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

Air pollution affects same-day hospital admissions for acute coronary syndromes, decompensated heart failure and arrhyth-mias. 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 protocolMethods: We enrolled 1292 patients with chronic coronary syndromes referred for clinically-driven dipyridamole ABCDE-SE (score resultsfrom 0= all parameters normal, to 5, all abnormal). Same day values of 5 pollutants were obtained on the same morning of testing (averageof 4 hours) from publicly available data sets of regional authority of environmental protection. Air pollution score (APS) of 5 items includedfine (PM 2.5) and <10 ?m 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 UKgovernment 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 individualpollutants were evaluated with individual items (from A to E) of SE score, NO2 concentration was correlated with rest (r=.089; p = 0.001) andpeak 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 withnormal (<= 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] ?g/m3, p< 0.001) and PM 2.5 (22.0 [9.1-23.5] vs 17.6 [8.6-22.2] ?g/m3, p< 0.001), with lower values of O3, a secondary pollutantdestroyed by NO2 (44.9 [26.7-59.5] vs 48.4 [28.5-67.4] ?g/m3, p= 0.040). At multivariable logistic regression analysis (Figure), NO2 predic-ted 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 morefrequent pulmonary congestion mirrored by B-lines at rest and during stress. The increased inflammatory stress mediated by NO2 and PM2.5 may increase the permeability of the alveolar capillary barrier to any given rise in pulmonary wedge pressure