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Background: The association between obesity, major adverse cardiovascular events (MACE), and mortality in patients with incident stroke is not well established. We assessed the relationship between body mass index (BMI) and MACE in patients with incident stroke. Methods: The population-based cohort study identified 30,702 individuals from the Clinical Practice Research Datalink (CPRD GOLD) and Hospital Episode Statistics (HES) databases from the United Kingdom. Individuals were aged 18 years with incident stroke between 1-1-1998 and 31-12-2017, a BMI recorded within 24 months before incident stroke, and no prior history of MACE. BMI was categorised as underweight (≤18.5 kg/m2), normal (18.5-24.9 kg/m2), overweight (25.0-29.9 kg/m2), obesity class I (30.0-34.9 kg/m2), class II (35.0-39.9 kg/m2) and class III (40 kg/m2). MACE was defined as a composite of incident coronary heart disease, recurrent stroke, peripheral vascular disease (PVD), heart failure, and cardiovascular-related mortality. Multivariable Cox regression was used to assess differences in MACE risk between BMI categories. Results: At baseline, 1,217 (4.0%) were underweight, 10,783 (35.1%) had a normal BMI, 10,979 (35.8%) had overweight, 5,206 (17.0%) had obesity class I, 1,749 (5.7%) class II, and 768 (2.5%) class III. In multivariable analysis, higher BMI were associated with lower risk of subsequent MACE [overweight: HR 0.96 95% CI 0.93-0.99)]; PVD [overweight: 0.65 (0.49-0.85); obesity class III: 0.19 (0.50-0.77)]; cardiovascular-related death [overweight: 0.80 (0.74-0.86); obesity class I: 0.79 (0.71-0.88); class II: 0.80 (0.67-0.96)]; and all-cause mortality [overweight: 0.75 (0.71-0.79); obesity class I: 0.75 (0.70-0.81); class II: 0.77 (0.68-0.86)] when compared to those with normal BMI. The results were similar irrespective of sex, diabetes mellitus, smoking or cancer at time of incident stroke. Conclusions: In patients with incident stroke, overweight or obesity were associated with a more favourable prognosis for subsequent MACE, PVD, and mortality, irrespective of sex, diabetes mellitus, smoking or cancer at baseline. As with other cohort studies, our study demonstrates an association. Randomised control trials should be considered to robustly evaluate the impact of weight management recommendations on subsequent cardiovascular outcomes in stroke survivors.

Up to 10% of patients with ischaemic stroke have comorbid cancer and stroke in these patients is thought to have a poor short-term prognosis. There is little known about the long-term cardiovascular morbidity and mortality outcomes after incident ischaemic stroke in patients with recent cancer history.To assess the risk of subsequent cardiovascular morbidity and mortality outcomes in patients with an incident ischaemic stroke and recent cancer history.Patients aged ≥18 years with an incident ischaemic stroke between 1998 and 2017, with any diagnosis of cancer within 12 months before the stroke event, and no prior history of serious vascular event were identified from UK Clinical Practice Research Datalink (CPRD GOLD) linked to Hospital Episode Statistics (HES) data. To minimize selection bias, these patients were propensity-score matched with patients with incident ischaemic stroke and no history of cancer. Propensity-score matching was done using covariates such as demographic data, vascular risk factors, comorbid conditions, and prescribed medication. Multivariable models (Competing risks and Cox regression) were used to determine the risk of subsequent major adverse cardiovascular event (MACE) outcomes and all-cause mortality.Our cohort included 22,460 patients with a median age of 75 (IQR 64-83) years and a follow-up of 12.3 (IQR 7.2-16.7) years. Recent cancer was identified in 1,149 patients (5.1%) at the time of incident ischaemic stroke. The patients with recent cancer history had a lower risk of composite MACE (sub-distribution hazard ratio (SHR) 0.83 [95% CI: 0.75-0.92]) and recurrent stroke (SHR 0.85 95% CI:0.75-0.96]) and a higher risk of all-cause mortality (hazard ratio 1.67 [95% CI:1.47-1.91]). The risk of coronary heart disease, peripheral vascular disease, heart failure, and CVD-related death outcomes did not differ significantly between the groups.After incident ischaemic stroke, patients with recent cancer history have a lower risk of composite MACE and recurrent stroke outcomes but a higher risk of all-cause mortality when compared with patients without a prior history of cancer.

Background Patients with ischemic stroke are considered a very high risk population for subsequent cardiovascular events and guidelines recommend intensive preventive strategies. However, there is no clear recommendation that patients with hemorrhagic stroke should also be regarded as a very high cardiovascular risk population. Objective To compare the risk of subsequent cardiovascular morbidity/mortality between patients with incident hemorrhagic and ischemic stroke. Methods Patients aged ≥18 years with incident hemorrhagic or ischemic stroke between 1998 and 2017 and no prior history of serious vascular event were identified from UK Clinical Practice Research Datalink (CPRD GOLD) linked to Hospital Episode Statistics data. Results The cohort included 32,091 patients with an overall follow-up of 381,237 person-years (median: 11.8 years). After adjusting for potential confounders, patients with incident hemorrhagic stroke had no significantly different risk of subsequent cardiovascular morbidity compared with patients with incident ischemic stroke—coronary heart disease (CHD; hazard ratio [HR]: 0.86, 95% confidence interval [CI]: 0.56–1.32), recurrent stroke (HR: 0.92, 95% CI: 0.83–1.02), peripheral vascular disease (PVD; HR: 1.15, 95% CI:0.56–2.38), or heart failure (HR: 1.03, 95% CI: 0.61–1.74). Patients with incident hemorrhagic stroke had significantly higher risk of subsequent cardiovascular disease (CVD)-related mortality (HR: 2.35, 95% CI: 2.04–2.72) and all-cause mortality (HR: 2.16, 95% CI: 1.94–2.41). Propensity-score matched analysis of 1,039 patients with hemorrhagic stroke and 1,039 with ischemic stroke showed similar risk in subsequent cardiovascular morbidity—CHD (stratified HR [sHR]: 0.92, 95% CI: 0.55–1.54), recurrent stroke (sHR: 0.93, 95% CI: 0.82–1.02), PVD (sHR: 1.04 95% CI: 0.45–2.41), or heart failure (sHR: 0.71, 95% CI: 0.39–1.27). Conclusion The risk of subsequent cardiovascular events is similar between patients with incident hemorrhagic and ischemic stroke. Patients with previous hemorrhagic stroke should be regarded as a population at very high risk for subsequent CVD.

Background Variability in low-density lipoprotein cholesterol (LDL-C) response to statins is underappreciated. We characterised patients by their statin response (SR), baseline risk of cardiovascular disease (CVD) and 10-year CVD outcomes. Methods and results A multivariable model was developed using 183,213 United Kingdom (UK) patients without CVD to predict probability of sub-optimal SR, defined by guidelines as Conclusions Patients with sub-optimal response to statins experienced significantly more MACE, regardless of baseline CVD risk. To enhance cholesterol management for primary prevention, statin response should be considered alongside risk assessment.

Background Although obesity is a well-recognised risk factor for cardiovascular disease (CVD), the impact of long-term body mass index (BMI) changes in overweight or obese adults, on the risk of heart failure, CVD and mortality has not been quantified. Methods This population-based cohort study used routine UK primary care electronic health data linked to secondary care and death-registry records. We identified adults who were overweight or obese, free from CVD and who had repeated BMI measures. Using group-based trajectory modelling, we examined the BMI trajectories of these individuals and then determined incidence rates of CVD, heart failure and mortality associated with the different trajectories. Cox-proportional hazards regression determined hazards ratios for incident outcomes. Results 264,230 individuals (mean age 49.5 years (SD 12.7) and mean BMI 33.8 kg/m2 (SD 6.1)) were followed-up for a median duration of 10.9 years. Four BMI trajectories were identified, corresponding at baseline, with World Health Organisation BMI classifications for overweight, class-1, class-2 and class-3 obesity respectively. In all four groups, there was a small, stable upwards trajectory in BMI (mean BMI increase of 1.06 kg/m2 (± 3.8)). Compared with overweight individuals, class-3 obese individuals had hazards ratios (HR) of 3.26 (95% CI 2.98–3.57) for heart failure, HR of 2.72 (2.58–2.87) for all-cause mortality and HR of 3.31 (2.84–3.86) for CVD-related mortality, after adjusting for baseline demographic and cardiovascular risk factors. Conclusion The majority of adults who are overweight or obese retain their degree of overweight or obesity over the long term. Individuals with stable severe obesity experience the worst heart failure, CVD and mortality outcomes. These findings highlight the high cardiovascular toll exacted by continuing failure to tackle obesity.

Background: Although obesity is a well-recognised risk factor for cardiovascular disease (CVD), the impact of long-term body mass index (BMI) changes in overweight or obese adults, on the risk of heart failure, CVD and mortality has not been quantified.Methods: This population-based cohort study used routine UK primary care electronic health data linked to secondary care and death-registry records. We identified adults who were overweight or obese, free from CVD and who had repeated BMI measures. Using group-based trajectory modelling, we examined the BMI trajectories of these individuals and then determined incidence rates of CVD, heart failure and mortality associated with the different trajectories. Cox-proportional hazards regression determined hazards ratios for incident outcomes. Results: 264,230 individuals (mean age 49.5 years (SD 12.7) and mean BMI 33.8kg/m2 (SD 6.1)) were followed-up for a median duration of 10.9 years. Four BMI trajectories were identified, corresponding at baseline, with World Health Organisation BMI classifications for overweight, class-1, class-2 and class-3 obesity respectively. In all four groups, there was a small, stable upwards trajectory in BMI (mean BMI increase of 1.06kg/m2 (± 3.8)). Compared with overweight individuals, class-3 obese individuals had a 3.3-fold increased risk of heart failure (HR 3.26 (95% CI 2.98-3.57)), 2.7-fold increased risk of all-cause mortality (HR 2.72 (2.58-2.87)) and 3.3-fold increased risk of CVD-related mortality (HR 3.31 (2.84-3.86)) after adjusting for baseline demographic and cardiovascular risk factors. Conclusion: The majority of adults who are overweight or obese retain their degree of overweight or obesity over the long term. Individuals with stable severe obesity experience the worst heart failure, CVD and mortality outcomes. These findings highlight the high cardiovascular toll exacted by continuing failure to tackle obesity.

Background and aims The UK Simon Broome (SB) familial hypercholesterolaemia (FH) register previously reported 3-fold higher standardised mortality ratio for cardiovascular disease (CVD) in women compared to men from 2009 to 2015. Here we examined sex differences in CVD morbidity in FH by national linkage of the SB register with Hospital Episode Statistics (HES). Methods Of 3553 FH individuals in the SB register (aged 20–79 years at registration), 2988 (52.5% women) had linked HES records. Standardised Morbidity Ratios (SMbR) compared to an age and sex-matched UK general practice population were calculated [95% confidence intervals] for first CVD hospitalisation in HES (a composite of coronary heart disease (CHD), myocardial infarction (MI), stable or unstable angina, stroke, TIA, peripheral vascular disease (PVD), heart failure, coronary revascularisation interventions). Results At registration, men had significantly (p 50 years, SMbR was 33% higher in women than men (6.11 [5.57–6.70] vs 4.59 [4.08–5.15]). Conclusions Excess CVD morbidity due to FH remains markedly elevated in women at all ages, but especially those aged 30–50 years. This highlights the need for earlier diagnosis and optimisation of lipid-lowering risk factor management for all FH patients, with particular attention to young women with FH., Graphical abstract Image 1, Highlights • Males with familial hypercholesterolaemia (FH) had more cardiovascular disease (CVD) risk factors and were commenced on lipid-lowering therapy at a younger age, than females with FH. • Individuals with FH had excess rates of hospitalisations for CVD, compared to the general population of non-FH individuals. • Excess CVD morbidity due to FH was higher in women than men aged 30 years and over, but especially in those aged 30–50 years.

Background and aims Familial hypercholesterolaemia (FH) is a known major cause of premature heart disease. However, the risks of atherosclerotic disease in other vascular regions are less known. We determined the risk of major cardiovascular disease (CVD) outcomes associated with clinical FH. Methods In a retrospective cohort study (1 January, 1999 to 22 July, 2016), we randomly-matched 14,097 UK subjects with clinical FH diagnoses or characteristics (Simon-Broome definite or Dutch Lipid Clinic Score >8) to 42,506 subjects without FH by age, sex, general practice. We excluded those with CVD at baseline. Incident rates for coronary heart disease (CHD), stroke or transient ischaemic attack (TIA) and peripheral vascular disease (PVD) were estimated. Cox proportional hazards regression, stratified on matched-pairs, determined adjusted hazards ratios (HR) for incident CVD. Results During follow-up (median 13.8 years), incidence rates (95% CI) of CVD (per 1000 person-years) were 25.6 (24.8–26.3) in FH and 2.9 (2.8–3.1) in non-FH subjects. The risk of CHD, stroke/TIA and PVD was higher in FH compared to non-FH subjects: CHD (HR 10.63, 95% CI 9.82–11.49), stroke/TIA (HR 6.74, 95% CI 5.84–7.77), PVD (HR 7.17, 95% CI 6.08–8.46). The risk of CVD was greater in those with FH characteristics (HR 13.52, 95% CI 12.48–14.65) than those with clinical diagnoses (HR 1.66, 95% CI 1.42–1.93). Conclusions In addition to the recognised increased risk of CHD, subjects with FH have greatly elevated risk of stroke/TIA and PVD. This emphasises need for early diagnosis and preventive interventions beyond CHD, to reduce CVD risk in these individuals.

ObjectiveTo assess low-density lipoprotein cholesterol (LDL-C) response in patients after initiation of statins, and future risk of cardiovascular disease (CVD).MethodsProspective cohort study of 165 411 primary care patients, from the UK Clinical Practice Research Datalink, who were free of CVD before statin initiation, and had at least one pre-treatment LDL-C within 12 months before, and one post-treatment LDL-C within 24 months after, statin initiation. Based on current national guidelines, Results84 609 (51.2%) patients had a sub-optimal LDL-C response to initiated statin therapy within 24 months. During 1 077 299 person-years of follow-up (median follow-up 6.2 years), there were 22 798 CVD events (12 142 in sub-optimal responders and 10 656 in optimal responders). In sub-optimal responders, compared with optimal responders, the HR for incident CVD was 1.17 (95% CI 1.13 to 1.20) and 1.22 (95% CI 1.19 to 1.25) after adjusting for age and baseline untreated LDL-C. Considering competing risks resulted in lower but similar sub-HRs for both unadjusted (1.13, 95% CI 1.10 to 1.16) and adjusted (1.19, 95% CI 1.16 to 1.23) cumulative incidence function of CVD.ConclusionsOptimal lowering of LDL-C is not achieved within 2 years in over half of patients in the general population initiated on statin therapy, and these patients will experience significantly increased risk of future CVD.

To the Editor Our recently published study using electronic health records from primary care setting in the UK examined low-density lipoprotein cholesterol (LDL-C) reduction among patients initiating statins.1 We are grateful to Dr Taher Modarressi, Dr Dieter Lutjohann, Professor Oliver Weingartner, Dr Tulin Muggleton and Dr Ellis Muggleton for their comments. With regards to the points raised: Suboptimal cholesterol response to initiation of statins and future risk of cardiovascular disease – Dr Taher Modarressi While biomarkers are useful to establish associations with various disease conditions including cardiovascular disease (CVD), often these biomarkers are not routinely offered or measured in primary care settings within the UK, and hence are not available in electronic health records. Lipoprotein(a) (Lp(a)), a large lipoprotein particle produced in the liver, is not routinely measured in patients in UK general practice. There is, however, evidence indicating Lp(a) might be a useful biomarker that has …

ObjectiveTo investigate relationships between maternal smoking status in pregnancy and infant development. The largest randomised controlled trial of nicotine replacement therapy (NRT) for smoking cessation in pregnancy, the smoking, nicotine and pregnancy (SNAP) trial, found that at 1 month after randomisation, smoking cessation rates were doubled in the NRT group compared with the placebo group. At delivery, there was no significant difference in cessation rates between groups. Surprisingly, infants born to women randomised to NRT were more likely to have unimpaired development at 2 years. We hypothesised that this apparently protective effect was due to smoking cessation caused by NRT and so, investigate this relationship using the same cohort.DesignSecondary analysis of a randomised controlled trial.SettingSeven antenatal hospitals in the Midlands and North-West England.ParticipantsEight hundred and eighty-four pregnant smokers randomised to receive either NRT patches or visually-identical placebo in the SNAP trial. Participants’ smoking behaviour were recorded at randomisation, 1 month after their target quit date and at delivery.MethodsUsing logistic regression models, we investigated associations between participants’ smoking measures and infant development (assessed using the Ages and Stages questionnaire) at 2 years.Main outcome measures2 year infant development.ResultsDevelopmental impairment was reported for 12.7% of study 2 year olds. Maternal heaviness of smoking at randomisation (OR: 1.26, 95% CI: 0.82 to 1.96, p=0.091), validated smoking abstinence recorded at 1 month after a quit date (OR: 1.02, 95% CI: 0.60 to 1.74, p=0.914) and validated smoking abstinence recorded at both 1 month after a quit date and at the end of pregnancy (OR: 1.52, 95% CI: 0.81 to 2.85, p=0.795) were not independently associated with infant developmental impairment at 2 years.ConclusionWe found no evidence that NRT treatment improved infants' developmental outcomes through smoking cessation.Trial registration numberCTA03057/0002/001-0001; Post-results

Studies have shown that for the same quantity of cigarettes smoked, women are more likely to develop heart disease than men, but studies in lung cancer have produced conflicting results. We studied the association between smoking quantity and lung cancer in men and women.Using data from The Health Improvement Network (a UK medical research database), we generated a data set comprising 12,121 incident cases of lung cancer and 48,216 age-, sex-, and general practice-matched control subjects. We used conditional logistic regression to calculate ORs for lung cancer according to highest-ever-quantity smoked in men and women separately.The odds of lung cancer in women who had ever smoked heavily compared with those who had never smoked were increased 19-fold (OR, 19.10; 95% CI, 16.98-21.49), which was more than for men smoking the same quantity (OR, 12.81; 95% CI, 11.52-14.24). There was strong evidence of a difference in effect of quantity smoked on lung cancer between men and women (interaction P.0001), which remained after adjusting for height (a proxy marker for lung volume).Moderate and heavy smoking carry a higher risk of lung cancer in women than in men, and this difference does not seem to be explained by lung volume. The findings suggest that extrapolating risk estimates for lung cancer in men to women will underestimate the adverse impact of smoking in women.

Background: The UK has poor lung cancer survival rates and high early mortality, compared to other countries. We aimed to identify factors associated with early death, and features of primary care that might contribute to late diagnosis. Methods: All cases of lung cancer diagnosed between 2000 and 2013 were extracted from The Health Improvement Network database. Patients who died within 90 days of diagnosis were compared with those who survived longer. Standardised chest X-ray (CXR) and lung cancer rates were calculated for each practice. Results: Of 20 142 people with lung cancer, those who died early consulted with primary care more frequently prediagnosis. Individual factors associated with early death were male sex (OR 1.17; 95% CI 1.10 to 1.24), current smoking (OR 1.43; 95% CI 1.28 to 1.61), increasing age (OR 1.80; 95% CI 1.62 to 1.99 for age ≥80 years compared to 65–69 years), social deprivation (OR 1.16; 95% CI 1.04 to 1.30 for Townsend quintile 5 vs 1) and rural versus urban residence (OR 1.22; 95% CI 1.06 to 1.41). CXR rates varied widely, and the odds of early death were highest in the practices which requested more CXRs. Lung cancer incidence at practice level did not affect early deaths. Conclusions: Patients who die early from lung cancer are interacting with primary care prediagnosis, suggesting potentially missed opportunities to identify them earlier. A general increase in CXR requests may not improve survival; rather, a more timely and appropriate targeting of this investigation using risk assessment tools needs further assessment.

Introduction In the UK, most people with lung cancer are diagnosed at a late stage when curative treatment is not possible. To aid earlier detection, the socio-demographic and early clinical features predictive of lung cancer need to be identified. Methods We studied 12 074 cases of lung cancer and 120 731 controls in a large general practice database. Logistic regression analyses were used to identify the socio-demographic and clinical features associated with cancer up to 2 years before diagnosis. A risk prediction model was developed using variables that were independently associated with lung cancer up to 4 months before diagnosis. The model performance was assessed in an independent dataset of 1 826 293 patients from the same database. Discrimination was assessed by means of a receiver operating characteristic (ROC) curve. Results Clinical and socio-demographic features that were independently associated with lung cancer were patients’ age, sex, socioeconomic status and smoking history. From 4 to 12 months before diagnosis, the frequency of consultations and symptom records of cough, haemoptysis, dyspnoea, weight loss, lower respiratory tract infections, non-specific chest infections, chest pain, hoarseness, upper respiratory tract infections and chronic obstructive pulmonary disease were also independently predictive of lung cancer. On validation, the model performed well with an area under the ROC curve of 0.88. Conclusions This new model performed substantially better than the current National Institute for Health and Clinical Excellence referral guidelines and all comparable models. It has the potential to predict lung cancer cases sufficiently early to make detection at a curable stage more likely by allowing general practitioners to better risk stratify their patients. A clinical trial is needed to quantify the absolute benefits to patients and the cost effectiveness of this model in practice.

Background There is pressing need to diagnose lung cancer earlier in the United Kingdom (UK) and it is likely that research using computerised general practice records will help this process. Linkage of these records to area-level geo-demographic classifications may also facilitate case ascertainment for public health programmes, however, there have as yet been no extensive studies of data validity for such purposes. Methods To first address the need for validation, we assessed the completeness and representativeness of lung cancer data from The Health Improvement Network (THIN) national primary care database by comparing incidence and survival between 2000 and 2009 with the UK National Cancer Registry and the National Lung Cancer Audit Database. Secondly, we explored the potential of a geo-demographic social marketing tool to facilitate disease ascertainment by using Experian's Mosaic Public Sector ™ classification, to identify detailed profiles of the sectors of society where lung cancer incidence was highest. Results Overall incidence of lung cancer (41.4/100, 000 person-years, 95% confidence interval 40.6-42.1) and median survival (232 days) were similar to other national data; The incidence rate in THIN from 2003-2006 was found to be just over 93% of the national cancer registry rate. Incidence increased considerably with area-level deprivation measured by the Townsend Index and was highest in the North-West of England (65.1/100, 000 person-years). Wider variations in incidence were however identified using Mosaic classifications with the highest incidence in Mosaic Public Sector ™types 'Cared-for pensioners, ' 'Old people in flats' and 'Dignified dependency' (191.7, 174.2 and 117.1 per 100, 000 person-years respectively). Conclusions Routine electronic data in THIN are a valid source of lung cancer information. Mosaic ™ identified greater incidence differentials than standard area-level measures and as such could be used as a tool for public health programmes to ascertain future cases more effectively.

Introduction: The majority of cases of both lung cancer and chronic obstructive pulmonary disease (COPD) are attributable to cigarette smoking, but whether COPD is an independent risk factor for lung cancer remains unclear. Methods: We used The Health Improvement Network, a U.K. general practice database, to identify incident cases of lung cancer and controls matched on age, sex, and practice. Using conditional logistic regression, we assessed the effects of timing of first diagnoses of COPD, pneumonia, and asthma on the odds of lung cancer, adjusting for smoking habit. Results: Of 11,888 incident cases of lung cancer, 23% had a prior diagnosis of COPD compared with only 6% of the 37,605 controls. The odds of lung cancer in patients who had COPD diagnosed within 6 months of their cancer diagnosis were 11-fold those of patients without COPD (odds ratio 11.47, 95% confidence interval 9.38–14.02). However, when restricted to earlier COPD diagnoses, with adjustment for smoking, the effect markedly diminished (for COPD diagnoses >10 years before lung cancer diagnosis, odds ratio: 2.18, 95% confidence interval: 1.87–2.54). The pattern was similar for pneumonia. The effect of COPD on lung cancer remained after excluding patients who had a codiagnosis of asthma. Conclusion: A diagnosis of COPD is strongly associated with a diagnosis of lung cancer, however, this association is largely explained by smoking habit, strongly dependent on the timing of COPD diagnosis, and not specific to COPD. It seems unlikely, therefore, that COPD is an independent risk factor for lung cancer.

Background The majority of cases of both lung cancer and COPD are attributable to cigarette smoking. Some consider COPD to be an independent risk factor for lung cancer, even after accounting for smoking, with estimates of increased risk up to 9-fold in previous studies. We undertook a large case-control study using prospectively collected data which allowed us to quantify this association in the UK population, whilst carefully controlling for smoking and the impact of timing of diagnoses. Methods We used The Health Improvement Network, a UK general practise database, to identify incident cases of lung cancer and controls matched on age, sex and the practise with which they were registered. Using conditional logistic regression, we assessed the effects of timing of first diagnoses of COPD, pneumonia and asthma on the odds of lung cancer, adjusting for smoking habit and socioeconomic status. Results Of 11,888 incident cases of lung cancer, 23% had a prior diagnosis of COPD compared with only 6% of the 37,605 controls. The odds of lung cancer in patients who had COPD diagnosed within 6 months of their cancer diagnosis were eleven-fold those of patients without COPD. However, when restricted to earlier COPD diagnoses, with adjustment for smoking, the effect markedly diminished (for COPD diagnoses >10 years before lung cancer diagnosis OR 2.18, 95% CI 1.87–2.54). The pattern was similar for pneumonia (see table). There was some diagnostic overlap between asthma and COPD but analyses which accounted for this produced similar results. Conclusion The association between COPD and lung cancer is largely explained by smoking habit, strongly dependent on the timing of COPD diagnosis and not specific to COPD. There is, however, an extremely strong unadjusted relationship of both COPD and pneumonia with lung cancer in the 6 months immediately prior to lung cancer diagnosis. This is useful in a clinical context highlighting the need to consider a diagnosis of lung cancer when making new diagnoses of COPD or pneumonia, and supporting the current NICE recommendation that all patients should have a chest radiograph looking for evidence of lung cancer at the time of COPD diagnosis.