title: Three ways to die suddenly: do they all require calcium calmodulin-dependent protein kinase II?
abstract: 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.
authors.affiliation: Iowa City, Iowa.
authors.forename: Mark E
authors.initials: ME
authors.lastname: Anderson
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000201:enzymology / Q000209:etiology* / Q000401:mortality / Q000503:physiopathology; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D016757:Death, Sudden, Cardiac / Q000209:etiology* / Q000517:prevention & control; D015195:Drug Design; D004789:Enzyme Activation; D006339:Heart Rate; D006801:Humans; D058990:Molecular Targeted Therapy; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D018384:Oxidative Stress; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use; D017382:Reactive Oxygen Species / Q000378:metabolism; D012084:Renin-Angiotensin System; D012307:Risk Factors; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000975:Antioxidants; D047428:Protein Kinase Inhibitors; D017382:Reactive Oxygen Species; D017871:Calcium-Calmodulin-Dependent Protein Kinases