QT dispersion in patients with social phobia

Nahshoni, Eitan; Gur, Shay; Marom, Sofi; Levin, Jennifer; Weizman, Abraham; Hermesh, Haggai

doi:10.1016/s0165-0327(02)00052-6

Cited by 24 publications

(27 citation statements)

References 21 publications

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“…It is showed with the meta-analysis studies that there is no association between gender and P-wave parameters and no significant association between Pmax and Pmin, and BMI; and no correlation, by any regression analysis, is found between age and Pd, Pmax, and Pmin values [15].…”

Section: Discussionmentioning

confidence: 91%

“…In those with common anxiety disorder, panic disorder and social phobia, increased anxiety and increased activation of the sympathetic nerve system of autonomic innervation and prolonged QTd have been shown [15,16]. Studies of eating disorders and conversion disorder have shown increased QTd in patients accompanied by high anxiety and depression scores [17,18].…”

Section: Introductionmentioning

confidence: 99%

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QT dispersion and P wave dispersion in schizophrenia

Baykara

Yılmaz

Baykara

2018

Psychiatry and Clinical Psychopharmacology

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BACKGROUND: The difference between maximum QT (QTmax) and minimum (QTmin) on electrocardiography (ECG) is known as QT dispersion (QTd). An increase in QTd carries the risk of ventricular arrhythmia and subsequent death. P wave dispersion (Pd) shows the difference between maximum P (Pmax) and minimum P (Pmin). Prolonged P wave duration and an increase in Pd are a risk for irregular electrical transmission and atrial fibrillation. OBJECTIVES: The aim of this study was to examine QTd and Pd values which indicate atrial fibrillation and ventricular arrhythmia in schizophrenia patients with whom cardiovascular diseases (CVD) are seen at a higher rate than the general population.

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Section: Discussionmentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

QT dispersion and P wave dispersion in schizophrenia

Baykara

Yılmaz

Baykara

2018

Psychiatry and Clinical Psychopharmacology

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“…Working from the assumption that an altered autonomic function may also be a feature of different psychiatric disorders, some authors have recently demonstrated significant alterations of the QT interval in clinical cohorts of psychiatric patients, including subjects with social phobia [12], panic disorder [13], and major depression [14]. The latter findings are of particular importance, because it is well-known that depressed patients show an increased risk for a number of cardiovascular complications, including ischemic heart disease [15], serious ventricular arrhythmias [16], and sudden cardiac death [17].…”

Section: Introductionmentioning

confidence: 99%

QT interval duration in apparently healthy men is associated with depression-related personality trait neuroticism

Minoretti

Politi

Martinelli

et al. 2006

Journal of Psychosomatic Research

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“…Emotions such as anger and anxiety are thought to increase sympathetic output, thereby increasing heart rate (HR) and risk of coronary heart disease or sudden cardiac death (Agelink et al, 2002;Johnsen et al, 2003;Kawachi et al, 1994;Nahshoni et al, 2004;Watkins et al, 1998;Wittstein et al, 2005;Yeragani et al, 2001Yeragani et al, , 2002. Alternatively, fear and feelings of hopelessness cause severe vagal activation resulting in bradycardia, which can lead to vasovagal syncope and asystole (Angrilli et al, 1997;Friedman et al, 1993;Hartel, 1987).…”

Section: Introductionmentioning

confidence: 99%

Facilitation of Cardiac Vagal Activity by CRF-R1 Antagonists during Swim Stress in Rats

Wood

Verhoeven

Savit

et al. 2006

Neuropsychopharmacol

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Exposure to stressors that elicit fear and feelings of hopelessness can cause severe vagal activation leading to bradycardia, syncope, and sudden death. These phenomena though documented, are difficult to diagnose, treat clinically, and prevent. Therefore, an animal model incorporating these cardiovascular conditions could be useful. The present study examined 'sinking' during a 2-h swim stress, a phenomenon that occurs in 50% of rats during 251C water exposure. Concurrent measurements of body temperature, immobility, heart rate (HR), and PR interval (a measure of vagal activity) were made. Neither decreases in immobility nor variations in hypothermia during swim were correlated with sinking. Bradycardia was more severe in sinking rats (average minimum HR7SEM; 143713 vs 247714; po0.01), and PR interval was elevated (po0.0001). To examine potential modulation of vagal activity during stress, corticotropinrelasing factor (CRF) receptor antagonists (antalarmin, R121919 and astressin B), a glucocorticoid receptor antagonist (RU486), and a peripherally acting cholinergic antagonist (methylatropine nitrate) were administered. The centrally acting CRF antagonist, antalarmin (32 mg/kg), produced elongation of the PR interval (po0.0001), robust bradycardia (135718; po0.001), and increased sinking (92%; po0.05), and methylatropine nitrate (3.2 mg/kg) blocked these effects. Corroborating these data, two different CRF antagonists, R121919 (30 mg/kg) and astressin B (intracerebroventricular (i.c.v.), 0.03 mg/rat) increased sinking to 100%. RU486 (20 mg/kg) blocked HPA axis negative feedback and decreased percent sinking to 25%. From these studies, we concluded that sinking during a 2-h water exposure was a result of extreme vagal hyperactivity. Furthermore, stress-induced CRF release may serve to protect against elevated cardiac vagal activity.

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QT dispersion in patients with social phobia

Cited by 24 publications

References 21 publications

QT dispersion and P wave dispersion in schizophrenia

QT dispersion and P wave dispersion in schizophrenia

QT interval duration in apparently healthy men is associated with depression-related personality trait neuroticism

Facilitation of Cardiac Vagal Activity by CRF-R1 Antagonists during Swim Stress in Rats

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