Introduction In response to the COVID-19 pandemic in Detroit, an earlier termination of resuscitation protocol was initiated in March 2020. To characterize pre-hospital cardiac arrest careduring COVID-19 in Detroit, we analyzed out-of-hospital cardiac arrest (OHCA) rate of ROSC (return of spontaneous circulation) and patient characteristics before and during the COVID-19 pandemic. Methods OHCA data was analyzed between March 10th, 2020 – April 30th,2020 and March 10th, 2019 – April 30th,2019. ROSC, patient demographics, arrest location, initial rhythms, bystander CPR and field termination were compared before and during the pandemic. Descriptive statistics were utilized to compare arrest characteristics between years, and the odds of achieving vs. not achieving ROSC. 2020 vs. 2019 as a predictor for ROSC was assessed with logistic regression. Results 471 patients were included. Arrests increased to 291 during the pandemic vs. 180 in 2019 (62% increase). Age (mean difference + 6; 95% CI: +2.4 to +9.5), arrest location (nursing home OR = 2.42; 95% CI: 1.42–4.31; public place OR = 0.47; 95% CI: 0.25–0.88), BLS response (OR = 0.68; 95% CI: 0.47–0.99), and field termination of resuscitation (OR = 2.36; 95% CI: 1.36–4.07) differed significantly in 2020 compared to 2019. No significant difference was found in the confounder-adjusted odds of ROSC in 2020 vs 2019 (OR = 0.61; 95% CI: 0.34–1.11). Conclusion OHCA increased by 62% during COVID-19 in Detroit, without a significant change in prehospital ROSC. The rate of ROSC remained similar despite the implementation of an early termination of resuscitation protocol in response to COVID-19.

Angiotensin-converting enzyme inhibitors (ACEi) are part of the indicated treatment in hypertensive African Americans. ACEi have blood pressure-independent effects that may make them preferred for certain patients. We aimed to evaluate the impact of ACEi on anti-fibrotic biomarkers in African American hypertensive patients with left ventricular hypertrophy (LVH). We conducted a post hoc analysis of a randomized controlled trial in which hypertensive African American patients with LVH and vitamin D deficiency were randomized to receive intensive antihypertensive therapy plus vitamin D supplementation or placebo. We selected patients who had detectable lisinopril (lisinopril group) in plasma using liquid-chromatography/mass spectrometry analysis and compared them to subjects who did not (comparison group) at the oneyear follow-up. The pro-fibrotic marker type 1 procollagen C-terminal propeptide (PICP) and the anti-fibrotic markers matrix metalloproteinase-1 (MMP-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), telopeptide of collagen type I (CITP), and N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) peptide were measured. Sixty-six patients were included, and the mean age was 46.2 ± 8 years. No difference was observed in the number and intensity of antihypertensive medications prescribed in each group. Patients with detectable lisinopril had lower blood pressure than those in the comparison group. The anti-fibrotic markers Ac-SDKP, MMP-1, and MMP-1/ TIMP-1 ratio were higher in patients with detectable ACEi (all p < .05). In a model adjusted for systolic blood pressure, MMP-1/TIMP-1 (p = .02) and Ac-SDKP (p < .001) levels were associated with lisinopril. We conclude that ACEi increase anti-fibrotic biomarkers in hypertensive African Americans with LVH, suggesting that they may offer added benefit over other agents in such patients.This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

ACEi are first line treatment in hypertension; however, there is controversy regarding the benefit over other antihypertensive drugs. ACEi have pressure independent effects that may make them preferable for certain patients. We aimed to evaluate the impact of ACEi on antifibrotic biomarkers in hypertensive patients with left ventricular hypertrophy (LVH). We conducted a post hoc analysis of a randomized controlled trial where hypertensive African American patients with LVH and vitamin D (VTD) deficiency were randomized to receive standard antihypertensive therapy plus VTD supplementation or placebo. We selected patients who had detectable lisinopril in plasma at one year follow-up and compared them to subjects who did not. The profibrotic marker propeptide of procollagen type I (CPIP) and the antifibrotic markers: matrix metalloproteinase-1 (MMP-1), tissue inhibitor of MMP1 (TIMP-1), the MMP-1/TIMP-1 ratio, telopeptide of collagen type I (CITP) and Ac-SDKP peptide were measured. Sixty six patients were included. Table 1 shows patients characteristics. Patients with lisinopril had lower blood pressure at one-year but no differences were observed in left ventricular mass index (LVMI). The antifibrotic markers Ac-SDKP (3.9±2.6 vs 6.3±2.8; p<0.001), MMP1 and MMP1/TIMP-1 ratio were higher in patients with detectable ACEi (all p<0.05). In a model adjusted for systolic blood pressure, low LVMI (p=0.01), MMP1/TIMP-1 (p=0.02) and Ac-SDKP (p<0.001) levels were associated with lisinopril. We conclude that ACEi increase antifibrotic biomarkers in African Americans with hypertension and LVH, suggesting that they may be offer added benefit over other agents in such patients.

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Isolated hyperglycinuria is a rare disorder that is associated with osteoporosis and renal calculi. We report findings in a middle-aged, black woman who presented for renal function evaluation with a history of transient hypobicarbonataemia associated with topiramate therapy. She displayed the full triad of high urinary glycine, early-onset osteopenia despite normal reproductive hormones, and renal calculus with high urinary oxalate, phosphate and uric acid. Parathyroid hormone and fibroblast growth factor 23 were both normal. Formal genetic testing did not reveal mutations in SLC6A20, SLC6A18, SLC6A19, SLC36A2, the known genes associated with glycinuria; however, black individuals are poorly represented in the genetic databases. It may well be that otherwise unidentified mutations may be present or that topiramate may result in a lingering proximal tubule defect even after cessation of the drug.