Carbon Monoxide Pollution Impairs Myocardial Perfusion Reserve: Implication of Coronary Endothelial Dysfunction

Abstract

Chronic exposure to simulated urban CO pollution is reported to be associated with cardiac dysfunction. Despite the potential implication of myocardial perfusion alteration in the pathophysiology of CO pollution, the underlying mechanisms remain today still unknown. Therefore, the aim of this work was to evaluate the effects of prolonged exposure to simulated urban CO pollution on the regulation of myocardial perfusion. Cardiac hemodynamics and myocardial perfusion were assessed under basal conditions and during the infusion of a β-Adrenergic agonist. The effects of CO exposure on capillary density, coronary endothelium-dependent vasodilatation, eNOS expression and eNOS uncoupling were also evaluated. Our main results were that prolonged CO exposure was associated with a blunted myocardial perfusion response to a physiological stress responsible for an altered contractile reserve. The impairment of myocardial perfusion reserve was not accounted for a reduced capillary density but rather by an alteration in coronary endothelium-dependent vasorelaxation (-45% of maximal relaxation to ACh). In addition, though chronic CO exposure did not change eNOS expression, it significantly increased eNOS uncoupling. Therefore, the present work underlines the fact that chronic CO exposure, at levels found in urban air pollution, is associated with reduced myocardial perfusion reserve. This phenomenon is explained at the coronary-vessel level by deleterious effects of CO exposure on the endothelium NO-dependent vasorelaxation via eNOS uncoupling.

Long-Term Exposures to Air Pollutants and Risk of Peripheral Arterial Occlusive Disease: A Nationwide Cohort Study in Taiwan

“…Moreover, long-term CO exposure could amount to an enhanced thickening of the carotid intima-media and elevated serum C-reactive protein, thereby conferring a higher risk for patients to develop CVD ( 31 ). Exposure to CO levels at urbanized regions has also been demonstrated to have an association with reduced myocardial perfusion reserve, implying coronary endothelial dysfunction ( 32 ). Furthermore, CO leads to atherogenic processes both in coronary arteries and in peripheral artery systems.…”

Carbon monoxide exposure in the urban environment: An insidious foe for the heart?

“…Tachycardia is also a common feature after CO exposure in newborn rat pups (500 ppm; 2 × 10 −5 mol L −1 for 32 days), and these effects persist in adults (Penney et al, 1988). As discussed before, chronic CO exposure (under conditions mimicking urban pollution) promotes ventricular remodelling and Ca 2+ -dependent ventricular arrhythmia (VA) that are exacerbated by a ␤-adrenergic challenge or I/R in healthy rats Meyer et al, 2011). Under these conditions, CO induces cardiac fibrosis and hypertrophy and depresses heart rate variability, indicating an alteration of the ANS .…”

Efeito da exposição precoce ao poluente 1,2-naftoquinona sobre a função vascular e cardíaca: papel dos canais iônicos receptores de potencial transitório (TRP).

“…No que diz respeito aos efeitos da poluição atmosférica no sistema cardiovascular podemos citar alterações importantes como uma maior susceptibilidade ao infarto agudo do miocárdio (Shah et al, 2013), maior probabilidade de ocorrência de episódios de arritmias, alterações tanto na plasticidade do tecido cardíaco (Andre et al, 2010;Bartell et al, 2013;Newby et al, 2015) quanto na estrutura e funcionalidade das artérias coronárias e pulmonar (Lemos et al, 2006;Meyer et al, 2011) e hipertensão (Adamopoulos et al, 2010).…”