Etiology and characteristics of non-aneurysmal thunderclap headache presenting to an acute setting.

OBJECTIVES: To describe the characteristics and causes of non-aneurysmal thunderclap headache (TCH) and compare serious from benign underlying causes. METHODS: Retrospective cohort study of consecutive adult patients with TCH presenting to a tertiary care academic medical center between 2010 and 2020. Aneurysmal subarachnoid hemorrhage cases were excluded. Cases were categorized into serious or benign; serious TCH was defined as any condition in which delayed diagnosis and treatment could result in neurological disability or death. Risk factors for serious TCH were analyzed. We adhere to standardized guidelines for reporting observational studies. RESULTS: A total of 932 patients presented with TCH. After exclusion of 393 patients with aneurysmal-type subarachnoid hemorrhage, 539 were included in the analysis. One-half (n = 275, 51.0 %) had a serious cause. Median age was 51 years, 69.0 % were female. Most frequent diagnoses were intracranial hemorrhage (n = 102, 18.9 %), reversible cerebral vasoconstriction syndrome (n = 97, 18.0 %), and idiopathic TCH (n = 102, 38.6 %). A multivariable logistic regression model for prediction of serious TCH included age, hypertension, migraines, recurrent TCH, level of consciousness and other clinical exam findings, and achieved an AUROC of 0.732. This score had a sensitivity of 79.9 % (95 % CI 73.5-83.5 %) for the identification of serious TCH. A 0.5-point increase in the risk score was associated with a 73 % increase in the odds of serious TCH (odds ratio 1.73, 95 % CI 1.53-1.95, p < 0.001). CONCLUSION: Our study describes the relative frequency of presentation and etiologies among patients with TCH This score can aide clinicians in recognising patients with potentially serious cause of TCH, for whom additional imaging and neurological consultation is necessary.

Safety of Diltiazem for Acute Management of Atrial Fibrillation (AF) in Patients with Heart Failure and Reduced Ejection Fraction in the Emergency Department.

BACKGROUND: Diltiazem is an effective rate control agent for atrial fibrillation with rapid ventricular rate (AF RVR). However, its negative inotropic effects may increase the risk for worsening heart failure in patients with a reduced ejection fraction (EF). OBJECTIVES: This observational study aims to describe the incidence of worsening heart failure in patients who receive intravenous diltiazem for acute atrial fibrillation management. METHODS: Adult patients that received diltiazem in the emergency department (ED) for AF RVR (heart rate ≥ 100 beats/min) from 2021 to 2022 and had a prior documented EF were included. The primary outcome is worsening heart failure within 24 h of diltiazem administration. Secondary outcomes include return ED visits and death within 7 days. EF percentage was compared across outcomes using Wilcoxon rank-sum tests. Outcomes were compared by reduced EF (< 50%) and preserved EF (≥ 50%). Continuous data were summarized with medians and interquartile ranges, and categorical features were summarized with frequency counts and percentages. Wilcoxon rank-sum tests were used for numeric outcomes and chi-squared tests or Fisher's exact tests for categorical outcomes, with a p-value < 0.05 considered statistically significant. RESULTS: There were 674 patients with AF RVR that received diltiazem, and 386 patients met the inclusion criteria for analysis. Baseline demographics included a median age of 72 (64-81) years, with 14.5% of patients having a prior diagnosis of congestive heart failure. EF < 50% was identified in 13.7% of patients (n = 53), of which approximately 30% of these patients safely discharged home after receiving i.v. diltiazem. The primary outcome of worsening heart failure occurred in 7/41 (17%) and 10/207 (4.8%) patients with reduced and preserved ejection fractions, respectively, who were admitted to the hospital (p = 0.005). CONCLUSION: The development of worsening heart failure is multifactorial and may include the use of diltiazem in critically ill patients requiring hospital admission.

A Pragmatic Study of Cardiovascular Disease During Long-Term COVID-19.

BACKGROUND: Many patients diagnosed with COVID-19 have persistent cardiovascular symptoms, but whether this represents a true cardiac process is unclear. This study assessed whether symptoms associated with long COVID among patients referred for cardiovascular evaluation are associated with objective abnormalities on cardiac testing to explain their clinical presentation. METHODS: A retrospective cohort study of 40,462 unique patients diagnosed with COVID-19 at our tertiary referral was conducted and identified 363 patients with persistent cardiovascular symptoms a minimum of 4 weeks after polymerase chain reaction confirmed COVID-19 infection. Patients had no cardiovascular symptoms prior to COVID-19 infection. Each patient was referred for cardiovascular evaluation at a tertiary referral center. The incidence and etiology of abnormalities on cardiovascular testing among patients with long COVID symptoms are reported here. The cohort was subsequently divided into 3 categories based on the dominant circulating severe acute respiratory syndrome coronavirus 2 variant at the time of initial infection for further analysis. RESULTS: Among 40,462 unique patients diagnosed with COVID-19 at our tertiary referral center from April 2020 to March 2022, 363 (0.9%) patients with long COVID were evaluated by Cardiology for possible cardiac sequelae from COVID and formed the main study cohort. Of these, 229 (63%) were vaccinated and 47 (12.9%) had severe initial infection, receiving inpatient treatment for COVID prior to developing long COVID symptoms. Symptoms were associated with a cardiac cause in 85 (23.4%), of which 52 (14.3%) were attributed to COVID; 39 (10.7%) with new cardiac disease from COVID, and 13 (3.6%) to worsening of pre-existing cardiac disease after COVID infection. The median troponin change in 45 patients with troponin measurements within 4 weeks of acute infection was +4 ng/dL (9 to 13 ng/dL). Among the total cohort with long COVID, 83.7% were diagnosed during the pre-Delta phase, 13.2% during the Delta phase, and 3.1% during the Omicron phase of the pandemic. There were 6 cases of myocarditis, 11 rhythm disorders, 8 cases of pericarditis, 5 suspected cases of endothelial dysfunction, and 33 cases of autonomic dysfunction. CONCLUSION: This pragmatic retrospective cohort study suggests that patients with long COVID referred for cardiovascular evaluation infrequently have new, objective cardiovascular disease to explain their clinical presentation. A multidisciplinary, patient-centered approach is warranted for symptom management along with conservative use of diagnostic testing.

Plasma thrombin generation kinetics vary by injury pattern and resuscitation characteristics in pediatric and young adult trauma patients.

BACKGROUND: Thrombin generation kinetics are not well studied in children. This study aimed to assess how thrombin generation kinetics vary in pediatric and young adult (YA) trauma patients by clinical characteristics and injury pattern. METHODS: Prospective cohort study where plasma samples were obtained from pediatric (ages 0-17 years) and YA (ages 18-21 years) trauma patients upon emergency department arrival. Thrombin generation (calibrated automated thrombogram [CAT]) was quantified as lag time (LT, minutes), peak height (PH, nM), time to peak (ttPeak, minutes), and endogenous thrombin potential (ETP, nM × minute). Results are expressed as median and quartiles [Q1, Q3] and compared using Wilcoxon rank sum testing with p < 0.05 considered significant. RESULTS: We enrolled 47 pediatric (median age, 15 [14, 17] years, 78% male, 87% blunt, median Injury Severity Score, 12) and 49 YA (median age 20 [18, 21] years, 67% male, 84% blunt, median Injury Severity Score, 12) patients. Pediatric and YA patients had similar rates of operative intervention (51% vs. 57%), transfusion (25% vs. 20%), and traumatic brain injury (TBI) (53% vs. 49%). Pediatric patients who required an operation had accelerated initiation of thrombin generation, with shorter LT than those who did not (2.58 [2.33, 2.67]; 2.92 [2.54, 3.00], p = 0.034). Shorter LT (2.41 [2.22, 2.67]; 2.67 [2.53, 3.00]) and ttPeak (4.50 [4.23, 4.73]; 5.22 [4.69, 5.75], both p < 0.01) were noted in pediatric patients who required transfusion as compared with those who did not. The YA patients requiring transfusion had shorter LT (2.33 [2.19, 2.74]; 2.83 [2.67, 3.27]) and ttPeak (4.48 [4.33, 5.65]; 5.33 [4.85, 6.28] both p < 0.04) than those who were not transfused. Young adults with TBI had greater ETP than those without (1509 [1356, 1671]; 1284 [1154, 1471], p = 0.032). CONCLUSION: Thrombin generation kinetics in pediatric trauma patients prior to intervention vary with need for operation and transfusion, while thrombin generation kinetics in young adult patients are influenced by TBI and need for operation or transfusion. This is a promising tool for assessing coagulopathy in young trauma patients. LEVEL OF EVIDENCE: Prognostic and Epidemiological; Level III.

TELOMERE LENGTH OF PERIPHERAL BLOOD MONONUCLEAR CELLS IS ASSOCIATED WITH DISCHARGE DISPOSITION IN OLDER TRAUMA PATIENTS.

Introduction: Little is known regarding peripheral blood mononuclear cell telomere length (PBMC-TL) and response to traumatic injury. The objective of this study was to characterize the role of PBMC-TL in coagulation and clinical outcomes after injury. Methods: Plasma and buffy coats were prospectively collected from trauma patients and healthy volunteers. DNA was purified and PBMC-TL quantified by quantitative polymerase chain reaction. Thrombin generation kinetics were expressed as lag time (in minutes), peak height (in nanometers), time to peak (in minutes), and endogenous thrombin potential (in nM × min). Results are in median and quartiles [Q1, Q3]. P < 0.05 was considered significant (Wilcoxon rank sum testing). Results: Forty-two younger patients (21 [20, 22] years, 69% were male) and 39 older patients (62 [61, 64] years, 79% were male) were included. There was no significant difference in Clinical Frailty Scores between groups. Younger patients had longer total PBMC-TL (0.40 Mb [0.30, 0.49] vs. 0.29 Mb [0.23, 0.33], P < 0.001) and longer average PBMC-TL per chromosome (4.3 kb [3.3, 5.3] vs. 3.2 kb [2.5, 3.7], P < 0.001). When older patients were stratified by 50th percentile of PBMC-TL, there were no differences in thrombin generation; however, those with shorter telomeres were less likely to be discharged home (29% vs. 77%, P = 0.004). Older patients in the bottom quartile of PBMC-TL had shorter lag time (2.78 min [2.33, 3.00] vs. 3.33 min [3.24, 3.89], P = 0.030) and were less likely to be discharged home (22% vs. 90%, P = 0.006) than those in the top quartile of PBMC-TL. Multivariable logistic regression models revealed both increased age and shorter PBMC-TL to be independent predictors of discharge disposition other than home. Conclusion: In older trauma patients, shorter PBMC-TL is associated with accelerated initiation of thrombin generation and lower likelihood of being discharged to home.