Circulating Microparticles From Patients With Coronary Artery Disease Cause Endothelial Dysfunction. Response

To the Editor,

I would like to thank the interesting comments of Bueno Jiménez et al. published in Revista Española de Cardiología in relation to the Editorial article¹ where I discussed the plausibility of the exposure to ambient ultrafine particles (UFP) as a risk factor for cardiovascular diseases. Numerous epidemiological studies support the association of exposure to ambient particulate matter (PM) with cardiovascular ischemic endpoints² and substantial experimental animal work support the feasibility for causality in the case of atherosclerosis.³ While it is likely that PM with a smaller particle size such as UFP carry greater cardiovascular toxicity than particles with larger size, the possibility that inhaled UFP could translocate and access the systemic circulation still awaits more definite confirmation.³ Ambient PM can lead to systemic vascular effects by several hypothetical mechanisms that still remain to be elucidated.¹ The author's comment about the need to employ novel biomarkers for endothelial dysfunction, such as circulating endothelium-derived microparticles (EMP), that can better capture the cardiovascular risk potentially attributable to ambient PM and UFP is very appropriate as they could also aid in the identification of pathogenic mechanisms. EMPs, characterized by different phenotypes such as CD31⁺/CD41⁻, CD31⁺/annexin V⁺, CD144⁺ and/or CD62e⁺ appear not only to reflect endothelial dysfunction and serve as an stratifying biomarker⁴ but also to exert pathogenic actions such as procoagulant effects.⁵ Likewise, other biomarkers such as the level and function of endothelial progenitor cells (EPC) could prove to be helpful to reflect endothelial damage caused by air pollutants, as it has been recently shown that exposure to ambient fine particles (PM<2.5μm) induced reversible vascular injury, reflected by depletion of circulating EPC levels, both in humans and mice.⁶ It would be valuable to determine whether exposure to ambient PM and UFP in particular result in increased levels of EMPs as well. Interestingly, exposure to secondhand smoking, thought to mimic some of the effects associated with PM exposure and to activate similar pathogenic mechanisms, have been shown to result in increased EMP as well as EPC.⁷ Therefore, it would be highly desirable to use these biomarkers in the assessment of vascular effects caused by the exposure to UFP, as suggested by the author.

Received 8 December 2011
Accepted 14 December 2011