Persistent Asthma Associated With Carotid Plaque Burden

Patients with persistent asthma have an increased carotid plaque burden and levels of inflammatory biomarkers compared with individuals without asthma, investigators reported in the Journal of the American Heart Association.

Study authors hypothesized that persistent asthma would be associated with carotid plaque presence and burden. They therefore analyzed data from the Multi-Ethnic Study of Atherosclerosis (MESA; ClinicalTrials.gov Identifier: NCT00005487), assessing risk factors for atherosclerotic cardiovascular disease (ASCVD) and disease progression in 6814 healthy participants aged 45 to 84 years who were free of known ASCVD at baseline at 6 US centers from 2000 to 2002.

B-mode ultrasound longitudinal images of patients’ right and left common, bifurcation, and internal carotid artery segments were recorded at baseline. Asthma was defined as self-reported, physician-diagnosed asthma at baseline, with patients with asthma stratified into 2 subgroups: persistent asthma (ie, patients on controller medications) and intermittent asthma (ie, those not taking controller medications).

The primary analysis included participants with baseline ASCVD risk factors and carotid ultrasound from July 2000 to August 2002 (n=5029). The participants had a mean (SD) age of 61.6 (10.0) years; 53% were female, 26% were Black, and 23% were Hispanic. Of the cohort, 109 participants had persistent asthma, 388 had intermittent asthma, and 4532 participants were without asthma. Patients who had persistent asthma were more likely to be women (70% vs 51.7%), have an increased body mass index (29.9 vs 28.1 kg/m²), and have higher high-density lipoprotein cholesterol levels (56.5 vs 50.6 mg/dL), compared with those without asthma.

Carotid plaque was observed in 50.5% of individuals without asthma, with a mean (SD) total plaque score (TPS) of 1.29 (1.80). Carotid plaque was also found in 49.5% of those with intermittent asthma, with a TPS of 1.25 (1.76), and in 67% of those with persistent asthma, with a TPS of 2.08 (2.35) (P ≤.003 for comparison of proportions, and P =.002 for comparison of means).

The patients with persistent asthma had significantly increased levels of C reactive protein (CRP) (mean, 6.49 [11.20] mg/L vs 3.61 [5.50] mg/L; P =.008) and interleukin-6 (IL-6) (mean, 1.89 [1.61] pg/mL vs 1.52 [1.21] pg/mL; P =.02), compared with participants without asthma. The patients with intermittent asthma had a higher average CRP level compared with individuals without asthma (mean, 4.54 [6.80] mg/L; P =.009) but not higher IL-6 (mean, 1.60 [1.21] pg/mL; P =.20).

Persistent asthma was associated with greater odds of carotid plaque in unadjusted analysis (odds ratio [OR], 1.97; 95% CI, 1.32-2.95; P <.01). This association occurred in models for biologic confounders as well (OR, 1.83; 95% CI, 1.21-2.76; P <.01). In addition, persistent asthma was associated with an increased carotid TPS (fully adjusted β = 0.62; 95% CI, 0.24-1.00; P <.001).

In fully adjusted models assessing the association of asthma subtype and carotid plaque or TPS, the addition of CRP or IL-6 did not attenuate the associations of asthma severity and carotid plaque or TPS.

Study limitations include the observational design, the potential for identified associations to not be causal, and possible misclassification bias due to the self-reporting of asthma diagnoses. Also, because asthma severity was defined in part by the need for daily controller medications, the study was unable to evaluate the effects of asthma medications on carotid plaque presence and TPS. Furthermore, the participants were free of ASCVD at baseline, and generalizability to the general population may be limited.

“Adjustment for baseline inflammatory biomarkers did not attenuate the association between carotid plaque and asthma subtype, indicating the increased ASCVD risk among individuals with persistent asthma may be multifactorial,” stated the researchers. “Because asthma prevalence continues to increase and ASCVD remains the leading cause of death in the United States, these diseases create a significant public health burden and emphasize the importance of additional studies to define their shared mechanistic underpinnings.”