COVID-19 drive-through testing survey: Measuring the burden on healthcare workers.

Objective: To survey individuals who tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) at 1 of 4 Trinity Health of New England drive-through testing centers to assess their demographic information, hospitalization rate, preexisting conditions, possible routes of exposures, duration of symptoms, and subsequent household infections of healthcare workers (HCWs) when compared to non-HCWs. Methods: Data were collected via a telephone survey using a standardized script. Between March 1, 2020 and June 17, 2020, 28,903 people were tested at 4 Connecticut drive-through testing centers. Individuals who tested positive between March 16 and April 21, 2020 were randomly contacted. Of those individuals, 100 people agreed to complete the survey. Bivariate analysis and logistic regression were performed. Results: HCWs comprised 46% of the 100 survey respondents during the study period. Similarly, HCWs comprised 42.1% of all individuals who tested positive and listed an employer between March 1 and June 17, 2020. HCWs reported a longer duration of symptoms (17.39 vs 13.44 days) and were more likely to report work as their route of exposure (80.4% vs 27.8%) than non-HCWs. Conclusions: HCWs may face a disproportionate risk of contracting COVID-19 and self-report a longer duration of symptoms than the general public. The data suggest a need for an increased recovery time away from work than is currently recommended by the Centers for Disease Control and Prevention, as well as an increase in infection precautions for HCWs.

Renal Denervation Promotes Atherosclerosis in Hypertensive Apolipoprotein E-Deficient Mice Infused with Angiotensin II.

Objective: To determine the effect of renal denervation (RDN) on the severity of atherosclerosis and aortic aneurysm in hypertensive mice. Methods: Hypertension, atherosclerosis and aortic aneurysm were induced by subcutaneous infusion of angiotensin II (1 µg/kg/min) for 28 days in apolipoprotein E-deficient mice. RDN was conducted using combined surgical and local chemical denervation. The norepinephrine concentration in the kidney was measured by high-performance liquid chromatography. Blood pressure was measured by the tail-cuff method. Atherosclerosis was assessed by Sudan IV staining of the aortic arch. The aortic diameter was measured by the morphometric method. The mRNA expression of genes associated with atherosclerosis and aortic aneurysm were analyzed by quantitative PCR. Results: RDN decreased the median norepinephrine content in the kidney by 93.4% (n = 5-7, P = 0.003) 5 days after the procedure, indicating that the RDN procedure was successful. RDN decreased systolic blood pressure in apolipoprotein E-deficient mice. Mice that had RDN had more severe aortic arch atherosclerosis (median percentage of Sudan IV positive area: 13.2% in control mice, n = 12, and 25.4% in mice having RDN, n = 12, P = 0.028). The severity of the atherosclerosis was negatively correlated with the renal norepinephrine content (spearman r = -0.6557, P = 0.005). RDN did not affect the size of aortic aneurysms formed or the incidence of aortic rupture in mice receiving angiotensin II. RDN significantly increased the aortic mRNA expression of matrix metalloproteinase-2 (MMP-2). Conclusion: RDN promoted atherosclerosis in apolipoprotein E-deficient mice infused with angiotensin II associated with upregulation of MMP-2. The higher MMP-2 expression could be the results of the greater amount of atheroma in the RDN mice. The findings suggest further research is needed to assess potentially deleterious effects of RDN in patients.

CD4⁺CD25⁺Foxp3⁺ regulatory T cells suppress cardiac fibrosis in the hypertensive heart.

BACKGROUND: CD4⁺CD25⁺Foxp3⁺ regulatory T cells (Tregs) are potent inhibitors of inflammation and autoimmune diseases. Because inflammation has been associated with development of cardiac fibrosis in experimental hypertension, here we investigated whether adoptively transferred Tregs would inhibit development of cardiac fibrosis initiated by elevating blood pressure. METHODS: Cardiac fibrosis was induced in mice by constricting the aorta between the two carotid arteries. Immediately after the operation mice received either vehicle or purified, cultured Tregs (1.5 × 106). Fourteen days later we assessed effects on developing left ventricular fibrosis, blood pressure, inflammation, myofibroblasts and the transforming growth factor-beta1 (TGF-ß1) system. RESULTS: Fourteen days after aortic constriction, marked left-ventricular fibrosis was apparent and this was greatly reduced in mice receiving adoptively transferred Tregs. This reduction in fibrosis was associated with attenuated inflammatory cell numbers, reduced interstitial myofibroblast numbers and attenuated activity of the TGF-ß1 system, indicated by reductions in the expression of TGF-ß1 and its receptors activin-like kinase-5 and type II TGF-ß receptor. Adoptively transferred Tregs did not affect blood pressure and exerted only a small effect on left-ventricular hypertrophy. CONCLUSIONS: These data indicate that Tregs attenuate cardiac fibrosis associated with hypertensive heart disease by suppressing inflammation.