Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5604885 | International Journal of Cardiology | 2017 | 9 Pages |
Abstract
Second, we need to recognize the fact that SCD in this population is a result of multiple potential mechanisms. And, the electrophysiologic substrates underlying these mechanisms are influenced by interactions with the autonomic nervous system and hemodynamic conditions. While most out-of-hospital cardiac arrests do not occur in persons with overt heart failure, the presence of heart failure clearly increases the risk for SCD, likely by a variety of mechanisms. There is increasing evidence that altered left ventricular geometry may not only reduce LV mechanical efficiency, but may also have direct effects on the electrophysiologic substrate. Although there is an abundance of evidence supporting the importance of autonomic interactions in the genesis of spontaneous arrhythmias, the utility of prospectively measuring autonomic indices to predict future arrhythmic events has to date not proven to be useful. Of course, that is not to discount the significant impact of beta-adrenergic blockade on survival and reducing arrhythmic events. Future works must focus more on both animal models of post-infarction arrhythmias, as well as integrating findings from such studies into human physiology, with subsequent testing in the form of randomized clinical trials.
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Authors
Alfred E. Buxton,