Particulate matter (PM) exposures are correlated in several studies with short-term increases of morbidity and mortality for cardiovascular diseases. Some of these effects are believed to be exacerbated by dysregulation of cardiac rhythm. We studied patients with antecedent myocardial infarction showing that a reduction of heart rate variability (HRV) correlates with the intensity of exposures to quasi-ultrafine particles (PM0.25). However, this correlation was not found in patients taking beta-blockers. These data suggest that the effects of PM could be mediated through a rapid imbalance of the autonomic regulation of the heart. Current mechanistic hypotheses are discussed leading to the conclusion that the most studied one, i.e. pulmonary inflammation, may trigger reflexes or, more likely PM interact with bronchial receptors directly, and inflammation may be simply bystander.