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Cardiac Surgical Research/Cardiothoracic Surgery, The Rayne Institute (King's College London), Guy's & St. Thomas' NHS Foundation Trust, St. Thomas' Hospital, London, United Kingdom
* Address correspondence to Dr Chambers, Cardiac Surgical Research/Cardiothoracic Surgery, The Rayne Institute (King's College London), Guy's & St. Thomas' NHS Foundation Trust, St. Thomas' Hospital, London, SE1 7EH, United Kingdom (Email: david.chambers@kcl.ac.uk).
In this issue, a series of three articles [1–3] examine the effects of mild hypothermia (reductions of
2°C to 4°C) on ischemia-reperfusion injury from regional ischemia (coronary occlusion). The authors sought to determine how this might influence (and hopefully reduce) the development of myocardial infarction and lead to improved myocardial protection. The studies are potentially, extremely relevant to current cardiologic practice of percutaneous coronary intervention (PCI), with the hope that this procedure will act as an additive therapy to complement that of the reperfusion procedure.
During the development and early years of cardiac surgery, profound hypothermia (to temperatures of 4°C to 10°C) was considered essential for myocardial protection of the globally ischemic heart. This was achieved either by topical cooling or infusion of cold crystalloid or blood cardioplegia [4]. More recently, however, "tepid" cardioplegia (ie, cooling the heart to around 32°C) has been shown to be effective [5–7].
Investigators studying regional ischemia to mimic acute myocardial infarction were likely encouraged by the results seen with global ischemia and "tepid" cardioplegia to suggest that mild hypothermia (of
2°C to 4°C reduction) may also be beneficial for patients undergoing coronary angioplasty or thrombolysis (with maintained beating working hearts). Thus, Chien and coworkers [8] showed that, in rabbit hearts, infarct size correlated positively with blood temperature (whole body cooling) over the range of 35°C to 42°C when maintained constantly throughout 30 minutes of ischemia and 180 minutes of reperfusion. This benefit was independent of heart rate, implying that reduced myocardial oxygen consumption (MVO2) was unlikely as a mechanism of action for this protection. Similarly, effective reduction of infarct size in rabbit hearts was achieved by topical regional hypothermia (2°C to 4°C reduction using an ice bag) of the myocardial risk zone before 30 minutes
Related Articles
Ann. Thorac. Surg. 2009 87: 157-163.
Ann. Thorac. Surg. 2009 87: 164-171.
Ann. Thorac. Surg. 2009 87: 172-177.
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