15 research outputs found

    Estimated detection rates for daily snapshot monitoring classified based on low/high CHADS<sub>2</sub> score and low/high AT/AF burden (n = 370).

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    <p>Estimated detection rates for daily snapshot monitoring classified based on low/high CHADS<sub>2</sub> score and low/high AT/AF burden (n = 370).</p

    Histogram of the patient’s AT/AF burden (n = 370).

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    <p>AT/AF burden was defined as the amount of time spent in AT/AF on a given day. Average AT/AF burden per day over the monitoring period (A), maximum daily AT/AF burden, defined as the single day with maximal burden over the monitoring period (B), and the percentage of days over the monitoring period that the patient experienced AT/AF (C) were determined for each of the 370 patients in the primary analysis and are shown as a histogram. Each bar in Fig 1A and 1B indicates the proportion of individuals who were assigned into the corresponding group divided by 1-hour interval of the aggregated AT/AF events among 370 patients. For example, the bar of 6 hours/day in Fig 1A indicates that the proportion of patients with an average AT/AF burden between 5 to 6 hours/day among the 370 patients was 0.5%.</p

    Atrial arrhythmia prevalence and characteristics for human immunodeficiency virus-infected persons and matched uninfected controls

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    <div><p>Background</p><p>Human Immunodeficiency Virus-Infected (HIV+) persons have elevated risks for various manifestations of cardiovascular disease (CVD). No studies to our knowledge have compared atrial fibrillation (AF) and atrial flutter (AFL) prevalence and associated characteristics for HIV+ persons and matched uninfected controls.</p><p>Methods and findings</p><p>Persons with diagnoses of HIV receiving care at a large urban academic medical center were frequency-matched 1:2 on age, sex, race, zip code, and clinic location with uninfected persons. Possible AF/AFL was screened for using administrative codes and diagnoses of AF/AFL were subsequently adjudicated using electrocardiography and physician notes; adjudication was performed given the inconsistent validity of administrative code-derived AF diagnoses found in previous studies. There were 101 confirmed AF/AFL cases (2.00%) among 5,052 HIV+ patients and 159 confirmed AF/AFL cases (1.57%) among 10,121 uninfected controls [Odds Ratio (OR) 1.27, 95% Confidence Interval (CI) 0.99–1.64; p = 0.056]. The association between HIV serostatus and AF/AFL was attenuated after adjustment for demographics and CVD risk factors. Among HIV+ persons, nadir CD4+ T cell count <200 cells/mm<sup>3</sup> was associated with approximately twofold elevated odds of AF/AFL even after adjustment for demographics and CVD risk factors (Multivariable-adjusted OR 1.98, 95% CI 1.21–3.25). There was no significant association between log<sub>10</sub> of peak HIV viral load and AF/AFL (Multivariable-adjusted OR 1.03, 95% CI 0.86–1.24). Older age, diabetes, hypertension, and chronic obstructive pulmonary disease were associated with similarly elevated odds of AF/AFL for HIV+ persons and uninfected controls.</p><p>Conclusion</p><p>HIV-related immunosuppression (nadir CD4 T cell count <200 cells/mm<sup>3</sup>) and traditional CVD risk factors are associated with significantly elevated odds of AF/AFL among HIV+ persons. Although atrial fibrillation and flutter was more common among HIV+ versus uninfected persons in this cohort, this difference was attenuated by adjustment for demographics and CVD risk factors.</p></div

    A Targeted, Differential Top-Down Proteomic Methodology for Comparison of ApoA‑I Proteoforms in Individuals with High and Low HDL Efflux Capacity

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    Top-down proteomics (TDP) allows precise determination/characterization of the different proteoforms derived from the expression of a single gene. In this study, we targeted apolipoprotein A-I (ApoA-I), a mediator of high-density-lipoprotein cholesterol efflux (HDL-E), which is inversely associated with coronary heart disease risk. Absolute ApoA-I concentration and allelic variation only partially explain interindividual HDL-E variation. Therefore, we hypothesize that differences in HDL-E are associated with the abundances of different ApoA-I proteoforms. Here, we present a targeted TDP methodology to characterize ApoA-I proteoforms in serum samples and compare their abundances between individuals. We characterized 18 ApoA-I proteoforms using selected-ion monitoring coupled to electron-transfer dissociation mass spectrometry. We then compared the abundances of these proteoforms between two groups of four participants, representing the individuals with highest and lowest HDL-E values within the Chicago Healthy Aging Study (<i>n</i> = 420). Six proteoforms showed significantly (<i>p</i> < 0.0005) higher intensity in high HDL-E individuals: canonical ApoA-I [fold difference (fd) = 1.17], carboxymethylated ApoA-I (fd = 1.24) and, with highest difference, four fatty acylated forms: palmitoylated (fd = 2.16), oleoylated (fd = 2.08), arachidonoylated (fd = 2.31) and one bearing two modifications: palmitoylation and truncation (fd = 2.13). These results demonstrate translational potential for targeted TDP in revealing, with high sensitivity, associations between interindividual proteoform variation and physiological differences underlying disease risk

    Relative risk reductions by blood pressure-lowering treatment, according to CVD risk and SBP treatment strategies.

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    <p>Hazard ratios of major cardiovascular events by blood pressure-lowering treatment, as a function of number of persons and proportion of sample treated using a CVD risk strategy (in green) and an SBP strategy (in red). Numbers associated with each curve represent the specific CVD risk level (percentage 5-y CVD risk) or SBP (mmHg) at the treatment threshold. Hazard ratios determined from persons above each treatment threshold. CVD, cardiovascular disease; SBP, systolic blood pressure.</p
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