Safety and feasibility of triage and rapid discharge of patients with chest pain from emergency room: a pragmatic, randomised non-inferiority control trial of the European Society of Cardiology (ESC) 0-1 hour pathway vs. conventional 0-3 hour accelerated diagnostic protocol.

Patients presenting with chest pain represent a significant proportion of Emergency Department (ED) attendances but only a minority, typically 10%, have a final diagnosis of myocardial infarction (MI). Prompt discharge of patients without MI will alleviate ED overcrowding as well as improve patient satisfaction and reduce exposure to risk of hospital acquired infections such as Covid 19. The measurement of cardiac troponin (cTn) by a high sensitivity method is recommended by the National Institute for health and Care Excellence (NICE) for rapid categorisation of patients presenting with chest pain. Strategies proposed include measurement on admission and one hour from admission (ESC 0-1-hour pathway, the recent guideline approved pathway which has not been implemented widely), and measurement on admission and three hours from admission (0-3-hour pathway, which is conventional and widely adopted). The primary objective of this study is twofold: firstly, to assess the safety, feasibility, and impact of implementing the ESC (European Society of Cardiology) 0-1-hour pathway in clinical practice by reference to the more established ESC 0-3-hour protocol. The principal outcome measure will be the safety of the ESC 0-1-hour protocol. However, there are concerns that the time from sample draw to result availability (typically around 60 minutes) will impact on the feasibility of the ESC 0-1-hour pathway. Secondly, therefore, our goal is to evaluate whether measurement of high sensitivity troponin by a bedside analyser (point of care testing, POCT), which will produce results in 15 minutes is a feasible alternative to laboratory testing. We will compare the results produced by POCT with the laboratory results in the context of the ESC 0-1 hour and 0-3-hour pathway, as a nested controlled study in the context of a randomised controlled trial. (clinicaltrials.gov: NCT05322395).

Evaluation of the analytical and clinical performance of a high-sensitivity troponin I point-of-care assay in the Mersey Acute Coronary Syndrome Rule Out Study (MACROS-2).

OBJECTIVES: The objective of this study is to evaluate the analytical and diagnostic performance of a high-sensitivity point-of-care (POC) cardiac troponin I assay, the Quidel TriageTrue™ (QuidelOrtho Inc, San Diego, USA), compared to central laboratory testing (CLT) in accelerated diagnostic protocols (ADP) in real time in a clinical environment. METHODS: In a nested sub-study of a pragmatic randomised control trial, consecutive patients with suspected acute coronary syndrome (ACS) and chest pain <12 h duration were randomised to the ESC 0/1 and 0/3-h ADP. Subjects underwent sampling for Quidel TriageTrue POC hs-TnI whole blood and plasma, CLT hs-TnT Roche Elecsys and a validated, NICE approved CLT High sensitivity cardiac troponin I (hs-TnI) (Siemens Attellica) at each time point. Assay imprecision was assessed by repeat analysis of whole blood samples at three levels (low, near 10 % CV 5-10 ng/L, medium, approximating 99th percentile 15-25 ng/L and high, 3-5 times the 99th percentile, 60-100 ng/L). Final diagnosis was adjudicated at 6 weeks by Roche hs-TnT using the 4th universal definition of myocardial infarction (MI). RESULTS: A total of 1,157 patients consented and had both investigational POC whole blood and plasma and central lab hs-cTn available. The median age was 59, 47.2 % were female and 15 % had suffered a previous MI. Assay imprecision of whole blood POC TriageTrue revealed 10 % CV at 8.6 ng/L (>50 % lower than 99th percentile [20.5 ng/L]) and a 20 % CV at 1.2 ng/L. Receiver operator characteristics (ROC) curves were computed for each assay against adjudicated index type 1 MI to study clinical performance. At all-time points there were excellent performance for whole blood POC TriageTrue: area under the curve (AUC) 0.97 [95 % CI 0.94-098], 0.98 [95 % CI 0.97-1.00] and 0.95 [95 % CI 0.92-0.98] at time 0, 1 and 3 h respectively. There was statistical equivalence for performance of whole blood and plasma POC TriageTrue hs-TnI and laboratory Siemens Atellica hs-TnI. CONCLUSIONS: The whole blood POC TriageTrue hs-TnI assay demonstrates imprecision levels consistent with high sensitivity characteristics and has a clinical performance equivalent to an established, validated and NICE approved laboratory Siemens Atellica hs-TnI.

No Effect of Coenzyme Q10 on Cognitive Function, Psychological Symptoms, and Health-related Outcomes in Schizophrenia and Schizoaffective Disorder: Results of a Randomized, Placebo-Controlled Trial.

BACKGROUND: Cognitive impairments, negative symptoms, affective symptoms, and low energy are highly prevalent features of schizophrenia. Mitochondrial dysfunction has been hypothesized as one of the numerous factors to underlie the manifestation of these symptoms. The objective of this study was to evaluate whether Coenzyme Q10 (CoQ10) has a role in the treatment of schizophrenia and schizoaffective disorder. METHODS: A double-blind, randomized, placebo-controlled trial was conducted to assess the effects of CoQ10 supplementation (300 mg/day) on the co-primary outcomes of attention and working memory performance after 3 and 6 months. Secondary outcomes included plasma CoQ10 levels, mitochondrial function, energy, depression, anxiety, negative symptoms, and quality oflife. FINDINGS: In total, 72 patients were randomized to intervention groups. Overall, there was no effect of CoQ10 supplementation on the primary outcome measures at 3 or 6 months. Further, with the exception of plasma CoQ10 levels, CoQ10 supplementation also had no effect on the secondary outcomes. At 3 months, CoQ10 concentration was significantly higher in the CoQ10 group (3.85 µg/mL) compared with placebo (1.13 µg/mL); this difference was not present at 6 months. CONCLUSIONS: The results of the study suggest that CoQ10 supplementation at 300 mg/day for 6 months is unlikely to be beneficial for cognitive, psychological and health-related outcomes in schizophrenia and schizoaffective disorder. However, a number of limitations including low adherence, modest sample size, and attrition, likely reduce estimates of effects. As such, results should be considered preliminary.

Liver steatosis and fibrosis in people with human immunodeficiency virus in West Africa and the relationship with hepatitis B virus coinfection.

There is a heavy burden of liver disease in West Africa. While the role of hepatitis B virus (HBV) infection is well recognized, less is known about the contributing role of liver steatosis and how the two interact in the context of human immunodeficiency virus (HIV) infection. Adults with HIV in Ghana underwent FibroScan measurements to determine prevalence of liver steatosis (expressed as controlled attenuation parameter [CAP]) and fibrosis (expressed as liver stiffness [LS]). We explored contributing factors in linear regression models, including demographics, lifestyle characteristics, medical history, HIV and HBV status, and measurements of metabolic syndrome. Among 329 adults (72.3% women; median age, 47 years), 322 (97.9%) were on antiretroviral therapy (median duration, 8.9 years). CD4 counts were preserved (median, 619 cells/mm3 ); plasma HIV RNA was fully suppressed in 162 (50.3%) of the treated participants. Cigarette smoking, excessive alcohol consumption, and use of traditional or herbal remedies were uncommon (6.1%, 1.8%, 3.3%, respectively). Largely undiagnosed metabolic syndrome was detected in 87 (26.4%) participants. We obtained readings indicative of ≥S2 steatosis and ≥F2 fibrosis in 43 (13.1%) and 55 (16.7%) participants, respectively. Higher CAP values were associated with metabolic syndrome and longer prior stavudine exposure. Higher LS values were associated with male sex, higher HIV RNA, and higher CAP values. Relative to people without HBV, those with HBV (n = 90) had a similar prevalence of ≥S2 steatosis but a higher prevalence of ≥F2 fibrosis (36.7% vs. 9.2%, p < 0.0001) and concomitant ≥S2 steatosis and ≥F2 fibrosis (9.1% vs. 1.3%, p < 0.001). Conclusion: Both HBV and liver steatosis pose a threat to long-term liver health among people with HIV in West Africa. Urgently required interventions include improving HIV suppression and diagnosing and managing determinants of the metabolic syndrome.