Psychological Stress Preceding Idiopathic Ventricular Fibrillation

Lane, Richard D.; Laukes, Cindi; Marcus, Frank I.; Chesney, Margaret A.; Sechrest, Lee; Gear, Kathleen; Fort, Carolyn; Priori, Silvia G.; Schwartz, Peter J.; Steptoe, Andrew

doi:10.1097/01.psy.0000160476.67536.41

Cited by 50 publications

(25 citation statements)

References 30 publications

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“…However, overstimulated SGK activity may be detrimental. For example, it has been reported that psychosocial stress plays a role in otherwise unexplained cardiac arrest (39). Furthermore, a gain-of-function SGK1 mutation has been reported in twins who displayed the shortened QT interval, which induces arrhythmias and sudden death (40,41).…”

Section: Discussionmentioning

confidence: 99%

The Serum- and Glucocorticoid-inducible Kinases SGK1 and SGK3 Regulate hERG Channel Expression via Ubiquitin Ligase Nedd4-2 and GTPase Rab11

Lamothe

Zhang

2013

Journal of Biological Chemistry

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Background:The cardiac hERG (I Kr ) potassium channel is important for cardiac repolarization. Results: Activation of SGK1 and SGK3 increases hERG expression by inhibiting Nedd4-2 activity and promoting Rab11-mediated hERG recycling. Conclusion: SGK1 and SGK3 regulate hERG through Nedd4-2 and Rab11 pathways. Significance: Identification of SGK effects on hERG extends our understanding of ion channel regulation and cardiac electrophysiology.

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Section: Discussionmentioning

confidence: 99%

The Serum- and Glucocorticoid-inducible Kinases SGK1 and SGK3 Regulate hERG Channel Expression via Ubiquitin Ligase Nedd4-2 and GTPase Rab11

Lamothe

Zhang

2013

Journal of Biological Chemistry

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“…It is at these brainstem and subcortical levels that central cardio-cardiac reflexes may exacerbate pathological autonomic responses to emotional challenges in cardiological patients placing them at risk of arrhythmia and sudden death (1,6,9). Beyond these brainstem centers, homoeostatic afferent information is conveyed by both basal and posterior ventromedial thalamic nuclei to the superior margin of the insula cortex, which supports a cortical representation of visceral state (9, 34, 37-42).…”

Section: Discussionmentioning

confidence: 99%

“…afferent homeostatic feedback ͉ electroencephalography ͉ heart beat-evoked potential ͉ insula cortex ͉ ischemia E motional events and mental stress can precipitate cardiac arrhythmia and sudden death in patients with heart disease (1-4). Electrocardiographic (ECG) indices of proarrhythmic electrical instability of the myocardium accompany psychological stress (5) and are associated with abnormalities in regional brain activity, suggesting abnormal efferent autonomic drive to the heart (1,6). Although a central efferent mechanism for arrhythmogenesis may also explain sudden death in disorders such as epilepsy (4,7), disturbances in cardiac afferent feedback may induce cardiogenic reflexes that enhance the vulnerability of cardiovascular disease patients to stress-induced arrhythmia (8).…”

mentioning

confidence: 99%

A cortical potential reflecting cardiac function

Gray

Taggart

Sutton

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

195

132

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Emotional trauma and psychological stress can precipitate cardiac arrhythmia and sudden death through arrhythmogenic effects of efferent sympathetic drive. Patients with preexisting heart disease are particularly at risk. Moreover, generation of proarrhythmic activity patterns within cerebral autonomic centers may be amplified by afferent feedback from a dysfunctional myocardium. An electrocortical potential reflecting afferent cardiac information has been described, reflecting individual differences in interoceptive sensitivity (awareness of one's own heartbeats). To inform our understanding of mechanisms underlying arrhythmogenesis, we extended this approach, identifying electrocortical potentials corresponding to the cortical expression of afferent information about the integrity of myocardial function during stress. We measured changes in cardiac response simultaneously with electroencephalography in patients with established ventricular dysfunction. Experimentally induced mental stress enhanced cardiovascular indices of sympathetic activity (systolic blood pressure, heart rate, ventricular ejection fraction, and skin conductance) across all patients. However, the functional response of the myocardium varied; some patients increased, whereas others decreased, cardiac output during stress. Across patients, heartbeat-evoked potential amplitude at left temporal and lateral frontal electrode locations correlated with stress-induced changes in cardiac output, consistent with an afferent cortical representation of myocardial function during stress. Moreover, the amplitude of the heartbeat-evoked potential in the left temporal region reflected the proarrhythmic status of the heart (inhomogeneity of left ventricular repolarization). These observations delineate a cortical representation of cardiac function predictive of proarrhythmic abnormalities in cardiac repolarization. Our findings highlight the dynamic interaction of heart and brain in stress-induced cardiovascular morbidity. afferent homeostatic feedback ͉ electroencephalography ͉ heart beat-evoked potential ͉ insula cortex ͉ ischemia

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“…In the sample studied by Chandra et al (1988, as cited in Carvalho-Filho, 2000, the prevalence was 93.2%, both for ventricular arrhythmias as well as supraventricular arrhythmias. However, age is only a risk factor for coronary diseases when over 65 years, though not for idiopathic arrhythmias, as demonstrated in the study of Lane et al (2005). These authors found that patients with idiopathic ventricular fibrillation were significantly younger (36.0  11.6 years) than patients with coronary disease (57.1  8.1 years).…”

mentioning

confidence: 48%