Definition of Polypharmacy in Heart Failure: A Scoping Review of the Literature

Patients with heart failure (HF) have a high prevalence of polypharmacy, which can lead to drug interactions, cognitive impairment, and medication non-compliance. However, the definition of polypharmacy in these patients is still inconsistent. The aim of this scoping review was to find the most common definition of polypharmacy in HF patients. We conducted a scoping review searching Medline, Embase, CINAHL, and Cochrane using terms including polypharmacy, HF and deprescribing, which resulted in 7,949 articles. Articles without a definition of polypharmacy in HF patients and articles which included patients \u3c 18 years of age were excluded; only 59 articles were included. Of the 59 articles, 49% (n = 29) were retrospective, 20% (n = 12) were prospective, 10% (n = 6) were cross-sectional, and 27% (n = 16) were review articles. Twenty percent (n = 12) of the articles focused on HF with reduced ejection fraction, 10% (n = 6) focused on HF with preserved ejection fraction and 69% (n = 41) articles either focused on both diagnoses or did not clarify the specific type of HF. The most common cutoff for polypharmacy in HF was five medications (59%, n = 35). There was no consensus regarding the inclusion or exclusion of over-the-counter medications, supplements, or vitamins. Some newer studies used a cutoff of 10 medications (14%, n = 8), and this may be a more practical and meaningful definition for HF patients

Coronary Artery Calcium Score on Standard of Care Oncologic CT Scans for the Prediction of Adverse Cardiovascular Events in Patients With Non-Small Cell Lung Cancer Treated With Concurrent Chemoradiotherapy

INTRODUCTION: Chemoradiotherapy (CRT) has been associated with increased incidence of cardiovascular (CV) adverse events (CVAE). Coronary artery calcium scoring (CAC) has shown to predict coronary events beyond the traditional CV risk factors. This study examines whether CAC, measured on standard of care, non-contrast chest CT (NCCT) imaging, predicts the development of CVAE in patients with non-small cell lung cancer (NSCLC) treated with CRT. METHODS: Patients with NSCLC treated with CRT at MD Anderson Cancer Center from 7/2009 until 4/2014 and who had at least one NCCT scan within 6 months from their first CRT were identified. CAC scoring was performed on NCCT scans by an expert cardiologist and a cardiac radiologist following the 2016 SCCT/STR guidelines. CVAE were graded based on the most recent Common Terminology Criteria for Adverse Events (CTCAE) version 5.0. CVAE were also grouped into (i) coronary/vascular events, (ii) arrhythmias, or (iii) heart failure. All CVAE were adjudicated by a board-certified cardiologist. RESULTS: Out of a total of 193 patients, 45% were female and 91% Caucasian. Mean age was 64 ± 9 years and mean BMI 28 ± 6 kg/m DISCUSSION: Cardiovascular adverse events are frequent in patients with NSCLC treated with CRT. CAC calculated on standard of care NCCT can predict the development of CVAEs and specifically coronary/vascular events, as well as OS, independently from other traditional risk factors and radiation mean heart dose

CD11b activation suppresses TLR-dependent inflammation and autoimmunity in systemic lupus erythematosus

Genetic variations in the ITGAM gene (encoding CD11b) strongly associate with risk for systemic lupus erythematosus (SLE). Here we have shown that 3 nonsynonymous ITGAM variants that produce defective CD11b associate with elevated levels of type I interferon (IFN-I) in lupus, suggesting a direct link between reduced CD11b activity and the chronically increased inflammatory status in patients. Treatment with the small-molecule CD11b agonist LA1 led to partial integrin activation, reduced IFN-I responses in WT but not CD11b-deficient mice, and protected lupus-prone MRL/ Lpr mice from end-organ injury. CD11b activation reduced TLR-dependent proinflammatory signaling in leukocytes and suppressed IFN-I signaling via an AKT/FOXO3/IFN regulatory factor 3/7 pathway. TLR-stimulated macrophages from CD11B SNP carriers showed increased basal expression of IFN regulatory factor 7 (IRF7) and IFN-β, as well as increased nuclear exclusion of FOXO3, which was suppressed by LA1-dependent activation of CD11b. This suggests that pharmacologic activation of CD11b could be a potential mechanism for developing SLE therapeutics