Low HRV may act as an intermediary in this association. The present study examined to what extent depression and anxiety differently predict 24-h HRV indices recorded post-myocardial infarction (MI).

Method. Ninety-three patients were recruited during hospitalization for MI and assessed on self-reported symptoms of depression and anxiety. Two months post-MI, patients were assessed on clinical diagnoses of lifetime depressive and anxiety disorder. Adequate 24-h ambulatory electrocardiography data were obtained from 82 patients on average 78 days post-MI.

Results. In unadjusted analyses, lifetime diagnoses

of major depressive disorder was predictive of lower SDNN [standard deviation of all normal-to-normal (NN) intervals; beta VX-661 price = -0.26, p =0.022] and SDANN (standard deviation of all 5-min mean NN intervals; beta = 0.25, p = 0.023), and lifetime anxiety disorder of lower RMSSD (root mean square of successive differences; beta = -0.23, p = 0.039). Depression and anxiety symptoms did not significantly predict HRV. After adjustment for age, sex, cardiac history and multi-vessel disease, lifetime depressive disorder was no longer predictive of HRV. Lifetime anxiety disorder predicted reduced high-frequency spectral power (beta = -0.22, p = 0.039) and RMSSD beta = -0.25, p = 0.019), even after additional adjustment of anxiety symptoms.

Conclusions. Clinical anxiety, but not depression, negatively influenced parasympathetic

modulation of heart rate in post-MI patients. These findings elucidate the physiological mechanisms underlying anxiety as a risk factor for adverse outcomes, but also raise questions https://www.selleckchem.com/products/SB-203580.html about the potential role of HRV as an intermediary between depression and post-MI prognosis.”
“Despite growing interest in the molecular epidemiology of influenza virus, the pattern of viral

spread within individual communities remains poorly understood. To determine the phylogeography of influenza virus in a single population, we examined the spatial diffusion of H1N1/09 influenza A virus within the student body of the University of California, San Diego Tanespimycin concentration (UCSD), sampling for a 1-month period between October and November 2009. Despite the highly focused nature of our study, an analysis of complete viral genome sequences revealed between 24 and 33 independent introductions of H1N1/09 into the UCSD community, comprising much of the global genetic diversity in this virus. These data were also characterized by a relatively low level of on-campus transmission as well as extensive spatial mixing, such that there was little geographical clustering by either student residence or city ZIP code. Most notably, students experiencing illness on the same day and residing in the same dorm possessed phylogenetically distinct lineages. H1N1/09 influenza A virus is therefore characterized by a remarkable spatial fluidity, which is likely to impede community-based methods for its control, including class cancellations, quarantine, and chemoprophylaxis.