Cardiovascular disease in Alpha 1 antitrypsin deficiency: an observational study assessing the role of neutrophil proteinase activity and the suitability of validated screening tools.

Alpha 1 anti-trypsin deficiency Arterial stiffness Cardiovascular disease Chronic obstructive pulmonary disease Emphysema Neutrophils Risk assessment

Journal

Orphanet journal of rare diseases
ISSN: 1750-1172
Titre abrégé: Orphanet J Rare Dis
Pays: England
ID NLM: 101266602

Informations de publication

Date de publication:
21 Mar 2024
Historique:
received: 26 04 2023
accepted: 03 03 2024
medline: 22 3 2024
pubmed: 22 3 2024
entrez: 22 3 2024
Statut: epublish

Résumé

Alpha 1 Antitrypsin Deficiency (AATD) is a rare, inherited lung disease which shares features with Chronic Obstructive Pulmonary Disease (COPD) but has a greater burden of proteinase related tissue damage. These proteinases are associated with cardiovascular disease (CVD) in the general population. It is unclear whether patients with AATD have a greater risk of CVD compared to usual COPD, how best to screen for this, and whether neutrophil proteinases are implicated in AATD-associated CVD. This study had three aims. To compare CVD risk in never-augmented AATD patients to non-AATD COPD and healthy controls (HC). To assess relationships between CVD risk and lung physiology. To determine if neutrophil proteinase activity was associated with CVD risk in AATD. Cardiovascular risk was assessed by QRISK2® score and aortic stiffness measurements using carotid-femoral (aortic) pulse wave velocity (aPWV). Medical history, computed tomography scans and post-bronchodilator lung function parameters were reviewed. Systemic proteinase 3 activity was measured. Patients were followed for 4 years, to assess CVD development. 228 patients with AATD, 50 with non-AATD COPD and 51 healthy controls were recruited. In all COPD and HC participants, QRISK2® and aPWV gave concordant results (with both measures either high or in the normal range). This was not the case in AATD. Once aPWV was adjusted for age and smoking history, aPWV was highest and QRISK2® lowest in AATD patients compared to the COPD or HC participants. Higher aPWV was associated with impairments in lung physiology, the presence of emphysema on CT scan and proteinase 3 activity following adjustment for age, smoking status and traditional CVD risk factors (using QRISK2® scores) in AATD. There were no such relationships with QRISK2® in AATD. AATD patients with confirmed CVD at four-year follow up had a higher aPWV but not QRISK2® at baseline assessment. aPWV measured CVD risk is elevated in AATD. This risk is not captured by QRISK2®. There is a relationship between aPWV, lung disease and proteinase-3 activity. Proteinase-driven breakdown of elastin fibres in large arteries and lungs is a putative mechanism and forms a potential therapeutic target for CVD in AATD.

Sections du résumé

BACKGROUND BACKGROUND
Alpha 1 Antitrypsin Deficiency (AATD) is a rare, inherited lung disease which shares features with Chronic Obstructive Pulmonary Disease (COPD) but has a greater burden of proteinase related tissue damage. These proteinases are associated with cardiovascular disease (CVD) in the general population. It is unclear whether patients with AATD have a greater risk of CVD compared to usual COPD, how best to screen for this, and whether neutrophil proteinases are implicated in AATD-associated CVD. This study had three aims. To compare CVD risk in never-augmented AATD patients to non-AATD COPD and healthy controls (HC). To assess relationships between CVD risk and lung physiology. To determine if neutrophil proteinase activity was associated with CVD risk in AATD. Cardiovascular risk was assessed by QRISK2® score and aortic stiffness measurements using carotid-femoral (aortic) pulse wave velocity (aPWV). Medical history, computed tomography scans and post-bronchodilator lung function parameters were reviewed. Systemic proteinase 3 activity was measured. Patients were followed for 4 years, to assess CVD development.
RESULTS RESULTS
228 patients with AATD, 50 with non-AATD COPD and 51 healthy controls were recruited. In all COPD and HC participants, QRISK2® and aPWV gave concordant results (with both measures either high or in the normal range). This was not the case in AATD. Once aPWV was adjusted for age and smoking history, aPWV was highest and QRISK2® lowest in AATD patients compared to the COPD or HC participants. Higher aPWV was associated with impairments in lung physiology, the presence of emphysema on CT scan and proteinase 3 activity following adjustment for age, smoking status and traditional CVD risk factors (using QRISK2® scores) in AATD. There were no such relationships with QRISK2® in AATD. AATD patients with confirmed CVD at four-year follow up had a higher aPWV but not QRISK2® at baseline assessment.
CONCLUSION CONCLUSIONS
aPWV measured CVD risk is elevated in AATD. This risk is not captured by QRISK2®. There is a relationship between aPWV, lung disease and proteinase-3 activity. Proteinase-driven breakdown of elastin fibres in large arteries and lungs is a putative mechanism and forms a potential therapeutic target for CVD in AATD.

Identifiants

pubmed: 38515138
doi: 10.1186/s13023-024-03124-x
pii: 10.1186/s13023-024-03124-x
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

130

Informations de copyright

© 2024. The Author(s).

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Auteurs

E Sapey (E)

Institute of Inflammation and Ageing, University of Birmingham, Birmingham, B15 2GW, UK.
University Hospitals Birmingham NHS Foundation Trust, Edgbaston, Birmingham, West Midlands, UK.

L E Crowley (LE)

Institute of Inflammation and Ageing, University of Birmingham, Birmingham, B15 2GW, UK. lxc097@bham.ac.uk.
University Hospitals Birmingham NHS Foundation Trust, Edgbaston, Birmingham, West Midlands, UK. lxc097@bham.ac.uk.

R G Edgar (RG)

Institute of Applied Health, University of Birmingham, Birmingham, West Midlands, UK.

D Griffiths (D)

University Hospitals Birmingham NHS Foundation Trust, Edgbaston, Birmingham, West Midlands, UK.

S Samanta (S)

UCL Respiratory, University College London, London, UK.

H Crisford (H)

Institute of Inflammation and Ageing, University of Birmingham, Birmingham, B15 2GW, UK.

C E Bolton (CE)

NIHR Nottingham BRC Respiratory Theme, School of Medicine, University of Nottingham, City Hospital NUH Trust, Nottingham, UK.

J R Hurst (JR)

UCL Respiratory, University College London, London, UK.

R A Stockley (RA)

University Hospitals Birmingham NHS Foundation Trust, Edgbaston, Birmingham, West Midlands, UK.

Classifications MeSH