Sudden cardiac death occurs due to a limited number of pathological events. The heart can beat too fast or too slow to maintain adequate cardiac output or the heart can rupture. Here we survey recent evidence that excessive activation of calcium calmodulin-dependent protein kinase II by three core neurohumoral pathways or by oxidant stress can lead to sudden cardiac death due to sinus node dysfunction and bradycardia, ventricular tachycardia or fibrillation, and cardiac rupture.
|Original language||English (US)|
|Number of pages||13|
|Journal||Transactions of the American Clinical and Climatological Association|
|State||Published - Jan 1 2014|
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