Micro- and nanoplastics in acute coronary thrombosis: exposure, enrichment, or a dual mechanism?

This commentary refers to ‘Micro- and nano-plastics in the coronary circulation and air pollution exposure in ischaemic heart disease presentation’, by P. Paolisso et al., https://doi.org/10.1093/eurheartj/ehag447 and the discussion piece ‘Coronary micro- and nanoplastics in ST-segment elevation myocardial infarction: antecedent exposure or post-thrombotic enrichment’, by J. Qin et al., https://doi.org/10.1093/eurheartj/ehag800. We thank Qin et al.1 for their thoughtful commentary on our study of micro- and nanoplastics (MNPs) in the coronary circulation across the spectrum of coronary artery disease. The authors raise two principal points: whether the proximal-to-peripheral gradient observed in ST-segment elevation myocardial infarction (STEMI) reflects antecedent exposure or post-thrombotic enrichment and whether smoking confounds the association between MNPs and acute coronary thrombosis. We welcome the opportunity to clarify these issues. We agree that our cross-sectional, single-timepoint sampling design cannot definitively separate focal accumulation preceding plaque rupture from secondary enrichment occurring after thrombotic occlusion. We emphasize that this local mechanism cannot alone account for our findings. Indeed, our most robust finding was not the concentration gradient itself but the markedly different rate of patients with detectable MNPs across the three groups, highest in STEMI, intermediate in chronic coronary syndromes, and lowest in controls, a binary difference in presence vs absence that local stasis or thrombus-related sequestration at a single occlusion site does not readily explain. Moreover, we deliberately used peripheral arterial blood, sampled at the vascular sheath and remote from the culprit lesion, as the reference compartment for this comparison to avoid confounding from local thrombus formation and flow disruption at the site of coronary occlusion. Peripheral arterial MNP concentrations were also significantly higher in STEMI than in chronic coronary syndromes or controls, a systemic difference that stasis or thrombus-related sequestration at the occlusion site cannot explain.2 We therefore view antecedent exposure and post-thrombotic local enrichment not as competing explanations but as plausibly coexisting phenomena: a higher systemic MNP burden predisposing to atherothrombotic events, superimposed on focal concentration once coronary flow is disrupted. The design proposed by the authors—comparing polymer burden and composition across peripheral blood, upstream and downstream coronary blood, aspirated thrombus, and plaque tissue from the same patient—is precisely the direction we are now pursuing, building on prior work demonstrating MNPs within coronary and peripheral thrombi and within atherosclerotic plaque itself.3–6