Coronary micro- and nanoplastics in ST-segment elevation myocardial infarction: antecedent exposure or post-thrombotic enrichment?

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 ‘Micro- and nanoplastics in acute coronary thrombosis: exposure, enrichment, or a dual mechanism?’, by R. Marfella et al., https://doi.org/10.1093/eurheartj/ehag803. We read with interest the study by Paolisso et al., who quantified micro- and nanoplastics (MNPs) in paired peripheral and coronary blood samples from patients with ST-segment elevation myocardial infarction (STEMI), chronic coronary syndromes, and angiographically normal coronary arteries. The paired sampling design, rigorous contamination controls, and complementary analytical methods are important strengths. However, the spatial gradient observed in STEMI permits an alternative interpretation.1 In STEMI, MNP concentrations were highest in coronary blood sampled upstream from the culprit occlusion before lesion crossing (Tube B), followed by downstream coronary blood after lesion crossing (Tube C) and peripheral arterial blood (Tube A). This pattern may reflect focal accumulation before plaque rupture, but all samples were obtained after a TIMI 0/1 thrombotic occlusion had formed. Markedly reduced flow and stasis near the occlusion, prolonged residence of circulating particles, or incorporation into thrombotic material could also produce secondary enrichment. Plastic polymers have been detected in coronary thrombi from patients with myocardial infarction and in thrombi retrieved from coronary, cerebral, and deep venous sites. These observations establish that thrombi can contain plastic particles, but not whether the particles promoted thrombosis or became incorporated during clot formation. The proximal-to-peripheral gradient should therefore be regarded as lesion-associated enrichment rather than evidence that focal deposition necessarily preceded the acute event.1–3