Hypothermia and atrial fibrillation

Authors

  • Geoffrey A. Donnan


The overarching themes in this edition are hypothermia as a neuroprotectant and atrial fibrillation. As we all know, the story of neuroprotection has been littered with challenges of translation, so that we currently have no therapies approved for clinical use. We are all very familiar with the numerous possibilities as to why this translation leap has been unsuccessful. Hypothermia remains one of the most powerful and consistently positive neuroprotectants in animal models, and has the strongest circumstantial evidence that it may be translatable. We know that trials of hypothermia in cardiac arrest have improved neurological outcomes, and the knowledge that the various hypothermic methods are used to preserve other organs of the body in humans prior to transplantation suggests that hypothermia is a strong human cellular protectant. Interestingly, this is also supported by the work of David Howells et al. who show that hypothermia clearly protects human neurons. Continuing on this theme is another interesting effect of hypothermia observed by McLeod et al. showing that hypothermia may prevent delayed intracranial pressure rise: another possible beneficial mechanism.

All of this should give heart to those conducting the EuroHYP-1 trials in acute stroke patients, the protocol which is also reported in this issue. This is a well-funded international study, the largest of its type, and certainly the most pragmatic. I'm sure we all hope that this time success will be realized.

Research into atrial fibrillation has been reenergized by the introduction of the new oral anticoagulants (NOACs). With the introduction of any new agent, there will always be areas of uncertainty in clinical management and this applies to the NOACs as for any other agent. Fortunately, we have an excellent review to help guide clinicians around the issues of uncertainty thrown up by the introduction of NOACs, particularly in areas such as: when thrombolysis can be given with those having had NOAC therapy; when to start NOACs after acute ischemic stroke and that old chestnut; when to start oral anticoagulants such as NOACs after intracerebral haemorrhage. In the absence of level-one evidence in these areas, the synthesis of opinion given by Haney and colleagues should be extremely helpful for practicing clinicians. The findings of Deguchi et al., correlating strongly with increasingly larger intracranial and extracranial vessel occlusion, further validate the usefulness of the CHADS scoring system. One interpretation may be that high scores are associated with large emboli.

Of course, there are many other articles of interest, ranging from a fascinating insight into the burden of stroke in the Philippines to the influence of racial differences on outcomes after thrombolytic therapy in acute ischemic stroke.

Wonderful summer reading for our northern hemisphere friends and winter comfort for our southern hemisphere colleagues. Happy reading!

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