We had the subjective impression that many patients admitted for resection of their lung cancer had first presented several months previously. The numerous steps in diagnosis and preoperative staging inevitably entail some delay, but the delay seemed to be longer than necessary. The survival of patients with lung cancer is well known to be correlated with the stage.' Naturally there is concern that delay in diagnosis and treatment allows tumour progression and thus reduces survival. The patient may also require more extensive resection. This is in addition to the high levels of anxiety that any delay can generate in patients who realise that they have lung cancer which may require surgery.This study was undertaken to assess the length and cause of delay from the first presentation to surgery and to identify the stages at which such delay occurs. Methods A retrospective study was made of all patients with lung tumours referred for lung resection at Papworth Hospital from 1 January 1993 to 31 December 1993. The names of the relevant patients were found from the operating theatre audit information. Data were obtained from medical records at the cardiothoracic regional centre and also at the referring hospitals. General practitioners and the departments of radiology and pathology were contacted for further details when required. The data collected were the dates on which each consultation, investigation and referral occurred, and the date of operation. The time of onset of symptoms was not recorded, since this would be very inaccurate in such a retrospective study and since it is not germane to the study. The tumour type and stage were also identified. From these data it was possible to identify the delay incurred by each patient at each stage in the investigative process. The hospital records for one patient were not available for this retrospective study, and this patient has therefore been excluded from the analysis.The delays studied were: (1) from first presentation to chest radiography, and (2) to chest physician referral; (3) from chest physician referral to chest clinic appointment; delays for (4) bronchoscopy, (5) CT scanning and (6) percutaneous needle biopsy; (7) from chest physician referral to surgical referral; (8) from this referral to surgical outpatient appointment; (9) from surgical referral to operation; and (10) the total delay from presentation to 903 on 10 May 2018 by guest. Protected by copyright.

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Background Myocardial fibrosis occurs in end-stage heart failure secondary to mitral regurgitation (MR), but it is not known whether this is present before onset of symptoms or myocardial dysfunction. This study aimed to characterise myocardial fibrosis in chronic severe primary MR on histology, compare this to tissue characterisation on cardiovascular magnetic resonance (CMR) imaging, and investigate associations with symptoms, left ventricular (LV) function, and exercise capacity. Methods Patients with class I or IIa indications for surgery underwent CMR and cardiopulmonary exercise testing. LV biopsies were taken at surgery and the extent of fibrosis was quantified on histology using collagen volume fraction (CVFmean) compared to autopsy controls without cardiac pathology. Results 120 consecutive patients (64 ± 13 years; 71% male) were recruited; 105 patients underwent MV repair while 15 chose conservative management. LV biopsies were obtained in 86 patients (234 biopsy samples in total). MR patients had more fibrosis compared to 8 autopsy controls (median: 14.6% [interquartile range 7.4–20.3] vs. 3.3% [2.6–6.1], P < 0.001); this difference persisted in the asymptomatic patients (CVFmean 13.6% [6.3–18.8], P < 0.001), but severity of fibrosis was not significantly higher in NYHA II-III symptomatic MR (CVFmean 15.7% [9.9–23.1] (P = 0.083). Fibrosis was patchy across biopsy sites (intraclass correlation 0.23, 95% CI 0.08–0.39, P = 0.001). No significant relationships were identified between CVFmean and CMR tissue characterisation [native T1, extracellular volume (ECV) or late gadolinium enhancement] or measures of LV function [LV ejection fraction (LVEF), global longitudinal strain (GLS)]. Although the range of ECV was small (27.3 ± 3.2%), ECV correlated with multiple measures of LV function (LVEF: Rho = − 0.22, P = 0.029, GLS: Rho = 0.29, P = 0.003), as well as NTproBNP (Rho = 0.54, P < 0.001) and exercise capacity (%PredVO2max: R = − 0.22, P = 0.030). Conclusions Patients with chronic primary MR have increased fibrosis before the onset of symptoms. Due to the patchy nature of fibrosis, CMR derived ECV may be a better marker of global myocardial status. Clinical trial registration Mitral FINDER study; Clinical Trials NCT02355418, Registered 4 February 2015, https://clinicaltrials.gov/ct2/show/NCT02355418