac arrest’ with normokalemic ALM microplegia [4]. The time has come for an extensive evaluation of benefits and harms of depolarized versus polarized cardiac arrest.