Background-Atherosclerosis is an inflammatory disease in which interferon (IFN)-␥, the signature cytokine of Th1 cells, plays a central role. We investigated whether interleukin (IL)-17, the signature cytokine of Th17 cells, is also associated with human coronary atherosclerosis. Methods and Results-Circulating IL-17 and IFN-␥ were detected in a subset of patients with coronary atherosclerosis and in referent outpatients of similar age without cardiac disease but not in young healthy individuals. IL-17 plasma levels correlated closely with those of the IL-12/IFN-␥/CXCL10 cytokine axis but not with known Th17 inducers such as IL-1␤, IL-6, and IL-23. Both IL-17 and IFN-␥ were produced at higher levels by T cells within cultured atherosclerotic coronary arteries after polyclonal activation than within nondiseased vessels. Combinations of proinflammatory cytokines induced IFN-␥ but not IL-17 secretion. Blockade of IFN-␥ signaling increased IL-17 synthesis, whereas neutralization of IL-17 responses decreased IFN-␥ synthesis; production of both cytokines was inhibited by transforming growth factor-␤1. Approximately 10-fold fewer coronary artery-infiltrating T helper cells were IL-17 producers than IFN-␥ producers, and unexpectedly, IL-17/IFN-␥ double producers were readily detectable within the artery wall. Although IL-17 did not modulate the growth or survival of cultured vascular smooth muscle cells, IL-17 interacted cooperatively with IFN-␥ to enhance IL-6, CXCL8, and CXCL10 secretion. Conclusions-Our findings demonstrate that IL-17 is produced concomitantly with IFN-␥ by coronary arteryinfiltrating T cells and that these cytokines act synergistically to induce proinflammatory responses in vascular smooth muscle cells.

Among HF patients in sinus rhythm, higher LVEFs were associated with a linear decrease in mortality up to an LVEF of 45%. However, increases above 45% were not associated with further reductions in mortality.

In a cohort of outpatients with established HF, higher BMIs were associated with lower mortality risks; overweight and obese patients had lower risk of death compared with those at a healthy weight. Understanding the mechanisms and impact of the "obesity paradox" in patients with HF is necessary before recommendations are made concerning weight and weight control in this population.

Background : Patients hospitalized for severe COVID-19 infection are at risk for in-hospital cardiac arrest (IHCA). It is unknown whether certain characteristics of cardiac arrest care and outcomes of IHCAs during the COVID-19 pandemic differed compared to a pre-COVID-19 period. Methods : All patients who experienced an IHCA at our hospital from March 1st through May 15th 2020, during the peak of the COVID-19 pandemic, and those who had an IHCA from January 1st 2019 to December 31st 2019 were identified. All patient data was extracted from our hospital's Get With The Guidelines-Resuscitation (GWTG-R) registry, a prospective hospital-based archive of IHCA data. Baseline characteristics of patients, interventions and overall outcomes of IHCAs during the COVID-19 pandemic were compared to IHCAs in 2019, prior to the COVID-19 pandemic. Results : There were 125 IHCAs during a 2.5-month period at our hospital during the peak of the COVID-19 pandemic compared to 117 IHCAs in all of 2019. IHCAs during the COVID-19 pandemic occurred more often on general medicine wards than in intensive care units (46% vs 33%; 19% vs 60% in 2019, p<0.001), were overall shorter in duration (median time of 11 min (8.5-26.5) vs 15 min (7.0-20.0), p=0.001), led to fewer endotracheal intubations (52% vs 85%, p<0.001) and had overall worse survival rates (3% vs 13%, p=0.007) compared to IHCAs prior to the COVID-19 pandemic. Conclusions : Patients who experienced an IHCA during the COVID-19 pandemic had overall worse survival compared to those who had an IHCA prior to the COVID-19 pandemic. Our findings highlight important differences between these two time periods. Further study is needed on cardiac arrest care in patients with COVID-19.