No abstract

There was no funding source for this study.

Several epidemiological studies found an association between acute exposure to fine particulate matter of less than 2.5 μm and 10 μm in aerodynamic diameter (PM2.5 and PM10) and cardiovascular diseases, ventricular fibrillation incidence and mortality. The effects of pollution on atrial fibrillation (AF) beyond the first several hours of exposure remain controversial. A total of 145 patients with implantable cardioverter-defibrillators (ICDs), cardiac resynchronization therapy defibrillators (ICD-CRT), or pacemakers were enrolled in this multicentric prospective study. Daily levels of PM2.5 and PM10 were collected from monitoring stations within 20 km of the patient’s residence. A Firth Logistic Regression model was used to evaluate the association between AF and daily exposure to PM2.5 and PM10. Exposure levels to PM2.5 and PM10 were moderate, being above the World Health Organization (WHO) PM2.5 and PM10 thresholds of 25 μg/m3 and 50 μg/m3, respectively, on 26% and 18% of the follow-up days. An association was found between daily levels of PM2.5 and PM10 and AF (95% confidence intervals (CIs) of 1.34–2.40 and 1.44–4.28, respectively) for an increase of 50 µg/m3 above the WHO threshold. Daily exposure to moderate PM2.5 and PM10 levels is associated with AF in patients who are not prone to AF.

No abstract

A neurogenic pathway, involving airway TRPV-1, has been implicated in acute cardiovascular events occurring after peaks of air pollution. We tested whether inhaled prostaglandin-E2 (PGE2) and bradykinin (BK) regulate TRPV-1 activity in vivo by changing cough response to capsaicin (CPS) and affecting heart rate variability (HRV), while also taking into account the influence of TRPV-1 polymorphisms (SNPs). Moreover, we assessed the molecular mechanism of TRPV-1 modulation in vitro. Seventeen healthy volunteers inhaled 100 μg PGE2, 200 μg BK or diluent in a randomized double-blind fashion. Subsequently, the response to CPS was assessed by cough challenge and the sympathetic activity by HRV, expressed by low (nLF) and high (nHF) normalized frequency components, as well as nLF/nHF ratio. Intracellular [Ca2+] was measured in HeLa cells, transfected with wild-type TRPV-1, pre-treated with increasing doses of PGE2, BK or diesel exhaust particulate (DEP), after CPS stimulation. Six functional TRPV-1 SNPs were characterized in DNA from each subject. Inhalation of PGE2 and BK was associated with significant increases in cough response induced by 30 μM of CPS (cough number after PGE2 = 4.20 ± 0.42; p < 0.001, and after BK = 3.64 ± 0.37; p < 0.01), compared to diluent (2.77 ± 0.29) and in sympathetic activity (nLF/nHF ratio after PGE2 = 6.1; p < 0.01, and after BK = 4.2; p < 0.05), compared to diluent (2.5–3.3). No influence of SNPs was observed on autonomic regulation and cough sensitivity. Unlike PGE2 and BK, DEP directly activated TRPV-1. Inhalation of PGE2 and BK sensitizes TRPV-1 and is associated with autonomic dysregulation of cardiac rhythm in healthy subjects.