Reduced lung function in patients with abdominal aortic aneurysm is associated with activation of inflammation and hemostasis, not smoking or cardiovascular disease

F. G. R. Fowkes, C. L. C. Anandan, Amanda Jane Lee, F. B. Smith, I. Tzoulaki, A. Rumley, J. T. Powell, G. D. O. Lowe

Research output: Contribution to journalArticle

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Abstract

Objective: Abdominal aortic aneurysms often coexist with reduced lung function and chronic obstructive pulmonary disease (COPD). These conditions are each associated with cigarette smoking, cardiovascular disease, and evidence of increased inflammatory and hemostatic activity. The aim of this study was to determine if these factors accounted for the link between aneurysms and pulmonary disease.

Methods. The design was a case-control study comparing patients with an asymptomatic abdominal aortic aneurysm with population-based controls without an aneurysm. Aneurysms were diagnosed by ultrasound scan, and pulmonary function was measured by respiratory questionnaire and spirometry. Activation of inflammation and hemostasis was measured by assay of plasma interleukin-6 (IL-6), fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (tPA) antigen, fibrin D-dimer, and plasmin antiplasmin complexes.

Results. Cases with an abdominal aortic aneurysm (n = 89) had more COPD and worse expiratory lung function as measured by forced expiratory volume in I second (FEVI) and forced vital capacity C) than controls (n = 98) (FEVI, 1.9 vs 2.2 L, P < .01; FEVI/FVC, 0.67 vs 0.75, P < .001) and did not differ in restrictive function (FVC, 2.9 vs 3.0 L, P = .33). Cases also had higher levels of lifetime cigarette smoking (30 vs 24 pack-years, P < 0.01), cardiovascular disease (35% vs 18%, P = .01), plasma fibrinogen (3.5 vs 3.1 g/L, P = .02), IL-6 (2.8 vs 1.8, pg/mL, P < .001), plasmin antiplasmin complexes (596 vs 384 mu g/L, P = .01), and D-dimer (442 vs 93 ng/mL, P < .001). On multiple logistic regression analysis of lung function and COPD on the risk of aneurysm, both cigarette smoking and cardiovascular disease had little effect on the relationships. For the markers of activated inflammation and hemostasis, plasmin antiplasmin complexes and D-dimer had the most important confounding effect on the odds ratios. All markers combined had a substantial effect: odds ratio of aneurysm for a one standard deviation decrease in FEVI fell from 2.3 (95% confidence interval [CI], 1.5 to 3.5) (P <.01) to 1.3 (95% CI, 0.55 to 2.4) (P >= 1.05).

Conclusion: The association between reduced respiratory function and abdominal aortic aneurysm was not accounted for by cigarette smoking or cardiovascular disease. We hypothesize that activation of inflammation and hemostasis in response to injury may be an important explanation of the association between aneurysm formation and reduced respiratory function. Further studies are required to test this hypothesis.

Original languageEnglish
Pages (from-to)474-480
Number of pages6
JournalJournal of Vascular Surgery
Volume43
DOIs
Publication statusPublished - Mar 2006

Keywords

  • OBSTRUCTIVE PULMONARY-DISEASE
  • GENERAL-POPULATION
  • NATURAL-HISTORY
  • BLOOD-PRESSURE
  • RISK-FACTORS
  • MEN BORN
  • ATHEROSCLEROSIS
  • RUPTURE
  • COHORT
  • METALLOPROTEINASES

Cite this

Reduced lung function in patients with abdominal aortic aneurysm is associated with activation of inflammation and hemostasis, not smoking or cardiovascular disease. / Fowkes, F. G. R.; Anandan, C. L. C.; Lee, Amanda Jane; Smith, F. B.; Tzoulaki, I.; Rumley, A.; Powell, J. T.; Lowe, G. D. O.

In: Journal of Vascular Surgery, Vol. 43, 03.2006, p. 474-480.

Research output: Contribution to journalArticle

Fowkes, F. G. R. ; Anandan, C. L. C. ; Lee, Amanda Jane ; Smith, F. B. ; Tzoulaki, I. ; Rumley, A. ; Powell, J. T. ; Lowe, G. D. O. / Reduced lung function in patients with abdominal aortic aneurysm is associated with activation of inflammation and hemostasis, not smoking or cardiovascular disease. In: Journal of Vascular Surgery. 2006 ; Vol. 43. pp. 474-480.
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abstract = "Objective: Abdominal aortic aneurysms often coexist with reduced lung function and chronic obstructive pulmonary disease (COPD). These conditions are each associated with cigarette smoking, cardiovascular disease, and evidence of increased inflammatory and hemostatic activity. The aim of this study was to determine if these factors accounted for the link between aneurysms and pulmonary disease.Methods. The design was a case-control study comparing patients with an asymptomatic abdominal aortic aneurysm with population-based controls without an aneurysm. Aneurysms were diagnosed by ultrasound scan, and pulmonary function was measured by respiratory questionnaire and spirometry. Activation of inflammation and hemostasis was measured by assay of plasma interleukin-6 (IL-6), fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (tPA) antigen, fibrin D-dimer, and plasmin antiplasmin complexes.Results. Cases with an abdominal aortic aneurysm (n = 89) had more COPD and worse expiratory lung function as measured by forced expiratory volume in I second (FEVI) and forced vital capacity C) than controls (n = 98) (FEVI, 1.9 vs 2.2 L, P < .01; FEVI/FVC, 0.67 vs 0.75, P < .001) and did not differ in restrictive function (FVC, 2.9 vs 3.0 L, P = .33). Cases also had higher levels of lifetime cigarette smoking (30 vs 24 pack-years, P < 0.01), cardiovascular disease (35{\%} vs 18{\%}, P = .01), plasma fibrinogen (3.5 vs 3.1 g/L, P = .02), IL-6 (2.8 vs 1.8, pg/mL, P < .001), plasmin antiplasmin complexes (596 vs 384 mu g/L, P = .01), and D-dimer (442 vs 93 ng/mL, P < .001). On multiple logistic regression analysis of lung function and COPD on the risk of aneurysm, both cigarette smoking and cardiovascular disease had little effect on the relationships. For the markers of activated inflammation and hemostasis, plasmin antiplasmin complexes and D-dimer had the most important confounding effect on the odds ratios. All markers combined had a substantial effect: odds ratio of aneurysm for a one standard deviation decrease in FEVI fell from 2.3 (95{\%} confidence interval [CI], 1.5 to 3.5) (P <.01) to 1.3 (95{\%} CI, 0.55 to 2.4) (P >= 1.05).Conclusion: The association between reduced respiratory function and abdominal aortic aneurysm was not accounted for by cigarette smoking or cardiovascular disease. We hypothesize that activation of inflammation and hemostasis in response to injury may be an important explanation of the association between aneurysm formation and reduced respiratory function. Further studies are required to test this hypothesis.",
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author = "Fowkes, {F. G. R.} and Anandan, {C. L. C.} and Lee, {Amanda Jane} and Smith, {F. B.} and I. Tzoulaki and A. Rumley and Powell, {J. T.} and Lowe, {G. D. O.}",
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TY - JOUR

T1 - Reduced lung function in patients with abdominal aortic aneurysm is associated with activation of inflammation and hemostasis, not smoking or cardiovascular disease

AU - Fowkes, F. G. R.

AU - Anandan, C. L. C.

AU - Lee, Amanda Jane

AU - Smith, F. B.

AU - Tzoulaki, I.

AU - Rumley, A.

AU - Powell, J. T.

AU - Lowe, G. D. O.

PY - 2006/3

Y1 - 2006/3

N2 - Objective: Abdominal aortic aneurysms often coexist with reduced lung function and chronic obstructive pulmonary disease (COPD). These conditions are each associated with cigarette smoking, cardiovascular disease, and evidence of increased inflammatory and hemostatic activity. The aim of this study was to determine if these factors accounted for the link between aneurysms and pulmonary disease.Methods. The design was a case-control study comparing patients with an asymptomatic abdominal aortic aneurysm with population-based controls without an aneurysm. Aneurysms were diagnosed by ultrasound scan, and pulmonary function was measured by respiratory questionnaire and spirometry. Activation of inflammation and hemostasis was measured by assay of plasma interleukin-6 (IL-6), fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (tPA) antigen, fibrin D-dimer, and plasmin antiplasmin complexes.Results. Cases with an abdominal aortic aneurysm (n = 89) had more COPD and worse expiratory lung function as measured by forced expiratory volume in I second (FEVI) and forced vital capacity C) than controls (n = 98) (FEVI, 1.9 vs 2.2 L, P < .01; FEVI/FVC, 0.67 vs 0.75, P < .001) and did not differ in restrictive function (FVC, 2.9 vs 3.0 L, P = .33). Cases also had higher levels of lifetime cigarette smoking (30 vs 24 pack-years, P < 0.01), cardiovascular disease (35% vs 18%, P = .01), plasma fibrinogen (3.5 vs 3.1 g/L, P = .02), IL-6 (2.8 vs 1.8, pg/mL, P < .001), plasmin antiplasmin complexes (596 vs 384 mu g/L, P = .01), and D-dimer (442 vs 93 ng/mL, P < .001). On multiple logistic regression analysis of lung function and COPD on the risk of aneurysm, both cigarette smoking and cardiovascular disease had little effect on the relationships. For the markers of activated inflammation and hemostasis, plasmin antiplasmin complexes and D-dimer had the most important confounding effect on the odds ratios. All markers combined had a substantial effect: odds ratio of aneurysm for a one standard deviation decrease in FEVI fell from 2.3 (95% confidence interval [CI], 1.5 to 3.5) (P <.01) to 1.3 (95% CI, 0.55 to 2.4) (P >= 1.05).Conclusion: The association between reduced respiratory function and abdominal aortic aneurysm was not accounted for by cigarette smoking or cardiovascular disease. We hypothesize that activation of inflammation and hemostasis in response to injury may be an important explanation of the association between aneurysm formation and reduced respiratory function. Further studies are required to test this hypothesis.

AB - Objective: Abdominal aortic aneurysms often coexist with reduced lung function and chronic obstructive pulmonary disease (COPD). These conditions are each associated with cigarette smoking, cardiovascular disease, and evidence of increased inflammatory and hemostatic activity. The aim of this study was to determine if these factors accounted for the link between aneurysms and pulmonary disease.Methods. The design was a case-control study comparing patients with an asymptomatic abdominal aortic aneurysm with population-based controls without an aneurysm. Aneurysms were diagnosed by ultrasound scan, and pulmonary function was measured by respiratory questionnaire and spirometry. Activation of inflammation and hemostasis was measured by assay of plasma interleukin-6 (IL-6), fibrinogen, von Willebrand factor (vWF), tissue plasminogen activator (tPA) antigen, fibrin D-dimer, and plasmin antiplasmin complexes.Results. Cases with an abdominal aortic aneurysm (n = 89) had more COPD and worse expiratory lung function as measured by forced expiratory volume in I second (FEVI) and forced vital capacity C) than controls (n = 98) (FEVI, 1.9 vs 2.2 L, P < .01; FEVI/FVC, 0.67 vs 0.75, P < .001) and did not differ in restrictive function (FVC, 2.9 vs 3.0 L, P = .33). Cases also had higher levels of lifetime cigarette smoking (30 vs 24 pack-years, P < 0.01), cardiovascular disease (35% vs 18%, P = .01), plasma fibrinogen (3.5 vs 3.1 g/L, P = .02), IL-6 (2.8 vs 1.8, pg/mL, P < .001), plasmin antiplasmin complexes (596 vs 384 mu g/L, P = .01), and D-dimer (442 vs 93 ng/mL, P < .001). On multiple logistic regression analysis of lung function and COPD on the risk of aneurysm, both cigarette smoking and cardiovascular disease had little effect on the relationships. For the markers of activated inflammation and hemostasis, plasmin antiplasmin complexes and D-dimer had the most important confounding effect on the odds ratios. All markers combined had a substantial effect: odds ratio of aneurysm for a one standard deviation decrease in FEVI fell from 2.3 (95% confidence interval [CI], 1.5 to 3.5) (P <.01) to 1.3 (95% CI, 0.55 to 2.4) (P >= 1.05).Conclusion: The association between reduced respiratory function and abdominal aortic aneurysm was not accounted for by cigarette smoking or cardiovascular disease. We hypothesize that activation of inflammation and hemostasis in response to injury may be an important explanation of the association between aneurysm formation and reduced respiratory function. Further studies are required to test this hypothesis.

KW - OBSTRUCTIVE PULMONARY-DISEASE

KW - GENERAL-POPULATION

KW - NATURAL-HISTORY

KW - BLOOD-PRESSURE

KW - RISK-FACTORS

KW - MEN BORN

KW - ATHEROSCLEROSIS

KW - RUPTURE

KW - COHORT

KW - METALLOPROTEINASES

U2 - 10.1016/j.jvs.2005.11.018

DO - 10.1016/j.jvs.2005.11.018

M3 - Article

VL - 43

SP - 474

EP - 480

JO - Journal of Vascular Surgery

JF - Journal of Vascular Surgery

SN - 0741-5214

ER -