Lung hyperinflation strongly associated with coronary artery disease in smokers: Study

Written By :  Medha Baranwal
Medically Reviewed By :  Dr. Kamal Kant Kohli
Published On 2021-09-21 05:30 GMT   |   Update On 2021-09-21 07:16 GMT

Pittsburgh, PA: A recent study has found a strong association between lung hyperinflation and clinical and subclinical coronary artery disease (CAD) in smokers, including those having airflow obstruction. Further, the study found no association of FEV1 and emphysema with CAD, after accounting for lung hyperinflation. The study is published in the Chest journal. Hyperinflation is caused...

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Pittsburgh, PA: A recent study has found a strong association between lung hyperinflation and clinical and subclinical coronary artery disease (CAD) in smokers, including those having airflow obstruction. Further, the study found no association of FEV1 and emphysema with CAD, after accounting for lung hyperinflation. The study is published in the Chest journal. 

Hyperinflation is caused by anything that limits the flow of air out of the lungs. The most common culprit is COPD (chronic obstructive pulmonary disease), caused mainly by smoking. Frank C. Sciurba, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, and colleagues addressed the question of which pulmonary phenotypes are associated with coronary artery disease (CAD) in smokers. 

The researchers analyzed the data from the University of Pittsburgh COPD Specialized Center for Clinically Oriented Research (SCCOR) cohort (n = 481) and the Genetic Epidemiology of COPD (COPDGene) cohort (n = 2,580). Participants included current and former smokers with > 10 pack-years of tobacco exposure. Because of methodologic differences, data from the two cohorts were analyzed. Lung hyperinflation was assessed by plethysmography in the SCCOR cohort and by inspiratory and expiratory CT scan lung volumes in the COPDGene cohort. 

Subclinical CAD was assessed as the coronary artery calcium score, whereas clinical CAD was defined as a self-reported history of CAD or myocardial infarction (MI). Analyses were performed in all smokers and then repeated in those with airflow obstruction (FEV1 to FVC ratio, < 0.70). 

Key findings include:

  • Pulmonary phenotypes, including airflow limitation, emphysema, lung hyperinflation, diffusion capacity, and radiographic measures of airway remodeling, showed weak to moderate correlations (r < 0.7) with each other.
  • In multivariate models adjusted for pulmonary phenotypes and CAD risk factors, lung hyperinflation was the only phenotype associated with calcium score, history of clinical CAD, or history of MI (per 0.2 higher expiratory and inspiratory CT scan lung volume; coronary calcium: OR, 1.2; clinical CAD: OR, 1.6; and MI in COPDGene: OR, 1.7).
  • FEV1 and emphysema were associated with increased risk of CAD in models adjusted for CAD risk factors; however, these associations were attenuated on adjusting for lung hyperinflation. Results were the same in those with airflow obstruction and were present in both cohorts.

Sciurba and colleagues concluded, "subsequent studies should consider measuring lung hyperinflation and examining its mechanistic role in CAD in current and former smokers."

Reference:

The study titled, "The Association Between Lung Hyperinflation and Coronary Artery Disease in Smokers," is published in the CHEST journal. 

DOI: https://journal.chestnet.org/article/S0012-3692(21)00889-8/fulltext

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Article Source : Chest

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