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Associations between COPD related manifestations: a cross-sectional study
Elisabeth A P M Romme1, David A McAllister, John T Murchison
1Department of Respiratory Medicine, Catharina Hospital, Eindhoven, The Netherlands. lisette.romme@catharinaziekenhuis.nl.
Insights
Cardiovascular disease markers like coronary artery calcification (CAC) and thoracic aortic calcification (TAC), along with emphysema extent, predict mortality in COPD patients. Higher CAC also correlates with increased arterial stiffness and lower bone density.
Area of Science:
- Pulmonary Medicine
- Cardiology
- Radiology
- Gerontology
Background:
- Chronic Obstructive Pulmonary Disease (COPD) is linked to cardiovascular disease, osteoporosis, and emphysema.
- The predictive value of these comorbidities for all-cause mortality in COPD patients remains unclear.
- This study investigates the associations between cardiovascular markers, bone density, emphysema, and mortality in COPD.
Purpose of the Study:
- To examine the relationship between cardiovascular disease markers (coronary artery calcification [CAC], thoracic aortic calcification [TAC], arterial stiffness), bone density, emphysema, and all-cause mortality in COPD patients.
- To determine if these factors predict mortality in a COPD cohort.
Main Methods:
- Low-dose chest computed tomography (CT) was used to assess CAC, TAC, and bone attenuation (vertebrae).
- Emphysema was quantified using PI-950 and 15th percentile measures.
- Arterial stiffness was measured via carotid-radial pulse wave velocity (PWV).
- Mortality data were obtained from the national register.
Main Results:
- 119 COPD subjects (mean age 67.8 years, 66% male, FEV1 46.0%) were studied.
- Higher CAC was associated with older age, male sex, hypertension, ischemic heart disease, increased arterial stiffness (PWV), and lower bone density.
- Cox proportional hazards models revealed that CAC, TAC, and emphysema extent (15th percentile) predicted all-cause mortality.
Conclusions:
- Increased coronary artery calcification (CAC) is linked to greater arterial stiffness and reduced bone density in COPD patients.
- Coronary artery calcification (CAC), thoracic aortic calcification (TAC), and the extent of emphysema are significant predictors of all-cause mortality in COPD.
Background:
Cardiovascular disease, osteoporosis and emphysema are associated with COPD. Associations between these factors and whether they predict all-cause mortality in COPD patients are not well understood. Therefore, we examined associations between markers of cardiovascular disease (coronary artery calcification [CAC], thoracic aortic calcification [TAC] and arterial stiffness), bone density (bone attenuation of the thoracic vertebrae), emphysema (PI-950 and 15th percentile) and all-cause mortality in a COPD cohort.
Methods:
We assessed CAC, TAC, bone attenuation of the thoracic vertebrae, PI-950 and 15th percentile on low-dose chest computed tomography in COPD subjects. We measured arterial stiffness as carotid-radial pulse wave velocity (PWV), and identified deaths from the national register.
Results:
We studied 119 COPD subjects; aged 67.8 ±7.3, 66% were males and mean FEV1% predicted was 46.0 ±17.5. Subjects were classified into three pre-specificed groups: CAC = 0 (n = 14), 0 < CAC ≤ 400 (n = 41) and CAC > 400 (n = 64). Subjects with higher CAC were more likely to be older (p < 0.001) and male (p = 0.03), and more likely to have higher systolic blood pressure (p = 0.001) and a history of hypertension (p = 0.002) or ischemic heart disease (p = 0.003). Higher CAC was associated with higher PWV (OR 1.62, p = 0.04) and lower bone attenuation (OR 0.32, p = 0.02), but not with 15th percentile, after adjustment for age, sex and pack-years of smoking. In a Cox proportional hazards model, CAC, TAC and 15th percentile predicted all-cause mortality (HR 2.01, 2.09 and 0.66, respectively).
Conclusions:
Increased CAC was associated with increased arterial stiffness and lower bone density in a COPD cohort. In addition, CAC, TAC and extent of emphysema predicted all-cause mortality.
Trial Registration:
Lothian NHS Board, Lothian Research Ethics Committee, LREC/2003/8/28.
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