Background: Unplanned readmissions after hospitalization for acute myocardial infarction (AMI) are among the leading causes of preventable morbidity, mortality, and healthcare costs. Digital health interventions (DHI) could be an effective tool in promoting self-management, adherence to guideline-directed therapy, and cardiovascular risk reduction. A DHI developed at Johns Hopkins-the Corrie Health Digital Platform (Corrie)-includes the first cardiology Apple CareKit smartphone application, which is paired with an Apple Watch and iHealth Bluetoothenabled blood pressure cuff. Corrie targets: (1) self-management of cardiac medications, (2) self-*

No abstract

Background Galectin-3, a beta-galactoside binding lectin involved in important regulatory roles in adhesion, inflammation, immunity, and fibrosis, may be relevant to atrial fibrillation (AF) etiology. Methods We included 8,436 participants free of AF at baseline (1996–98) and with measures of plasma galectin-3 from the Atherosclerosis Risk in Communities (ARIC) study. We ascertained incident AF through 2013 from study visit ECGs, hospitalizations and death certificates. Multivariable Cox proportional hazards models, adjusted for AF risk factors plus incident HF and CHD, were used to estimate hazard ratios for the association between galectin-3 and incident AF. Results The mean age (SD) of participants was 62.6 (5.6) years and was comprised of 58.7% women and 21.2% blacks. During a median follow-up of 15.7 years, 1,185 incident cases of AF were observed. After adjusting for AF risk factors, participants with galectin-3 levels ≥ 90th percentile (19.5 ng/mL) had a significantly higher risk of incident AF when compared to the lowest quartile (4.4 – 11.9 ng/mL), with hazard ratios (95% confidence interval) of 1.40 (1.04 – 1.89) for the 90th – <95th percentile and 1.51 (1.11 – 2.06) for the 95th – 100th percentile. This association was attenuated and no longer statistically significant after accounting for incident CHD and HF as time dependent variables. Conclusions Elevated plasma galectin-3 is associated with increased risk of incident AF. Galectin-3 may increase AF risk via pathways involving CHD and HF.

Resting heart rate (RHR) is independently associated with cardiovascular disease (CVD) risk. We determined whether RHR, measured in mid-life, is also associated with cognitive decline. We studied 13,720 middle-aged white and black ARIC participants without a prior history of stroke or atrial fibrillation. RHR was obtained from a 12-lead resting electrocardiogram at the baseline visit (1990)(1991)(1992) and categorized into groups as <60 (reference), 60-69, 70-79 and ≥80 bpm. Cognitive scores were obtained at baseline and at up to two additional visits (1996-1998 and 2011-2013). The primary outcome was a global composite cognitive score (Z-score) derived from 3 tests: delayed word recall, digit symbol substitution, and word fluency. The associations of RHR with

Self-collection methods are a viable option for collecting samples for STI testing in adult men based on their high feasibility, acceptability, and validity. Implementation of self-collection procedures in STI testing venues should be performed to expand opportunities for STI detection and treatment.

CVD ancillary study, was involved in the CT data collection, and provided critical revisions to the paper. Dr. Budoff interpreted the cardiac CT scans for the study (CT Core Lab) and provided critical revisions to the paper. Dr. Otvos provided the GlycA measurements and provided critical revisions to the paper. Drs. Zhao, Brown, Guallar, Palella, Martinson, Akinkuolie, Haberlen, and Mora provided critical revisions to the paper. Dr. Michos, Fashanu, and Tibuakuu take full responsibility for its content. All authors reviewed the final draft and approve of its submission. The manuscript was also approved by the MACS Executive Committee. Disclosures: Dr. Brown has served as a consultant to Gilead Sciences, Merck, BMS, EMD-Serono, and Theratechnologies. Dr. Budoff has received research funds from GE Healthcare. Dr. Otvos is employed by LabCorp (formally LipoScence). Dr. Mora has received research grant support from Atherotech Diagnostics, and has received consulting fees from Quest Diagnostics for work outside the current study. Dr. Mora has a patent application on the use of GlycA for predicting risk of colorectal cancer. No other authors report any conflicts.

No abstract

Background: GlycA, a nuclear magnetic resonance composite marker of systemic inflammation, reflects serum concentration and glycosylation state of main acute phase reactants. Prior studies have shown plasma GlycA levels were associated with cardiovascular disease even after adjusting for other inflammatory markers. However, little is known about the association of GlycA with the heart failure (HF) subtypes: heart failure with preserved ejection fraction (HFpEF) or heart failure with reduced ejection fraction. We examined the association of GlycA with incident HF and its subtypes in a multiethnic cohort. Methods: We studied 6507 Multi-Ethnic Study of Atherosclerosis participants aged 45 to 84 without baseline cardiovascular disease or HF who had data on GlycA and incident hospitalized HF. We used multivariable-adjusted Cox hazards models to evaluate the association of GlycA with incident total HF, HFpEF, and heart failure with reduced ejection fraction. Models were adjusted for sociodemographics, cardiovascular disease risk factors, and inflammatory biomarkers. Results: The mean (SD) for age was 62 (10) years and for GlycA was 375 (82) μmol/L; 53% women. Over a median follow-up of 14.0 years, participants in the highest quartile of GlycA, compared with the lowest, experienced increased risk of developing any HF (hazard ratio, 1.48 [95% CI, 1.01–2.18]) in fully adjusted models. However, this increased risk was only seen for HFpEF (2.18 [1.15–4.13]) and not heart failure with reduced ejection fraction [1.06 (0.63–1.79)]. There was no significant interaction by sex, age, or race/ethnicity. Conclusions: GlycA was associated with an increased risk of any HF, and in particular, HFpEF. Future studies should examine mechanisms that might explain differential association of GlycA with HF subtypes, and whether therapeutic lowering of GlycA can prevent HFpEF development. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00005487.