Key result
Severe CAC >400 is linked to ~68% higher all-cause mortality in smokers.
Why the study?
Little is known about how coronary artery calcium (CAC) interacts with and predicts all-cause mortality in patients with chronic obstructive pulmonary disease (COPD).
Does the presence and severity of coronary artery calcium on noncontrast thoracic CT predict all-cause mortality in smokers with and without COPD?
Cohort (n=6,842)
Does the presence and severity of coronary artery calcium on noncontrast thoracic CT predict all-cause mortality in smokers with and without COPD?
Coronary artery calcium identified on routine noncontrast thoracic CT is independently associated with increased all-cause mortality in smokers, with risk increasing alongside COPD severity.
A lthough coronary artery calcium (CAC) has extensive validation for predicting clinical events, little is known about how CAC interacts and predicts mortality in patients with chronic obstructive pulmonary disease (COPD).We evaluated the contribution of CAC to all-cause mortality and assessed the association of CAC with mortality varied by sex, race/ethnicity, and COPD GOLD category (Global Initiative for Chronic Obstructive Lung Disease) using the COPDGene study (Genetic Epidemiology of COPD).Smoking is not only the leading cause of lung cancer and COPD, but also a major risk factor for heart disease and associated with significantly higher atherosclerosis burden. 1 Smokers are more likely to die of cardiovascular disease (CVD) than lung cancer, which accounted for only 24.1% of all deaths in the National Lung Screening Trial. 1 Ungated low-dose multidetector row computerized tomography (CT), which is generally used for the assessment of lung cancer and COPD, can evaluate CAC. 2 Assessment of CAC during chest CT represents an opportunity to simultaneously identify asymptomatic individuals at increased CVD risk.3 Thus, we sought to evaluate the relationship between the presence and severity of CAC and the risk of all-cause mortality in smokers with and without COPD.COPDGene is a large, observational cohort study, evaluating the development of COPD in persons with a >10 pack-year smoking history and scientific data available at www.copdgene.org.3,4 Overall, 6842 participants had both CAC measured from noncontrast CT scans and follow-up for mortality (median, 81.3 months).COPD GOLD stage is based on forced expiratory volume (FEV 1 ).Cox proportional hazards regression was used to evaluate the independent effect of CAC on allcause mortality adjusting for age, sex, race, diabetes mellitus, self-reported hypercholesterolemia and hypertension, body mass index, cigarette pack-years, smoking status, and COPD GOLD stage.The study was approved by an institutional review board, and subjects gave informed consent.Over a median of 81.3 months of follow-up, 850 of 6842 (12.4%) participants died.Mortality in the CAC=0 group was 8.4%; in the 1 to 100 group, mortality was 9.3%; in the 101 to 400 group, mortality was 12.7%; and in the >400 group, mortality was 24.4% (P<0.0001, Figure 1).GOLD 0 (no obstruction) included 3039, GOLD 1 (FEV 1 ≥80%) included 552, GOLD 2 (FEV 1 50-79%) included 1288, GOLD 3 (FEV 1 30-49%) included 751, and GOLD 4 (FEV 1 <30%) included 388 participants.The highest CAC category (>400) was associated with increased mortality adjusted for known risk factors (hazard ratio [HR], 1.68; 95% CI, 1.30-2.03;P<0.0001), in comparison with individuals with no CAC.There was a strong interaction with COPD GOLD stage and CAC, where worsening mortality was independently associated with CAC and overall COPD (GOLD stages 1-4) (HR, 2.73; 95% CI, 2.27-3.28;P<0.0001).HRs increased across stages of COPD GOLD (stage 1 HR=1.24;stage 2 HR=2.16;stage 3 HR=3.96;and stage 4 HR=11.17).
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Budoff et al. (2018) conducted a cohort in smokers with and without COPD (n=6,842). Coronary artery calcium (CAC) >400 vs. No CAC (CAC=0) was evaluated on all-cause mortality (HR 1.68, 95% CI 1.30-2.03, p=<0.0001). In smokers with and without COPD, severe coronary artery calcium (>400) was associated with increased all-cause mortality compared to no CAC (HR 1.68; 95% CI 1.30-2.03; P<0.0001).
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