Asthma, type 2 inflammation associated with coronary artery disease
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Key takeaways:
- Patients were aged 40 to 69 years when they were recruited.
- 96.4% of patients with asthma had evidence of type 2 inflammation.
- Higher eosinophil counts also were linked to coronary artery disease.
SAN DIEGO — Type 2 inflammation and asthma were significantly associated with higher risk for coronary artery disease, according to a presentation at the American Thoracic Society International Conference.
Higher eosinophil counts also were significantly associated with coronary artery disease, Christa McPhee, MD, pulmonary and critical care medicine fellow, division of pulmonary, critical care and sleep medicine, Icahn School of Medicine at Mount Sinai, and colleagues wrote.
“It’s well known that asthma is a risk factor for cardiovascular disease. Our team wanted to investigate what inflammatory factors could be driving that risk,” McPhee told Healio.
Although certain types of inflammation have appeared to have a protective effect against cardiovascular disease, McPhee said that she and her colleagues are finding that this might not be the case.
“As a result of recent work showing ties between inflammation and cardiovascular disease in various populations, we investigated whether patients with asthma and type 2 inflammation have a significantly associated risk for coronary artery disease,” she said.
The researchers examined data from 11,226 adults (54.2% women, 94.6% white) from the UK Biobank on steps 2 through 5 of the Global Initiative for Asthma treatment guidelines. These patients were aged 40 to 69 years (median age, 57 years) when they were recruited between 2006 and 2010 from 22 centers across the United Kingdom.
Also, these patients had evidence of type 2 inflammation based on an eosinophil count that was higher 150 cells/µL or a history of eczema, allergies, nasal polyps or hay fever.
Patients with interstitial lung disease, COPD, emphysema, bronchiectasis, pneumoconiosis, hypersensitivity pneumonitis, pulmonary edema, pneumonitis or heart failure were excluded.
Patients who were current smokers with a diagnosis of asthma aged older than 60 years also were excluded. McPhee said that smoking status and history were important to the main outcome.
“The majority of our patients studied were never smokers followed by previous smokers,” she said. “We controlled for pack years and smoking status in our analysis.”
The study also controlled for BMI, HDL, LDL, cholesterol, diabetes and medications for diabetes and hypertension.
The cohort included 10,828 patients (96.4%) with evidence of type 2 inflammation. The odds ratio for coronary artery disease among these patients was 1.117, which the researchers called a significant association (P < .001).
After controlling for sex and age, higher eosinophil counts also had a positive association with coronary artery disease (P < .001).
The broad evidence of type 2 inflammation among patients with asthma indicate the importance of further understanding asthma endotypes, the researchers noted, in addition to these associations between coronary artery disease and inflammation, asthma and eosinophil counts.
“Providers should be aware of the association between asthma and cardiovascular disease, especially if patients have evidence of high type 2 inflammation,” McPhee said.
Also, physicians should provide prompt “referral to a pulmonologist for dedicated asthma care when indicated, as ongoing uncontrolled airways inflammation likely has impacts systemically,” she said.
Prospective studies and studies using a greater amount of more complex data could further delineate the relationship between airways disease and cardiovascular disease development, she continued.
“Studies designed to investigate current asthma medications, particularly biologics, for potential protective effects against cardiovascular disease would be impactful,” McPhee said.
For more information:
Christa McPhee, MD, can be reached at christa.mcphee@mountsinai.org.