Multiple COVID-19 Clusters on a University Campus - North Carolina, August 2020.

Preventing transmission of SARS-CoV-2, the virus that causes coronavirus disease 2019 (COVID-19), in institutes of higher education presents a unique set of challenges because of the presence of congregate living settings and difficulty limiting socialization and group gatherings. Before August 2020, minimal data were available regarding COVID-19 outbreaks in these settings. On August 3, 2020, university A in North Carolina broadly opened campus for the first time since transitioning to primarily remote learning in March. Consistent with CDC guidance at that time (1,2), steps were taken to prevent the spread of SARS-CoV-2 on campus. During August 3-25, 670 laboratory-confirmed cases of COVID-19 were identified; 96% were among patients aged <22 years. Eighteen clusters of five or more epidemiologically linked cases within 14 days of one another were reported; 30% of cases were linked to a cluster. Student gatherings and congregate living settings, both on and off campus, likely contributed to the rapid spread of COVID-19 within the university community. On August 19, all university A classes transitioned to online, and additional mitigation efforts were implemented. At this point, 334 university A-associated COVID-19 cases had been reported to the local health department. The rapid increase in cases within 2 weeks of opening campus suggests that robust measures are needed to reduce transmission at institutes of higher education, including efforts to increase consistent use of masks, reduce the density of on-campus housing, increase testing for SARS-CoV-2, and discourage student gatherings.

Worsening Renal Function during Management for Chronic Heart Failure with Reduced Ejection Fraction: Results From the Pro-BNP Outpatient Tailored Chronic Heart Failure Therapy (PROTECT) Study.

OBJECTIVES: To assess prognostic meaning of worsening renal failure (WRF) occurring during management of chronic heart failure (HF) with reduced ejection fraction. BACKGROUND: When WRF develops during titration of HF medical therapy, it commonly leads to less aggressive care. METHODS: A total of 151 patients enrolled in a prospective, randomized study of standard of care (SOC) HF therapy versus SOC plus a goal N-terminal pro-B type natriuretic peptide (NT-proBNP) < 1000 pg/mL were examined. Cardiovascular (CV) event (defined as worsening HF, hospitalization for HF, significant ventricular arrhythmia, acute coronary or cerebral ischemia, or CV death) at 1 year relative to WRF (defined as any reduction in estimated glomerular filtration rate) 90 days postenrollment were tabulated. RESULTS: Those developing WRF by 3 months had an average 14% reduction in estimated glomerular filtration rate. There was no difference in incidence of WRF between study arms (43% in SOC, 57% in NT-proBNP, P = .29). During the first 3 months of therapy titration, incident WRF was associated with numerically fewer CV events at 1 year compared with those without WRF (mean 0.81 vs 1.16 events, P = .21). WRF was associated trend toward fewer CV events in the SOC arm (hazard ratio 0.45, 95% confidence interval 0.16-1.24, P = .12); the NT-proBNP-guided arm had numerically lower CV event rates regardless of WRF. Subjects with NT-proBNP <1000 pg/mL and WRF received higher doses of guideline directed medical therapies, lower doses of loop diuretics, and had significantly lower CV event rates (P < .001). CONCLUSIONS: Modest degrees of WRF are common during aggressive HF with reduced ejection fraction management, but we found no significant association with CV outcomes. HF care guided by NT-proBNP was not associated with more WRF compared with SOC, and led to benefit regardless of final renal function.

Incident Type 2 Myocardial Infarction in a Cohort of Patients Undergoing Coronary or Peripheral Arterial Angiography.

BACKGROUND: Despite growing recognition of type 2 myocardial infarction (T2MI; related to supply/demand mismatch), little is known about its risk factors or its association with outcome. METHODS: A single-center cohort of patients undergoing coronary or peripheral angiography with or without intervention was prospectively enrolled and followed for incident type 1 and T2MI, and major adverse cardiovascular events (MACE, a composite of all-cause death, nonfatal myocardial infarction [MI], heart failure, stroke, transient ischemic attack, peripheral arterial complication, and cardiac arrhythmia), as well. T2MI was adjudicated using criteria from the Third Universal Definition of MI. Baseline characteristics, blood samples, and angiography information were obtained. Major end points subsequent to first MI were assessed using landmark analyses to compare the rates of first events only where everyone with a prior history of any MACE before MI were censored and adjusted for follow-up times. Cox proportional hazard models were used for time-to-event analyses with age and sex forced into all models and additional covariates evaluated by using the stepwise option for the selection. RESULTS: One thousand two hundred fifty-one patients were enrolled and followed for a median of 3.4 years. Of these patients, 152 (12.2%) had T2MI during follow-up; T2MI was frequently recurrent. Multivariable predictors of T2MI were older age, lower systolic blood pressure, history of coronary artery disease, heart failure, chronic obstructive pulmonary disease, diabetes mellitus, nitrate use, and elevated concentrations of glucose, N-terminal pro-B type natriuretic peptide, and cystatin C. Patients with T2MI had higher rates of subsequent adverse events than those without T2MI (per 100 person-years: MACE, 53.7 versus 21.1, P<0.001; all-cause death, 23.3 versus 3.3, P<0.001; cardiovascular death, 17.5 versus 2.6, P<0.001; heart failure events, 22.4 versus 7.4, P<0.001); these rates are similar to those seen in patients with type 1 MI. Incident diagnosis of T2MI strongly predicted risk for subsequent MACE (adjusted hazard ratio, 1.90; 95% confidence interval, 1.46-2.48; P<0.001), all-cause death (adjusted hazard ratio, 2.96; 95% confidence interval, 2.01-4.36; P<0.001), and cardiovascular death (adjusted hazard ratio, 2.16; 95% confidence interval, 1.36-3.43; P=0.001). CONCLUSIONS: T2MI is common and associated with poor prognosis. Studies evaluating treatment strategies for management of T2MI are needed. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00842868.

Clinical Interventions to Reduce Preventable Hospital Readmission After Percutaneous Coronary Intervention.

Hospital readmissions are common and costly and, in some cases, may be related to problems with care processes. We sought to reduce readmissions after percutaneous coronary intervention (PCI) in a large tertiary care facility through programs to target vulnerabilities predischarge, after discharge, and during re-presentation to the emergency department. During initial hospitalization, we assessed patients' readmission risk with a validated risk score and used a discharge checklist to ensure access to appropriate medications and close follow-up for high-risk patients. We also developed patient education videos about chest discomfort and heart failure. After discharge, we established a new follow-up clinic with cardiology fellows. A computerized system was developed to automatically notify cardiologists when patients presented to the emergency department within 30 days of PCI to enhance patient access to cardiology care in the emergency department. Early cardiologist assessment and assistance with triage was encouraged, and the emergency department used a risk stratification algorithm derived from a local database of patients to triage patients presenting with chest discomfort after PCI. We tracked the number of patients readmitted after PCI to our hospital. With our interventions, from 2011 to 2015, the index hospital readmission rate has declined from 9.6% to 5.3%. This program could provide tangible structural changes that can be implemented in other healthcare centers, both reducing the cost of care and improving the quality of care for patients with PCI.

The Importance of Worsening Heart Failure in Ambulatory Patients: Definition, Characteristics, and Effects of Amino-Terminal Pro-B-Type Natriuretic Peptide Guided Therapy.

OBJECTIVES: The goal of this study was to define and assess the significance of worsening heart failure (WHF) in patients with chronic ambulatory heart failure with reduced ejection fraction (HFrEF). BACKGROUND: WHF has been identified as a potentially relevant clinical event in patients with acute heart failure (HF) and is increasingly used as an endpoint in clinical trials. No standardized definition of WHF exists. It remains uncertain how WHF relates to risk for other HF events or how treatment may affect WHF. METHODS: A total of 151 symptomatic patients with chronic HFrEF were randomized to standard of care HF management or a goal to lower N-terminal pro-B-type natriuretic peptide (NT-proBNP) concentrations ≤1,000 pg/ml in addition to standard of care. WHF was prospectively defined as: 1) new or progressive symptoms and/or signs of decompensated HF; and 2) unplanned intensification of diuretic therapy. RESULTS: Over a mean follow-up of 10 months, 45 subjects developed WHF. At baseline, patients developing incident WHF had higher ejection fraction (31% vs. 25%; p = 0.03), were more likely to have jugular venous distension and edema (p < 0.02), were less likely to receive angiotensin-converting enzyme inhibitors or received these agents at lower doses (p < 0.04), and also received higher loop diuretic doses (p < 0.001). Occurrence of WHF was strongly associated with subsequent HF hospitalization/cardiovascular death (hazard ratio, landmark analysis: 18.8; 95% confidence interval: 5.7 to 62.5; p < 0.001). NT-proBNP-guided care reduced the incidence of WHF in adjusted analyses (hazard ratio: 0.52; p = 0.06) and improved event-free survival (log-rank test p = 0.04). CONCLUSIONS: In chronic HFrEF, WHF was associated with substantial risk for morbidity and mortality. NT-proBNP-guided care reduced risk for WHF.

Biomarcadores en la insuficiencia cardiaca aguda / Biomarkers in acute heart failure

La asistencia de los pacientes con descompensación aguda de la insuficiencia cardiaca está cambiando gracias a la disponibilidad y el conocimiento de varios nuevos biomarcadores de la insuficiencia y otros que están apareciendo. Los patrones de referencia como biomarcadores en la insuficiencia cardiaca son el péptido natriurético tipo B y la fracción aminoterminal del propéptido natriurético tipo B, que desempeñan un papel importante en el diagnóstico, el pronóstico y el tratamiento de la insuficiencia cardiaca aguda descompensada. Los nuevos biomarcadores que se relacionan de manera creciente con los procesos de lesión miocárdica, activación neurohormonal y remodelado ventricular son prometedores para mejorar el diagnóstico y el pronóstico de los pacientes con insuficiencia cardiaca aguda descompensada. Entre ellos se encuentran la región media del propéptido natriurético auricular, la ST2 soluble, la galectina-3, la troponina de alta sensibilidad y la región media de proadrenomedulina. También se ha asistido a la aparición de biomarcadores para la evaluación de la insuficiencia cardiaca aguda descompensada que facilitan el diagnóstico diferencial de la disnea, como la procalcitonina (para la identificación de la neumonía aguda), así como de marcadores que predicen las complicaciones de la insuficiencia cardiaca aguda descompensada, como son los marcadores de la lesión renal. En este artículo se examina la fisiopatología y la utilidad de los biomarcadores establecidos y los nuevos biomarcadores surgidos para el diagnóstico clínico, el pronóstico y el tratamiento de la insuficiencia cardiaca aguda descompensada (AU)

The care of patients with acutely decompensated heart failure is being reshaped by the availability and understanding of several novel and emerging heart failure biomarkers. The gold standard biomarkers in heart failure are B–type natriuretic peptide and N-terminal pro-B-type natriuretic peptide, which play an important role in the diagnosis, prognosis, and management of acute decompensated heart failure. Novel biomarkers that are increasingly involved in the processes of myocardial injury, neurohormonal activation, and ventricular remodeling are showing promise in improving diagnosis and prognosis among patients with acute decompensated heart failure. These include midregional proatrial natriuretic peptide, soluble ST2, galectin–3, highly–sensitive troponin, and midregional proadrenomedullin. There has also been an emergence of biomarkers for evaluation of acute decompensated heart failure that assist in the differential diagnosis of dyspnea, such as procalcitonin (for identification of acute pneumonia), as well as markers that predict complications of acute decompensated heart failure, such as renal injury markers. In this article, we will review the pathophysiology and usefulness of established and emerging biomarkers for the clinical diagnosis, prognosis, and management of acute decompensated heart failure (AU)

Biomarkers in acute heart failure.

The care of patients with acutely decompensated heart failure is being reshaped by the availability and understanding of several novel and emerging heart failure biomarkers. The gold standard biomarkers in heart failure are B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide, which play an important role in the diagnosis, prognosis, and management of acute decompensated heart failure. Novel biomarkers that are increasingly involved in the processes of myocardial injury, neurohormonal activation, and ventricular remodeling are showing promise in improving diagnosis and prognosis among patients with acute decompensated heart failure. These include midregional proatrial natriuretic peptide, soluble ST2, galectin-3, highly-sensitive troponin, and midregional proadrenomedullin. There has also been an emergence of biomarkers for evaluation of acute decompensated heart failure that assist in the differential diagnosis of dyspnea, such as procalcitonin (for identification of acute pneumonia), as well as markers that predict complications of acute decompensated heart failure, such as renal injury markers. In this article, we will review the pathophysiology and usefulness of established and emerging biomarkers for the clinical diagnosis, prognosis, and management of acute decompensated heart failure.

Chronic psychosocial stressors and salivary biomarkers in emerging adults.

We investigated whole saliva as a source of biomarkers to distinguish individuals who have, and who have not, been chronically exposed to severe and threatening life difficulties. We evaluated RNA and DNA metrics, expression of 37 candidate genes, and cortisol release in response to the Trier Social Stress Test, as well as clinical characteristics, from 48 individuals stratified on chronic exposure to psychosocial stressors within the last year as measured by the Life Events and Difficulties Schedule. Candidate genes were selected based on their differential gene expression ratio in circulating monocytes from a published genome-wide analysis of adults experiencing different levels of exposure to a chronic stressor. In univariate analyses, we observed significantly decreased RNA integrity (RIN) score (P = 0.04), and reduced expression of glucocorticoid receptor-regulated genes (Ps < 0.05) in whole saliva RNA from individuals exposed to chronic stressors, as compared to those with no exposure. In those exposed, we observed significantly decreased BMI (P < 0.001), increased ever-smoking and increased lifetime alcohol abuse or dependence (P ≤ 0.03), and a reduction of cortisol release. In post hoc multivariate analyses including clinical and biospecimen-derived variables, we consistently observed significantly decreased expression of IL8 (Ps<0.05) in individuals exposed, with no significant association to RIN score. Alcohol use disorders, tobacco use, a reduced acute stress response and decreased salivary IL8 gene expression characterize emerging adults chronically exposed to severe and threatening psychosocial stressors.