Same-day air pollution and ABCDE stress echo results: nitrogen dioxide increases vulnerability to pulmonary congestion

Abstract

Abstract Funding Acknowledgements Type of funding sources: None. OnBehalf StressEcho 2030 study group Background Air pollution affects same-day hospital admissions for acute coronary syndromes, decompensated heart failure and arrhythmias. The present study hypothesis is that air pollution also may affect results of comprehensive cardiac functional testing unmasking a pre-clinical vulnerability. Aim To assess the effects of air pollution on stress echocardiography (SE) performed with ABCDE protocol Methods We enrolled 1292 patients with chronic coronary syndromes referred for clinically-driven dipyridamole ABCDE-SE (score results from 0= all parameters normal, to 5, all abnormal). Same day values of 5 pollutants were obtained on the same morning of testing (average of 4 hours) from publicly available data sets of regional authority of environmental protection. Air pollution score (APS) of 5 items included fine (PM 2.5) and <10 µm diameter particulate matter, ozone (O3), sulfur dioxide and nitrogen dioxide (NO2). According to predetermined, internationally established thresholds, APS ranged from 0 (all parameters normal or near normal, index value ≤3 in the 1 to 10 scale of UK government air quality index 2014) to 5 (all parameters abnormal). Results There was no significant correlation (r=-0.032, p = 0.276) between SE score (0.82 ± 1.08) and APS (1.96 ± 1.09). When individual pollutants were evaluated with individual items (from A to E) of SE score, NO2 concentration was correlated with rest (r=.089; p = 0.001) and peak stress B-lines in step B (r=.099; p < 0.001). Patients with abnormal (> 2) B-lines at peak stress (n = 247) were compared with those with normal (≤ 1) response (n= 1, 045). B-liners showed higher values of same-day NO2 (median value 23.1 [I.Q. range 16.2-31.0] vs 19.7 [12.5-27.4] µg/m3, p< 0.001) and PM 2.5 (22.0 [9.1-23.5] vs 17.6 [8.6-22.2] µg/m3, p< 0.001), with lower values of O3, a secondary pollutant destroyed by NO2 (44.9 [26.7-59.5] vs 48.4 [28.5-67.4] µg/m3, p= 0.040). At multivariable logistic regression analysis (Figure), NO2 predicted stress B-lines with age, hypertension, diabetes, and reduced (< 50%) ejection fraction. Conclusion Air pollution may modulate cardiac functional testing results. Higher concentration of NO2 and PM 2.5 are associated with more frequent pulmonary congestion mirrored by B-lines at rest and during stress. The increased inflammatory stress mediated by NO2 and PM 2.5 may increase the permeability of the alveolar capillary barrier to any given rise in pulmonary wedge pressure. Abstract table