4,019 research outputs found

    A cortical potential reflecting cardiac function

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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

    Intergalactic Dust Extinction in Hydrodynamic Cosmological Simulations

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    Recently Menard et al. detected a subtle but systematic change in the mean color of quasars as a function of their projected separation from foreground galaxies, extending to comoving separations of ~10Mpc/h, which they interpret as a signature of reddening by intergalactic dust. We present theoretical models of this remarkable observation, using SPH cosmological simulations of a (50Mpc/h)^3 volume. Our primary model uses a simulation with galactic winds and assumes that dust traces the intergalactic metals. The predicted galaxy-dust correlation function is similar in form to the galaxy-mass correlation function, and reproducing the MSFR data requires a dust-to-metal mass ratio of 0.24, about half the value in the Galactic ISM. Roughly half of the reddening arises in dust that is more than 100Kpc/h from the nearest massive galaxy. We also examine a simulation with no galactic winds, which predicts a much smaller fraction of intergalactic metals (3% vs. 35%) and therefore requires an unphysical dust-to-metal ratio of 2.18 to reproduce the MSFR data. In both models, the signal is dominated by sightlines with E(g-i)=0.001-0.1. The no-wind simulation can be reconciled with the data if we also allow reddening to arise in galaxies up to several x 10^10 Msun. The wind model predicts a mean visual extinction of A_V ~0.0133 mag out to z=0.5, with a sightline-to-sightline dispersion similar to the mean, which could be significant for future supernova cosmology studies. Reproducing the MSFR results in these simulations requires that a large fraction of ISM dust survive its expulsion from galaxies and its residence in the intergalactic medium. Future observational studies that provide higher precision and measure the dependence on galaxy type and environment will allow detailed tests for models of enriched galactic outflows and the survival of IG dust.Comment: Matches version accepted by MNRA
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