Neural respiratory drive predicts clinical deterioration and safe discharge in exacerbations of COPD.

RATIONALE: Hospitalised patients with acute exacerbation of COPD may deteriorate despite treatment, with early readmission being common. OBJECTIVES: To investigate whether neural respiratory drive, measured using second intercostal space parasternal muscle electromyography (EMGpara), would identify worsening dyspnoea and physician-defined inpatient clinical deterioration, and predict early readmission. METHODS: Patients admitted to a single-site university hospital with exacerbation of COPD were enrolled. Spirometry, inspiratory capacity (IC), EMGpara, routine physiological parameters, modified early warning score (MEWS), modified Borg scale for dyspnoea and physician-defined episodes of deterioration were recorded daily until discharge. Readmissions at 14 and 28 days post discharge were recorded. MEASUREMENTS AND MAIN RESULTS: 120 patients were recruited (age 70 ± 9 years, forced expiratory volume in 1 s (FEV1) of 30.5 ± 11.2%). Worsening dyspnoea, defined as at least one-point increase in Borg scale, was associated with increases in EMGpara%max and MEWS, whereas an increase in EMGpara%max alone was associated with physician-defined inpatient clinical deterioration. Admission-to-discharge change (Δ) in the normalised value of EMGpara (ΔEMGpara%max) was inversely correlated with ΔFEV1 (r = -0.38, p < 0.001) and ΔIC (r = -0.44, p < 0.001). ΔEMGpara%max predicted 14-day readmission (OR 1.13, 95% 1.03 to 1.23) in the whole cohort and 28-day readmission in patients under 85 years (OR 1.09, 95% CI 1.01 to 1.18). Age (OR 1.08, 95% CI 1.03 to 1.14) and 12-month admission frequency (OR 1.29, 1.01 to 1.66), also predicted 28-day readmission in the whole cohort. CONCLUSIONS: Measurement of neural respiratory drive by EMGpara represents a novel physiological biomarker that may be helpful in detecting inpatient clinical deterioration and identifying the risk of early readmission among patients with exacerbations of COPD. TRIAL REGISTRATION: NCT01361451.

Prospective RandOmised Trial of Emergency Cardiac Computerised Tomography (PROTECCT).

OBJECTIVE: Many patients presenting with suspected acute coronary syndrome (ACS) have high-sensitivity cardiac troponin (hs-cTn) concentrations between rule-in and rule-out thresholds and hence need serial testing, which is time consuming. The Prospective RandOmised Trial of Emergency Cardiac Computerised Tomography (PROTECCT) assessed the utility of coronary CT angiography (CCTA) in patients with suspected ACS, non-ischaemic ECG and intermediate initial hs-cTn concentration. METHODS: Patients were randomised to CCTA-guided management versus standard of care (SOC). The primary outcome was hospital length of stay (LOS). Secondary outcomes included cost of in-hospital stay and major adverse cardiac events (MACE) at 12 months of follow-up. Data are mean (SD); for LOS harmonic means, IQRs are shown. RESULTS: 250 (aged 55 (14) years, 25% women) patients were randomised. Harmonic mean (IQR) LOS was 7.53 (6.0-9.6) hours in the CCTA arm and 8.14 (6.3-9.8) hours in the SOC arm (p=0.13). Inpatient cost was £1285 (£2216) and £1108 (£3573), respectively, p=0.68. LOS was shorter in the CCTA group in patients with <25% stenosis, compared with SOC; 6.6 (5.6-7.8) hours vs 7.5 (6.1-9.4) hours, respectively; p=0.021. More referrals for cardiology outpatient clinic review and cardiac CT-related outpatient referrals occurred in the SOC arm (p=0.01). 12-month MACE rates were similar between the two arms (7 (5.6%) in the CCTA arm and 8 (6.5%) in the SOC arm-log-rank p=0.78). CONCLUSIONS: CCTA did not lead to reduced hospital LOS or cost, largely because these outcomes were influenced by the detection of ≥25% grade stenosis in a proportion of patients. TRIAL REGISTRATION NUMBER: NCT03583320.

A need to reconsider guidelines on management of primary spontaneous pneumothorax?

BACKGROUND: The key guidelines in the management of primary spontaneous pneumothorax (PSP) include the 2010 British Thoracic Society (BTS) Pleural Disease guideline and 2001 American College of Chest Physicians (ACCP) Consensus Statement. Current recommendations are dependent on radiographic measures which differ between these two guidelines. The aim of this study is to compare size classification of PSP cases, according to BTS and ACCP guidelines, and to evaluate guideline compliance. FINDINGS: We conducted a retrospective evaluation of all PSP episodes presenting to St Thomas' Hospital, London, between February 2013 and December 2014. Data was recorded from review of chest X-rays and patient records. Eighty-seven episodes of PSP in 72 patients were identified (median age 25 years, IQR 22-32.25). Classification of "large" and "small" showed the greatest disparity in those managed conservatively (12/27, 44%) or with aspiration only (11/23, 48%). In this UK study, BTS guidelines were followed in 70% of episodes with adherence to ACCP guidelines in 32% of episodes. CONCLUSIONS: There is a poor agreement in size classification between BTS and ACCP guidelines, resulting in conflicting recommendations for management of PSP. Robust clinical trial evidence is required to achieve international consensus on the management of PSP.

Esomeprazole 40 mg and 20 mg is efficacious in the long-term management of patients with endoscopy-negative gastro-oesophageal reflux disease: a placebo-controlled trial of on-demand therapy for 6 months.

BACKGROUND: On-demand therapy may offer an effective approach to the long-term management of gastro-oesophageal reflux disease (GORD) without oesophagitis. AIM: To examine the efficacy of the novel proton pump inhibitor esomeprazole as on-demand therapy in endoscopy-negative GORD. PATIENTS AND METHODS: Endoscopy-negative GORD patients who achieved complete resolution of heartburn after short-term esomeprazole or omeprazole treatment (n = 721) were randomized to esomeprazole 20 mg (n = 282), 40 mg (n = 293) or placebo (n = 146) on demand (maximum one dose/day) for 6 months. The primary and secondary efficacy endpoints were time to study discontinuation due to (i) unwillingness to continue and (ii) inadequate control of heartburn, respectively. RESULTS: Both doses of esomeprazole were more effective than placebo. During the 6-month period, 42% of placebo recipients discontinued treatment due to unwillingness to continue, compared with 8% and 11% of esomeprazole 20 mg and 40 mg recipients, respectively. Overall, more patients treated with esomeprazole were free from gastrointestinal symptoms after 6 months of on-demand therapy. CONCLUSIONS: Esomeprazole 20 mg was superior to placebo for on-demand treatment of GORD; a higher dose did not confer additional clinical benefit. Over 90% of patients were willing to continue on-demand treatment with esomeprazole 20 mg over a 6-month period.

17ss oestradiol does not attenuate the response to angiotensin I and II during long term therapy in postmenopausal women.

PURPOSE: It is thought that oestrogen replacement therapy may reduce the conversion of angiotensin I to angiotensin II in postmenopausal women by inhibiting angiotensin converting enzyme. We sought to determine the effects of 3 months oestrogen replacement therapy (ERT) on the response to angiotensin I and II in postmenopausal women. METHODS: Eighteen postmenopausal women were randomised to either three months of 2 mg oral oestradiol or placebo in a double blind, placebo controlled, protocol. Change in forearm blood flow (FBF), in response to brachial arterial infusion of increasing concentrations of angiotensin I and angiotensin II was measured, pre-randomisation, after 1 months randomised therapy and after 3 months therapy, using venous occlusion plethysmography. RESULTS: Oestrogen treatment had no effect on baseline FBF. The mean (SD) peak reductions in FBF with 64 pmol/min angiotensin I pre-randomisation, after 1 month and after 3 months treatment with placebo were 62(11), 65(15) and 57(8)%. The corresponding reductions with the peak dose of angiotensin II (16 pmol/min) were 53(8), 48(12) and 47(11)%. In the oestradiol group, the peak responses to angiotensin I were 56(8), 53(11) and 44(29)% pre-randomisation, after 1 months treatment and after 3 months treatment. The corresponding reductions in response to angiotensin II were 37(15), 47(15) and 45(19)%. Oestradiol did not affect the response to either angiotensin I or angiotensin II. CONCLUSION: This study does not support the idea that ERT might exert a cardioprotective effect through inhibition of the renin-angiotensin system.