A Multicenter Evaluation of Survival After In-Hospital Cardiac Arrest in Coronavirus Disease 2019 Patients.

IMPORTANCE: In-hospital cardiac arrest survival among coronavirus disease 2019 patients has been reported to range from 0% to 12%. These numbers are significantly lower than reported prepandemic in-hospital cardiac arrest survival rates of approximately 20-25% in the United States for non-coronavirus disease 2019 patients. OBJECTIVE: To assess the incidence of in-hospital cardiac arrest survival of coronavirus disease 2019 patients. DESIGN: A retrospective cohort study of adult patients with coronavirus disease 2019 subsequently found to have in-hospital cardiac arrest and underwent cardiopulmonary resuscitation (cardiopulmonary resuscitation). SETTING: Multiple hospitals of the Cleveland Clinic Health System. PATIENTS: All adult patients (age ≥ 18 yr) admitted to Cleveland Clinic Health System with a diagnosis of coronavirus disease 2019 who experienced in-hospital cardiac arrest requiring cardiopulmonary resuscitation. MEASUREMENTS AND MAIN RESULTS: From March 01, 2020 to October 15, 2020, 3,555 patients with coronavirus disease 2019 were hospitalized; 1,372 were admitted to the ICU; 58 patients had in-hospital cardiac arrest. Median age of this cohort was 66.5 years (interquartile range, 55.0-76.0 yr). Patients were predominantly male (62.5%), White (53.4%), with a median body mass index of 29.7 (interquartile range, 25.8-34.6). Most in-hospital cardiac arrests were in critical care environments (ICU), 51 of 58 (87.9%); seven of 58 (12.1%) were on ward locations. Thirty-four of 58 patients (58.6%) were on mechanical ventilation prior to in-hospital cardiac arrest with a median duration of mechanical ventilation of 9 days (interquartile range, 2-18 d). Twenty-four of 58 patients (44%) were on vasopressors prior to arrest. Initial arrest rhythm was pulseless electrical activity at (63.8%), asystole (29.3%), and pulseless ventricular tachycardia/fibrillation (6.9%). Of the 58 patients, 35 (60.3%) attained return of spontaneous circulation, and 13 of 58 (22.4%) were discharged alive. CONCLUSIONS: We report a 22% survival to discharge after in-hospital cardiac arrest in coronavirus disease 2019 patients, a survival rate similar to before the coronavirus disease 2019 pandemic.

CSF lipocalin-2 increases early in subarachnoid hemorrhage are associated with neuroinflammation and unfavorable outcome.

Lipocalin-2 mediates neuro-inflammation and iron homeostasis in vascular injuries of the central nervous system (CNS) and is upregulated in extra-CNS systemic inflammation. We postulate that cerebrospinal fluid (CSF) and blood lipocalin-2 levels are associated with markers of inflammation and functional outcome in subarachnoid hemorrhage (SAH). We prospectively enrolled 67 SAH subjects, serially measured CSF and plasma lipocalin-2, matrix metallopeptidase 9 (MMP-9), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) on post-SAH days 1-5 and assessed outcome by modified Rankin Scale (mRS) every 3 months. Unfavorable outcome is defined as mRS > 2. Twenty non-SAH patients undergoing lumbar drain trial were enrolled as controls. Lipocalin-2 was detectable in the CSF and significantly higher in SAH compared to controls (p < 0.0001). Higher CSF LCN2 throughout post-SAH days 1-5 was associated with unfavorable outcome at 3 (p = 0.0031) and 6 months (p = 0.014). Specifically, higher CSF lipocalin-2 on post-SAH days 3 (p = 0.036) and 5 (p = 0.016) were associated with unfavorable 3-month outcome. CSF lipocalin-2 levels positively correlated with CSF IL-6, TNF-α and MMP-9 levels. Higher plasma lipocalin-2 levels over time were associated with worse 6-month outcome. Additional studies are required to understand the role of lipocalin-2 in SAH and to validate CSF lipocalin-2 as a potential biomarker for SAH outcome.

Does inpatient hyperglycemia predict a worse outcome in COVID-19 intensive care unit patients?

BACKGROUND: We undertook this study to evaluate the association between hyperglycemia and outcomes in patients with coronavirus disease 2019 (COVID-19) admitted to the intensive care unit (ICU). METHODS: We conducted a multicenter retrospective study involving all adults with COVID-19 admitted to the ICU between March and May 2020. Patients were divided into normoglycemic (average blood glucose <140 mg/dL) and hyperglycemic (average blood glucose ≥140 mg/dL) groups. Outcomes such as mortality, need and duration of mechanical ventilation, and length of hospital and ICU stays were measured. RESULTS: Among 495 patients, 58.4% were male with a median age of 68 years (interquartile range [IQR]: 58.00-77.00), and baseline average blood glucose was 186.6 (SD ± 130.8). Preexisting diabetes was present in 35.8% of the studied cohort. Combined ICU and hospital mortality rates were 23.8%; mortality and mechanical ventilation rates were significantly higher in the hyperglycemic group with 31.4% vs 16.6% (P = .001) and 50.0% vs 37.2% (P = .004), respectively. Age above 60 years (hazard ratio [HR] 3.21; 95% CI 1.78, 5.78) and hyperglycemia (HR 1.79; 95% CI 1.14, 2.82) were the only significant predictors of in-hospital mortality. Increased risk for hyperglycemia was found in patients with steroid use (odds ratio [OR] 1.521; 95% CI 1.054, 2.194), triglycerides ≥150 mg/dL (OR 1.62; 95% CI 1.109, 2.379), and African American race (OR 0.79; 95% CI 0.65, 0.95). CONCLUSIONS: Hyperglycemia in patients with COVID-19 is significantly associated with a prolonged ICU length of stay, higher need of mechanical ventilation, and increased risk of mortality in the critical care setting. Tighter blood glucose control (≤140 mg/dL) might improve outcomes in COVID-19 critically ill patients; evidence from ongoing clinical trials is needed.

Systemic inflammation in hemorrhagic strokes - A novel neurological sign and therapeutic target?

Growing evidences suggest that stroke is a systemic disease affecting many organ systems beyond the brain. Stroke-related systemic inflammatory response and immune dysregulations may play an important role in brain injury, recovery, and stroke outcome. The two main phenomena in stroke-related peripheral immune dysregulations are systemic inflammation and post-stroke immunosuppression. There is emerging evidence suggesting that the spleen contracts following ischemic stroke, activates peripheral immune response and this may further potentiate brain injury. Whether similar brain-immune crosstalk occurs in hemorrhagic strokes such as intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH) is not established. In this review, we systematically examined animal and human evidence to date on peripheral immune responses associated with hemorrhagic strokes. Specifically, we reviewed the impact of clinical systemic inflammatory response syndrome (SIRS), inflammation- and immune-associated biomarkers, the brain-spleen interaction, and cellular mediators of peripheral immune responses to ICH and SAH including regulatory T cells (Tregs). While there is growing data suggesting that peripheral immune dysregulation following hemorrhagic strokes may be important in brain injury pathogenesis and outcome, details of this brain-immune system cross-talk remain insufficiently understood. This is an important unmet scientific need that may lead to novel therapeutic strategies in this highly morbid condition.

Association of Short Sleep Duration and Atrial Fibrillation.

BACKGROUND: Short sleep may be a risk factor for atrial fibrillation. However, previous investigations have been limited by lack of objective sleep measurement and small sample size. We sought to determine the association between objectively measured sleep duration and atrial fibrillation. METHODS: All 31,079 adult patients undergoing diagnostic polysomnography from 1999 to 2015 at multiple sites within a large hospital network were identified from electronic medical records. Prevalent atrial fibrillation was identified by continuous ECG during polysomnography. Incident atrial fibrillation was identified by diagnostic codes and 12-lead ECGs. Logistic regression and Cox proportional hazards modeling were used to examine the association of sleep duration and atrial fibrillation prevalence and incidence, respectively, adjusting for age, sex, BMI, hypertension, coronary artery disease, cerebrovascular disease, peripheral vascular disease, heart failure, and sleep apnea severity. RESULTS: We identified 404 cases of prevalent atrial fibrillation among 30,061 individuals (mean age ± SD, 51.0 ± 14.5 years; 51.6% women) undergoing polysomnography. After adjustment, each 1-h reduction in sleep duration was associated with a 1.17-fold (95% CI, 1.11-1.30) increased risk of prevalent atrial fibrillation. Among 27,589 patients without atrial fibrillation at baseline, we identified 1,820 cases of incident atrial fibrillation over 4.6 years median follow-up. After adjustment, each 1-h reduction in sleep duration was associated with a 1.09-fold (95% CI, 1.05-1.13) increased risk for incident atrial fibrillation. CONCLUSIONS: Short sleep duration is independently associated with prevalent and incident atrial fibrillation. Further research is needed to determine whether interventions to extend sleep can lower atrial fibrillation risk.

Lipoprotein-associated phospholipase A2 and its relationship with markers of subclinical cardiovascular disease: A systematic review.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is an enzyme that exhibits proinflammatory properties and has been associated with subclinical cardiovascular disease. OBJECTIVE: The relationship between Lp-PLA2 and subclinical CVD remains unclear. The goal of this systematic review was to clarify this relationship. METHODS: An extensive literature search of the MEDLINE database using Ovid and PubMed was performed. From an initial search of 444 articles, 13 met the inclusion and exclusion criteria and were included in the review. RESULTS: Of the 13 studies included in the review, 6 examined the relationship between Lp-PLA2 and coronary artery calcification, of which 3 showed a significant correlation. Two studies examined the relationship between Lp-PLA2 and endothelial dysfunction, and 1 reported a significant relationship. Five studies investigated the association of Lp-PLA2 with carotid intima-media thickness (CIMT), and 3 reported a significant relationship. CONCLUSIONS: This review shows a variable association between Lp-PLA2 and subclinical disease. This finding has broad implications for the future of public health and clinical practice. Future research is needed to clarify what role Lp-PLA2 has in guiding treatment and if it is involved in plaque instability, which would make it a useful tool for risk prognostication.