Interview with the ECM Award winner 2022 and introducing the new ECM members

Support statement: J. Cruz acknowledges the support of the Center for Innovative Care and Health Technology (ciTechCare) of the Polytechnic of Leiria, which is funded by Portuguese national funds provided by Fundação para a Ciência e Tecnologia (FCT) (UIDB/05704/2020).This article presents the interview with the ERS Early Career Member Awardee 2022 (@MathioudakisAG) and provides a brief introduction to the new ECM members https://bit.ly/3BSRgV2 The Early Career Member (ECM) Award is intended to honour promising members of the European Respiratory Society (ERS) at an early stage of their professional career, based on their curriculum vitae, involvement in the ERS and potential for future scientific contributions. This award is given during the ERS International Congress, where the ECM Awardee is invited to give the Mina Gaga lecture during the ECM session. In this article, we present an interview conducted with the 2022 ECM Award winner, Alexander Mathioudakis, where he discussed his work and visions for the future and shared some tips for ECMs starting a career in respiratory research. We also provide a brief introduction to the new members of the ECM Committee (ECMC) from Assemblies 2 (Respiratory intensive care), 3 (Basic and translational sciences), 7 (Paediatrics) and 8 (Thoracic surgery and transplantation).info:eu-repo/semantics/publishedVersio

Low-density lipoprotein cholesterol and risk of COPD: Copenhagen General Population Study

Background Randomised controlled trials found that low-density lipoprotein (LDL) cholesterol-lowering statins increase lung function and possibly decrease rate of exacerbations in individuals with COPD. However, it is unknown whether high levels of LDL cholesterol are associated with increased susceptibility to COPD. Methods We tested the hypothesis that high LDL cholesterol is associated with increased risk of COPD, severe COPD exacerbation and COPD-specific mortality. We examined 107 301 adults from the Copenhagen General Population Study. COPD outcomes were ascertained at baseline and prospectively through nationwide registries. Results In cross-sectional analysis, low LDL cholesterol was associated with increased risk of COPD (odds ratio for 1st versus 4th quartile: 1.07 (95% CI 1.01–1.14)). Prospectively, low LDL cholesterol was associated with increased risk of COPD exacerbations with hazard ratios of 1.43 (1.21–1.70) for 1st versus 4th quartile, 1.21 (1.03–1.43) for 2nd versus 4th quartile, and 1.01 (0.85–1.20) for 3rd versus 4th quartile of LDL cholesterol (p-value for trend=6×10−6). Finally, low LDL cholesterol was likewise associated with increased risk of COPD-specific mortality (log-rank test: p=0.0009). Sensitivity analyses with death as competing risk provided similar results. Conclusion Low LDL cholesterol was associated with increased risks of severe COPD exacerbation and COPD-specific mortality in the Danish general population. As this is opposite of that observed in randomised controlled trials with statins, our findings might be a result of reverse causation indicating that individuals with severe phenotypes of COPD have lower plasma levels of LDL cholesterol due to wasting

α1-Antitrypsin deficiency associated with increased risk of heart failure

Background Individuals with α1-antitrypsin deficiency have increased elastase activity resulting in continuous degradation of elastin and early onset of COPD. Increased elastase activity may also affect elastic properties of the heart, which may impact risk of heart failure. We tested the hypothesis that α1-antitrypsin deficiency is associated with increased risk of heart failure in two large populations. Methods In a nationwide nested study of 2209 patients with α1-antitrypsin deficiency and 21 869 controls without α1-antitrypsin deficiency matched on age, sex and municipality, we recorded admissions and deaths due to heart failure during a median follow-up of 62 years. We also studied a population-based cohort of another 102 481 individuals from the Copenhagen General Population Study including 187 patients from the Danish α1-Antitrypsin Deficiency Registry, all with genetically confirmed α1-antitrypsin deficiency. Results Individuals with versus without α1-antitrypsin deficiency had increased risk of heart failure hospitalisation in the nationwide cohort (adjusted hazard ratio 2.64, 95% CI 2.25–3.10) and in the population-based cohort (1.77, 95% CI 1.14–2.74). Nationwide, these hazard ratios were highest in those without myocardial infarction (3.24, 95% CI 2.70–3.90), without aortic valve stenosis (2.80, 95% CI 2.38–3.29), without hypertension (3.44, 95% CI 2.81–4.22), without atrial fibrillation (3.33, 95% CI 2.75–4.04) and without any of these four diseases (6.00, 95% CI 4.60–7.82). Hazard ratios for heart failure-specific mortality in individuals with versus without α1-antitrypsin deficiency were 2.28 (95% CI 1.57–3.32) in the nationwide cohort and 3.35 (95% CI 1.04–10.74) in the population-based cohort. Conclusion Individuals with α1-antitrypsin deficiency have increased risk of heart failure hospitalisation and heart failure-specific mortality in the Danish population

Severe α₁-antitrypsin deficiency associated with lower blood pressure and reduced risk of ischemic heart disease:a cohort study of 91,540 individuals and a meta-analysis

BACKGROUND: Increased elastase activity in α(1)-antitrypsin deficiency may affect elasticity of the arterial walls, and thereby blood pressure and susceptibility to cardiovascular disease. We hypothesized that severe α(1)-antitrypsin deficiency is associated with reduced blood pressure and susceptibility to cardiovascular disease. METHODS: We genotyped 91,353 adults randomly selected from the Danish general population and 187 patients from the Danish α(1)-Antitrypsin Deficiency Registry and recorded baseline blood pressure, baseline plasma lipids and cardiovascular events during follow-up. 185 participants carried the ZZ genotype, 207 carried the SZ genotype and 91,148 carried the MM genotype. RESULTS: α(1)-Antitrypsin deficiency was associated with decreases in blood pressure of up to 5 mmHg for systolic blood pressure and up to 2 mmHg for diastolic blood pressure, in ZZ vs SZ vs MM individuals (trend test, P’s ≤ 0.01). Plasma triglycerides and remnant cholesterol were reduced in ZZ individuals compared with MM individuals (t-test, P’s < 0.001). α(1)-Antitrypsin deficiency was associated with lower risk of myocardial infarction (trend test P = 0.03), but not with ischemic heart disease, ischemic cerebrovascular disease or hypertension (trend test, P’s ≥ 0.59). However, when results for ischemic heart disease were summarized in meta-analysis with results from four previous studies, individuals with versus without α(1)-antitrypsin deficiency had an odds ratio for ischemic heart disease of 0.66 (95% CI:0.53–0.84). CONCLUSIONS: Individuals with severe α(1)-antitrypsin deficiency have lower systolic and diastolic blood pressure, lower plasma triglycerides and remnant cholesterol, reduced risk of myocardial infarction, and a 34% reduced risk of ischemic heart disease. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12931-022-01973-3