99 research outputs found

    Psychological Distress and Arrhythmia: Risk Prediction and Potential Modifiers

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    The connection between the heart and the brain has long been anecdotally recognized but has systematically been studied only relatively recently. Cardiac arrhythmias, especially ventricular arrhythmias that can lead to sudden cardiac death, remain a major public health concern and there is mounting evidence that psychological distress plays a critical role both as a predictor of high-risk cardiac substrate and as an inciting trigger. The transient, unpredictable nature of emotions and cardiac arrhythmias has made their study challenging, but evolving technologies in monitoring and imaging along with larger epidemiological data sets have encouraged more sophisticated studies examining this relationship. Here we review the research on psychological distress including anger, depression and anxiety on cardiac arrhythmias, insights into proposed mechanisms, and potential avenues for future research

    Antipsychotic medications and sudden cardiac arrest: More than meets the eye?

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    Sudden cardiac arrest (SCA) remains an important public health problem and is stubbornly difficult to predict or prevent. A growing literature has emerged studying psychiatric conditions, such as depression and schizophrenia, and risk of arrhythmia and SCA.1–3 This field is challenging from an epidemiologic perspective, partly because of the rarity of SCA events in the general population without known heart disease and the potential confounding factors that may influence findings.4 For instance, there is increased recognition that treatments for mental illness may themselves raise cardiac risk

    Ibutilide Increases the Variability and Complexity of Atrial Fibrillation Electrograms: Antiarrhythmic Insights Using Signal Analyses

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    Introduction Intravenous ibutilide is used to convert atrial fibrillation (AF) to sinus rhythm (SR) due to its Class III antiarrhythmic mechanisms. However, the effects of ibutilide on local electrograms (EGMs) during AF have not been elucidated. Methods and Results We used EGM analysis techniques to characterize how ibutilide administration changes the frequency, morphology, and repeatability of AF EGM signals, thereby providing insight into ibutilide's antiarrhythmic mechanism of action. AF recordings were collected from 21 patients with AF, both before and after ibutilide administration. The effects of ibutilide on the following AF EGM parameters were assessed: (1) dominant frequency (DF), (2) variations in EGM amplitude and overall morphology, (3) repetition of EGM patterns, and (4) complexity of the AF frequency spectra. When comparing pre- versus post-ibutilide administration EGMs, DF decreased from 5.45 Hz to 4.02 Hz (P < 0.0001). There was an increase in the variability of both AF EGM amplitudes (P = 0.003) and overall AF EGM morphologies (P = 0.003). AF EGM pattern repetitiveness decreased (P = 0.01), and the AF frequency spectral profile manifested greater complexity (P = 0.02). Conclusions Novel EGM signal analysis techniques reveal that ibutilide administration causes increased complexity in the atrial electrical activation pattern with decreasing rate. These findings may be explained by the progressive destabilization of higher frequency, more homogeneous primary drivers of AF over the course of ibutilide administration, and/or less uniform propagation of atrial activation, until AF maintenance becomes more difficult and either transforms to atrial tachycardia or terminates to SR

    Global Psychological Distress and Risk of Atrial Fibrillation Among Women: The Women's Health Study

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    Background Symptoms of psychological distress and depression have been associated with risk of ventricular arrhythmias and sudden cardiac death. Their relationship with atrial arrhythmias, however, is less well studied. Methods and Results We sought to assess the long-term relations between psychological distress and risk of atrial fibrillation (AF) in the Women's Health Study of female health professionals. We measured psychological symptoms with the Mental Health Inventory-5. Incident AF was assessed annually and verified through medical records. Among 30 746 women without history of cardiovascular disease or AF, 771 cases of AF occurred during a median follow-up of 125 months (interquartile range, 117–130 months). Global psychological distress was not associated with AF risk in age-stratified (P=0.61 for linear trend) or multivariable proportional-hazards models that included antidepressant use (P=0.34). A proxy measure for depression, consisting of Mental Health Inventory-5 score <53, antidepressant use, or both, was also not associated with AF risk in multivariable models (hazard ratio=0.99; 95% confidence interval, 0.78–1.25; P=0.93). In post hoc analyses of individual symptoms from the Mental Health Inventory-5, positive affect, “feeling happy some/a good bit of the time,” was associated with reduced risk of AF (hazard ratio=0.69; 95% confidence interval, 0.49–0.99; P=0.04); other depressive and anxious symptoms were not. Conclusions In this prospective study of women without known cardiovascular disease, global psychological distress and specific depressive symptoms were unrelated to AF risk

    Depression and Risk of Sudden Cardiac Death and Coronary Heart Disease in Women Results From the Nurses' Health Study

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    ObjectivesWe assessed the association between depression and sudden cardiac death (SCD) and cardiac events among individuals without baseline coronary heart disease (CHD).BackgroundDepression is a risk factor for cardiac events and mortality among those with CHD, possibly from arrhythmia.MethodsWe studied depressive symptoms and a proxy variable for clinical depression consisting of severe symptoms and/or antidepressant medication use and their relationship to cardiac events in the Nurses' Health Study. Questionnaires in 1992, 1996, and 2000 assessed symptoms with the Mental Health Index (MHI-5), and antidepressant use was assessed in 1996 and 2000. Primary end points included SCD, fatal CHD, and nonfatal myocardial infarction.ResultsAmong 63,469 women without prior CHD/stroke in 1992, 7.9% had MHI-5 scores <53, previously found to predict clinical depression. Depressive symptoms were associated with CHD events, and the relationship was strongest for fatal CHD, where the association remained significant even after controlling for CHD risk factors (hazard ratio [HR]: 1.49; 95% confidence interval [CI]: 1.11 to 2.00 for MHI-5 score <53). In models from 1996 onward, our proxy variable for clinical depression was most associated with SCD in multivariable models (HR: 2.33, 95% CI: 1.47 to 3.70), and this risk was primarily due to a specific relationship between antidepressant use and SCD (HR: 3.34, 95% CI: 2.03 to 5.50).ConclusionsIn this cohort of women without baseline CHD, depressive symptoms were associated with fatal CHD, and a measure of clinical depression including antidepressant use was specifically associated with SCD. Although antidepressant use might be a marker of worse depression, its specific association with SCD merits further study
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