Effects of the COVID-19 pandemic on out-of-hospital cardiac arrest care in Detroit.

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.

Treatment and outcome variation in out-of-hospital cardiac arrest among four urban hospitals in Detroit.

AIMS: To determine whether out-of-hospital cardiac arrest (OHCA) post-resuscitation management and outcomes differ between four Detroit hospitals. INTRODUCTION: Significant variation exists in treatment/outcomes from OHCA. Disparities between hospitals serving a similar population is not well known. METHODS: Retrospective OHCA data was collected from the Detroit-Cardiac Arrest Registry (DCAR) between January 2014 to December 2019. Four hospitals were compared on two treatments (angiography, do not resuscitate (DNR)) and two outcomes (cerebral performance category (CPC) ≤ 2, in-hospital death). Models for death and CPC were tested with and without coronary angiography and DNR status. RESULTS: 999 patients at hospitals A - D differed (p < 0.05) before multivariable adjustment by age, race, witnessed arrest, dispatch-emergency department (ED) time, TTM, coronary angiography, DNR order, and in-hospital death. Rates of death and CPC ≤ 2 were worse in Hospital A (82.8%, 10%, respectively) compared to others (69.1%, 14.1%). After multivariable adjustment, Hospital A performed angiography less compared to B (OR = 0.17) and was more likely to initiate new DNR status than B (OR = 2.9), C (OR = 16.1), or D (OR = 3.6). CPC ≤ 2 were worse in Hospital A compared to B (OR = 0.27) and D (OR = 0.35). After sensitivity analysis, CPC ≤ 2 odds did not differ for A versus B (OR = 0.58, adjusted for angiography) or D (OR = 0.65, adjusted for DNR). Odds of death, despite angiography and DNR differences, were worse in Hospital A compared to B (OR = 1.87) and D (OR = 1.81). CONCLUSION: Differing rates of DNR and coronary angiography was associated with observed disparities in favorable neurologic outcome, but not death, between four Detroit hospitals.

Hyperglycinuria: diagnosis in middle age.

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.

Angiotensin-converting enzyme inhibitors increase anti-fibrotic biomarkers in African Americans with left ventricular hypertrophy.

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 one-year 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.