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1.
Artigo em Inglês | MEDLINE | ID: mdl-30878439

RESUMO

OBJECTIVES: This study used optical coherence tomography to investigate the mechanism of false lumen (FL) formation in spontaneous coronary artery dissection (SCAD) by studying: 1) differences between fenestrated and nonfenestrated SCAD; 2) vasa vasorum density; and 3) light attenuation characteristics of the FL. BACKGROUND: SCAD is an increasingly recognized cause of acute coronary syndromes, characterized by FL formation and compression of the true lumen (TL). The mechanisms underlying FL formation remain poorly understood. METHODS: A total of 65 SCAD patients (68 vessels) who underwent acute OCT imaging as part of routine clinical care were included. Images were classified by the absence or presence of a connection (fenestration) between the TL and FL. Indexed measurements of TL stenosis, external elastic lamina (EEL) area, FL area, and light attenuation of the FL were assessed. Vasa vasorum densities of SCAD cases were compared with those in control non-SCAD myocardial infarction cases. RESULTS: In nonfenestrated cases, there was significantly larger expansion of the EEL area (9.1% vs. -1.9%; p <0.05) and a larger FL area (73.6% vs. 53.2%, respectively; p <0.05) in dissected segments. No significant differences were found between vasa vasorum density in SCAD and those in control subjects. The FL contents were heterogeneous but attenuated less light than whole blood or thrombus (4.28 ± 0.55 mm-1 vs. 5.08 ± 0.56 mm-1; p < 0.05; vs. 4.96 ± 0.56 mm-1; p < 0.05). CONCLUSIONS: These observational data suggest that the absence of a fenestration leads to increased FL pressure and compression of the TL. Although vasa vasorum may still be implicated in pathogenesis, increased vasa vasorum density could be an epiphenomenon of vascular healing.

2.
J Am Coll Cardiol ; 73(1): 58-66, 2019 Jan 08.
Artigo em Inglês | MEDLINE | ID: mdl-30621952

RESUMO

BACKGROUND: Spontaneous coronary artery dissection (SCAD) is an increasingly recognized cause of acute coronary syndromes (ACS) afflicting predominantly younger to middle-aged women. Observational studies have reported a high prevalence of extracoronary vascular anomalies, especially fibromuscular dysplasia (FMD) and a low prevalence of coincidental cases of atherosclerosis. PHACTR1/EDN1 is a genetic risk locus for several vascular diseases, including FMD and coronary artery disease, with the putative causal noncoding variant at the rs9349379 locus acting as a potential enhancer for the endothelin-1 (EDN1) gene. OBJECTIVES: This study sought to test the association between the rs9349379 genotype and SCAD. METHODS: Results from case control studies from France, United Kingdom, United States, and Australia were analyzed to test the association with SCAD risk, including age at first event, pregnancy-associated SCAD (P-SCAD), and recurrent SCAD. RESULTS: The previously reported risk allele for FMD (rs9349379-A) was associated with a higher risk of SCAD in all studies. In a meta-analysis of 1,055 SCAD patients and 7,190 controls, the odds ratio (OR) was 1.67 (95% confidence interval [CI]: 1.50 to 1.86) per copy of rs9349379-A. In a subset of 491 SCAD patients, the OR estimate was found to be higher for the association with SCAD in patients without FMD (OR: 1.89; 95% CI: 1.53 to 2.33) than in SCAD cases with FMD (OR: 1.60; 95% CI: 1.28 to 1.99). There was no effect of genotype on age at first event, P-SCAD, or recurrence. CONCLUSIONS: The first genetic risk factor for SCAD was identified in the largest study conducted to date for this condition. This genetic link may contribute to the clinical overlap between SCAD and FMD.

4.
BMJ Case Rep ; 20162016 Jan 22.
Artigo em Inglês | MEDLINE | ID: mdl-26802063

RESUMO

This case describes a patient who presented with an occluded and ectatic right coronary artery. Initial aspiration and, later, guide catheter thrombectomy, liberated large volumes of thrombus but did not appear to restore significant flow. Thrombolysis in myocardial infarction (TIMI) 3 flow was, however, evident 2 weeks later, demonstrating the combined effect of vigorous thrombectomy and autolysis on a heavily thrombotic section of coronary artery.


Assuntos
Trombose Coronária/cirurgia , Vasos Coronários/patologia , Trombectomia/métodos , Cateteres Cardíacos , Sistema de Condução Cardíaco/fisiopatologia , Humanos , Infarto do Miocárdio/cirurgia , Sucção/métodos , Trombectomia/efeitos adversos , Trombectomia/instrumentação , Resultado do Tratamento
5.
BMJ Case Rep ; 20142014 Sep 08.
Artigo em Inglês | MEDLINE | ID: mdl-25201873

RESUMO

A 37-year-old woman was admitted into the coronary care unit following chest pain after using cocaine. She was found to have significant myocardial ischaemia on blood and ECG investigations despite a recent coronary angiogram that had not demonstrated flow-limiting coronary disease. This case report summarises the risks of myocardial ischaemia and/or infarction for patients taking cocaine and the pathophysiology behind it, focusing in particular on the risks of delayed reaction some time after cocaine ingestion.


Assuntos
Transtornos Relacionados ao Uso de Cocaína/complicações , Cocaína/efeitos adversos , Isquemia Miocárdica/induzido quimicamente , Adulto , Dor no Peito/diagnóstico , Dor no Peito/etiologia , Angiografia Coronária , Eletrocardiografia , Feminino , Humanos , Infarto/induzido quimicamente , Infarto do Miocárdio/induzido quimicamente , Infarto do Miocárdio/diagnóstico , Isquemia Miocárdica/diagnóstico , Vasoconstritores/efeitos adversos
7.
J Immunol ; 189(11): 5155-64, 2012 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-23087405

RESUMO

1,25-Dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], the active form of vitamin D, exerts potent effects on several tissues including cells of the immune system, where it affects T cell activation, differentiation and migration. The circulating, inactive form of vitamin D, 25(OH)D(3), is generally used as an indication of vitamin D status. However, use of this precursor depends on its uptake by cells and subsequent conversion by the enzyme 25(OH)D(3)-1α-hydroxylase (CYP27B1) into active 1,25(OH)(2)D(3). Using human T cells, we show in this study that addition of inactive 25(OH)D(3) is sufficient to alter T cell responses only when dendritic cells (DCs) are present. Mechanistically, CYP27B1 is induced in DCs upon maturation with LPS or upon T cell contact, resulting in the generation and release of 1,25(OH)(2)D(3), which subsequently affects T cell responses. In most tissues, vitamin D binding protein acts as a carrier to enhance the use of vitamin D. However, we show that vitamin D binding protein modulates T cell responses by restricting the availability of inactive 25(OH)D(3) to DC. These data indicate that the level of free 25(OH)D(3) available to DCs determines the inflammatory/regulatory balance of ensuing T cell responses.


Assuntos
25-Hidroxivitamina D3 1-alfa-Hidroxilase/metabolismo , Calcifediol/imunologia , Calcitriol/imunologia , Células Dendríticas/imunologia , Linfócitos T/imunologia , 25-Hidroxivitamina D3 1-alfa-Hidroxilase/imunologia , Calcifediol/metabolismo , Calcitriol/metabolismo , Comunicação Celular/efeitos dos fármacos , Comunicação Celular/imunologia , Diferenciação Celular/efeitos dos fármacos , Diferenciação Celular/imunologia , Técnicas de Cocultura , Células Dendríticas/efeitos dos fármacos , Células Dendríticas/enzimologia , Ativação Enzimática/efeitos dos fármacos , Ativação Enzimática/imunologia , Humanos , Lipopolissacarídeos/imunologia , Lipopolissacarídeos/farmacologia , Ativação Linfocitária/efeitos dos fármacos , Cultura Primária de Células , Transdução de Sinais/efeitos dos fármacos , Linfócitos T/efeitos dos fármacos , Linfócitos T/metabolismo , Fator de Crescimento Transformador beta/imunologia , Fator de Crescimento Transformador beta/farmacologia
8.
Eur Respir J ; 40(3): 561-9, 2012 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-22700846

RESUMO

There is inherent daily variability of sputum inflammatory mediators in stable-state patients with usual chronic obstructive pulmonary disease (COPD). The variability of pulmonary inflammation in patients with α(1)-antitrypsin deficiency (A1ATD) is unknown. Our study aimed to quantify this variability, in comparison to patients with usual COPD, in order to facilitate power calculations for proof of concept trials of putative specific anti-inflammatory agents in both groups. Sputum interleukin (IL)-8, myeloperoxidase (MPO), leukotriene B(4) (LTB(4)) and differential cell counts were measured in 12 usual COPD patients and 12 A1ATD patients on nine occasions over a 1-month period. All samples were obtained in the stable clinical state. There was significant daily variability in all mediators in all patients. A1ATD patients had higher sputum concentrations of IL-8 and LTB(4) compared with usual COPD, but lower levels of MPO and absolute neutrophil counts. Patients with usual COPD had more intra-patient variability, A1ATD patients demonstrated greater inter-patient variability. There are increased concentrations of pulmonary inflammatory mediators but fewer sputum neutrophils in A1ATD compared with usual COPD. The daily variability of inflammatory mediators and cell counts was significantly reduced in both groups by averaging sequential samples. This can be utilised to perform power calculations for future proof of concept studies; averaging three sequential samples appears optimum.


Assuntos
Mediadores da Inflamação/metabolismo , Doença Pulmonar Obstrutiva Crônica/metabolismo , Escarro/química , Deficiência de alfa 1-Antitripsina/metabolismo , Adulto , Idoso , Contagem de Células , Feminino , Humanos , Mediadores da Inflamação/análise , Interleucina-8/análise , Leucotrieno B4/análise , Masculino , Pessoa de Meia-Idade , Peroxidase/análise
9.
Respir Res ; 13: 16, 2012 Feb 22.
Artigo em Inglês | MEDLINE | ID: mdl-22356581

RESUMO

BACKGROUND: The development of COPD in subjects with alpha-1 antitrypsin (AAT) deficiency is likely to be influenced by modifier genes. Genome-wide association studies and integrative genomics approaches in COPD have demonstrated significant associations with SNPs in the chromosome 15q region that includes CHRNA3 (cholinergic nicotine receptor alpha3) and IREB2 (iron regulatory binding protein 2).We investigated whether SNPs in the chromosome 15q region would be modifiers for lung function and COPD in AAT deficiency. METHODS: The current analysis included 378 PIZZ subjects in the AAT Genetic Modifiers Study and a replication cohort of 458 subjects from the UK AAT Deficiency National Registry. Nine SNPs in LOC123688, CHRNA3 and IREB2 were selected for genotyping. FEV1 percent of predicted and FEV1/FVC ratio were analyzed as quantitative phenotypes. Family-based association analysis was performed in the AAT Genetic Modifiers Study. In the replication set, general linear models were used for quantitative phenotypes and logistic regression models were used for the presence/absence of emphysema or COPD. RESULTS: Three SNPs (rs2568494 in IREB2, rs8034191 in LOC123688, and rs1051730 in CHRNA3) were associated with pre-bronchodilator FEV1 percent of predicted in the AAT Genetic Modifiers Study. Two SNPs (rs2568494 and rs1051730) were associated with the post-bronchodilator FEV1 percent of predicted and pre-bronchodilator FEV1/FVC ratio; SNP-by-gender interactions were observed. In the UK National Registry dataset, rs2568494 was significantly associated with emphysema in the male subgroup; significant SNP-by-smoking interactions were observed. CONCLUSIONS: IREB2 and CHRNA3 are potential genetic modifiers of COPD phenotypes in individuals with severe AAT deficiency and may be sex-specific in their impact.


Assuntos
Proteína 2 Reguladora do Ferro/genética , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Receptores Nicotínicos/genética , Deficiência de alfa 1-Antitripsina/genética , Adulto , Cromossomos Humanos Par 15/genética , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Polimorfismo de Nucleotídeo Único , Enfisema Pulmonar/genética , Enfisema Pulmonar/fisiopatologia , Testes de Função Respiratória , Índice de Gravidade de Doença , Fatores Sexuais , Deficiência de alfa 1-Antitripsina/fisiopatologia
10.
Mamm Genome ; 23(3-4): 241-9, 2012 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-22076419

RESUMO

Animal models that closely resemble human disease can present a challenge. Particularly so in alpha-1 antitrypsin deficiency (α(1)ATD), as the mouse alpha-1 antitrypsin (α(1)AT) cluster encodes five highly related genes compared with the one in humans. The mouse PI2 homologue is closest to the α(1)AT human gene. We have changed the equivalent mouse site that results in the Z variant in man (Glu342Lys) and made both the "M" and "Z" mouse PI2 α(1)AT proteins. We have tested the ability of a small-molecular-weight compound CG to alleviate polymerisation of these mouse α(1)AT proteins as it has been shown to reduce aggregates of Z α(1)AT in man. We found that (1) CG specifically reduces the formation of polymers of recombinant mouse "Z" protein but not "M" protein; (2) whereas there is significantly more α(1)AT secreted from Chinese Hamster Ovary cells transfected with the mouse "M" α(1)AT gene than with the "Z" (20.8 ± 3.9 and 6.7 ± 3.6, respectively; P < 0.005), CG increased the α(1)AT levels secreted from "Z" cells (21.2 ± 0.01) to that of "M" (20.2 ± 0.02). The data support the concept that the murine "Z" gene is a potential model for the study of α(1)ATD and that mice expressing this gene would be relevant for testing treatments in vivo.


Assuntos
Modelos Biológicos , Bibliotecas de Moléculas Pequenas/farmacologia , Deficiência de alfa 1-Antitripsina/tratamento farmacológico , alfa 1-Antitripsina/genética , Animais , Células CHO , Cricetinae , Feminino , Humanos , Masculino , Camundongos , Transfecção , alfa 1-Antitripsina/química , alfa 1-Antitripsina/metabolismo , Deficiência de alfa 1-Antitripsina/genética , Deficiência de alfa 1-Antitripsina/metabolismo
12.
J Interv Cardiol ; 24(5): 389-96, 2011 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-21585544

RESUMO

BACKGROUND: It is normally necessary to use more than 1 coronary catheter in primary percutaneous coronary intervention (PPCI) for ST elevation myocardial infarction (STEMI). We explored the utility of a single guide catheter (Q) strategy for complete coronary assessment and treatment in PPCI. METHODS: Fifty-seven consecutive STEMI cases undergoing invasive management were included. Radial access was the default route (6 cases via femoral access). Among radial cases, a TIG catheter was used first on 6 occasions (perceived low likelihood of subsequent PCI) and a Judkins right followed by an EBU catheter on three occasions (stock issue). A Q guide was used as initial default in the remaining 42 cases. Two anterior STEMI cases had recently undergone angiography and did not require right coronary reinspection. Procedural and outcomes data were recorded prospectively. RESULTS: The Q catheter allowed complete assessment and treatment in 33 cases, 6 cases requiring a second catheter and one patient dying prior to right coronary imaging. Territories of infarction were: anterior (n = 18), inferior (n = 14), inferoposterior (n = 3), lateral (n = 1), inferolateral (n = 2), inferoposterolateral (n = 2). Sixty-three out of 65 lesions were treated successfully. Median catheterization laboratory door to balloon time was 18 minutes (IQR 15-21 minutes). There were no catheter-related complications. CONCLUSIONS: A default Q guide catheter allows rapid effective imaging and treatment of both left and right coronaries in the majority of STEMI cases suitable for radial access PPCI.


Assuntos
Angioplastia Coronária com Balão/instrumentação , Cateteres , Vasos Coronários/patologia , Infarto do Miocárdio/terapia , Artéria Radial , Idoso , Angioplastia Coronária com Balão/métodos , Stents Farmacológicos , Feminino , Indicadores Básicos de Saúde , Humanos , Masculino , Infarto do Miocárdio/tratamento farmacológico , Infarto do Miocárdio/mortalidade , Infarto do Miocárdio/cirurgia , Estudos Retrospectivos , Índice de Gravidade de Doença , Estatísticas não Paramétricas , Resultado do Tratamento
15.
Catheter Cardiovasc Interv ; 78(1): 54-7, 2011 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-21413121

RESUMO

Perforation and disruption of the artery used for access is a recognized complication of coronary angiography. There is an increasing trend toward use of the radial artery for angiography and angioplasty, particularly in the primary angioplasty setting, because of the reduced risk of hemorrhagic complications. On the rare occasions when radial artery perforation occurs, operators have had a tendency to switch to a second arterial access route. This article describes a technique for managing peri-procedural perforation which does not require use of a second artery for access. We show two cases where this technique was used successfully, demonstrating an angiographically normal radial artery at the end of the procedure.


Assuntos
Angioplastia Coronária com Balão/efeitos adversos , Angiografia Coronária/efeitos adversos , Hemorragia/prevenção & controle , Técnicas Hemostáticas , Artéria Radial/lesões , Lesões do Sistema Vascular/terapia , Angioplastia Coronária com Balão/instrumentação , Hemorragia/diagnóstico por imagem , Hemorragia/etiologia , Humanos , Masculino , Pessoa de Meia-Idade , Artéria Radial/diagnóstico por imagem , Ruptura , Stents , Resultado do Tratamento , Lesões do Sistema Vascular/diagnóstico por imagem , Lesões do Sistema Vascular/etiologia
17.
Occup Environ Med ; 67(8): 556-61, 2010 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-20519748

RESUMO

INTRODUCTION: Outdoor air pollutants are associated with respiratory morbidity and mortality, but little longitudinal work has been undertaken in this area in chronic obstructive pulmonary disease (COPD). Patients with alpha-1-antitrypsin deficiency (AATD) typically exhibit faster decline of lung function than subjects with usual COPD and thus represent a group in whom studies of factors influencing decline may be more easily clarified. METHODS: Decline of FEV(1) and KCO in subjects of the PiZZ genotype from the UK AATD registry were studied. Pollution levels (PM(10), ozone, sulphur dioxide, nitrogen dioxide) during the exposure window were extracted from GIS maps, matching the measurement to each patient's home address. Clinical predictors of decline were sought using generalised estimating equations, and pollutants added to these subsequently. Single pollutant models were used due to multicollinearity. RESULTS: In the FEV(1) decline analysis, higher baseline FEV(1) was associated with rapid decline of FEV(1) (p<0.001). High PM(10) exposure predicted more rapid decline of FEV(1) (p=0.024). In a similar analysis for KCO decline, higher baseline KCO predicted rapid decline (p<0.001) as did higher exposure to ozone (p=0.018). High PM(10) exposure also showed a trend towards this effect (p=0.056). CONCLUSIONS: Exposure to ozone and PM(10) predicts decline of lung function in AATD.


Assuntos
Poluição do Ar/efeitos adversos , Exposição Ocupacional/efeitos adversos , Ozônio/toxicidade , Doença Pulmonar Obstrutiva Crônica/fisiopatologia , Dióxido de Enxofre/toxicidade , Deficiência de alfa 1-Antitripsina/fisiopatologia , Feminino , Volume Expiratório Forçado/fisiologia , Humanos , Masculino , Pessoa de Meia-Idade , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Testes de Função Respiratória , Inquéritos e Questionários , Reino Unido/epidemiologia , Deficiência de alfa 1-Antitripsina/epidemiologia
18.
Am J Respir Crit Care Med ; 182(2): 192-9, 2010 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-20299531

RESUMO

RATIONALE: Chronic obstructive pulmonary disease (COPD) has a genetic component, explaining susceptibility. Tumor necrosis factor (TNF)-alpha polymorphisms have been associated with COPD, but it is unclear if genotype influences clinical phenotype, protein expression, and bioactivity. OBJECTIVES: To determine if a functional polymorphism was important by assessing TNF-alpha expression and activity and its association with clinical severity over time. METHODS: Patients with COPD with rs361525 polymorphism were matched to patients with COPD without rs361525 polymorphism. TNF-alpha, its antagonists, and downstream mediators were measured in plasma and sputum. To determine TNF-alpha bioactivity, IL-8 secretion from primary bronchial epithelial cells (PBECs) was measured, and neutrophil migration was assessed using sputum from both subject groups in the presence and absence of TNF-alpha antibody. Subjects were followed annually and compared. MEASUREMENTS AND MAIN RESULTS: Patients with polymorphism had more chronic bronchitis, a lower body mass index, and a greater annual decline in FEV(1) than patients with COPD without rs361525 polymorphism. TNF-alpha concentrations were 100-fold higher in airway secretions from the patients with the rs361525 polymorphism, with no difference in TNF-alpha antagonists. Their lung secretions contained more IL-8 and myeloperoxidase, consistent with downstream inflammation. Sputum from patients with rs361525 polymorphism induced greater secretion of IL-8 from PBECs and increased neutrophil migration. These effects could be abrogated by TNF-alpha antibody, demonstrating the bioactivity of TNF-alpha in lung secretions from this group. CONCLUSIONS: This TNF-alpha polymorphism is associated with clinical features of disease including progression. There is clear evidence of TNF-alpha overexpression and bioactivity with neutrophilic inflammation. The polymorphism is likely to be a factor that influences a COPD disease phenotype and its progression.


Assuntos
Polimorfismo Genético , Doença Pulmonar Obstrutiva Crônica/genética , Fator de Necrose Tumoral alfa/genética , Adulto , Idoso , Índice de Massa Corporal , Brônquios/citologia , Bronquite/epidemiologia , Estudos de Casos e Controles , Movimento Celular , Progressão da Doença , Células Epiteliais/metabolismo , Feminino , Volume Expiratório Forçado , Genótipo , Humanos , Interleucina-8/metabolismo , Masculino , Pessoa de Meia-Idade , Neutrófilos/fisiologia , Peroxidase/metabolismo , Fenótipo , Índice de Gravidade de Doença , Escarro/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
19.
Genome Med ; 1(11): 112, 2009 Nov 30.
Artigo em Inglês | MEDLINE | ID: mdl-19951401

RESUMO

Chronic obstructive pulmonary disease (COPD) is a common problem worldwide, and it is recognized that the term encompasses overlapping sub-phenotypes of disease. The development of a sub-phenotype may be determined in part by an individual's genetics, which in turn may determine response to treatment. A growing understanding of the genetic factors that predispose to COPD and its sub-phenotypes and the pathophysiology of the condition is now leading to the suggestion of individualized therapy based on the patients' clinical phenotype and genotype. Pharmacogenetics is the study of variations in treatment response according to genotype and is perhaps the next direction for genetic research in COPD. Here, we consider how knowledge of the pathophysiology and genetic risk factors for COPD may inform future management strategies for affected individuals.

20.
Respir Med ; 103(10): 1540-7, 2009 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-19443188

RESUMO

BACKGROUND: Four hundred and eighty-eight PiZ alpha-1-antitrypsin deficient patients, who had joined the UK registry over a 9-year period, were followed in an observational study to determine mortality. None had received A1AT augmentation therapy. METHODS: Cause of death was confirmed from death certification and medical records. Patients were censored according to length of time on the program or until they withdrew from the program. RESULTS: There were 56 deaths of which 30 were attributed to respiratory causes. Of the remaining 26 deaths, 4 were due to complications from lung transplant, 6 due to liver disease (including 2 post-liver transplant) and the other 16 due to a variety of causes. Kaplan-Meier plots indicated a cumulative hazard for mortality of 18.1% in 9 years, correcting for time of follow up. When categorised for FEV1 percent-predicted, the group with severe impairment had increased mortality (p = <0.001) compared with the mild group and there was a direct relationship between severity and mortality. The severe group had increased mortality compared with the mild group when categorised for KCO percent-predicted (p<0.001), RV/TLC ratio (p<0.001) or emphysema score on CT scan (p<0.001 upper zone). Cox regression analyses indicated that these relationships remained when corrected for age. There were no differences in mortality after categorisation for educational level or occupational group. CONCLUSION: Mortality in a cohort of A1AT deficient patients (PiZ phenotype) in the UK was 2% per year and was associated with lung function impairment and emphysema severity on CT scan, but not social status.


Assuntos
Enfisema Pulmonar/mortalidade , Deficiência de alfa 1-Antitripsina/mortalidade , Causas de Morte , Feminino , Volume Expiratório Forçado/fisiologia , Humanos , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Enfisema Pulmonar/diagnóstico por imagem , Enfisema Pulmonar/fisiopatologia , Tomografia Computadorizada por Raios X , Reino Unido/epidemiologia , Deficiência de alfa 1-Antitripsina/diagnóstico por imagem , Deficiência de alfa 1-Antitripsina/fisiopatologia
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