P6204Enhanced cardiovascular susceptibility to air pollution: A 4 years echocardiographic study of pulmonary circulation

Abstract

Background: Air particle matter (PM) was identified as an important risk factor for congestive heart failure. We recently reported that acute exposure to standardized level of PM alters pulmonary vascular function in healthy volunteers. Purpose: We aim to investigate the effect of ambient air pollution on echocardiographic parameters of pulmonary vascular function and identify potential susceptibility factors. Methods: From 2009 to 2013, 16295 patients had a transthoracic echocardiography in our University Hospital. Effects of lag 1, 5 and 10 days of PM10, PM2.5, NO2 and O3 air pollutants on pulmonary acceleration time (PVaccT), tricuspid regurgitation velocity jet (TRVmax) and right ventricular systolic function (TAPSE) were assessed. The data was analyzed through a general linear model in a multiway analysis of covariance (ANCOVA) in which all 2-way interactions between categorical clinical variable and environmental covariate were explored. A square root transformation of PVAccT and a cubic root of TRVmax were required to ensure Gaussian distributed model residuals. Results: Presence of pulmonary hypertension (PHT, ESC guidelines definition) was consistently associated with enhanced PVAcctT decrease and enhanced TRVmax increase following respectively lag 10 and lag 1 days to PM10 exposure (fig. 1, all p interaction <0.05). In PHT population, lag 5 days exposure to O3 was also associated with further decreased of TAPSE (p interaction <0.05). Left ventricle diastolic dysfunction and diabetes potentiated the decrease in PVAcctT observed with lag 10 days exposure to PM10 (all p interaction <0.001). Obstructive sleep apnea further increased the TRVmax observed with lag 10 days exposure to PM10 (p<0.05). Conclusion: Air pollution influences echo parameters of pulmonary circulation. Patients suffering of PHT are more susceptible to the effect of sustained increase in PM. Other factors as diastolic dysfunction, diabetes and obstructive sleep apnea may also enhance effect of PM on pulmonary circulation. (Figure Presented).