Micro- and nano-plastics in the coronary circulation and air pollution exposure in ischaemic heart disease presentation

Background and Aims. Micro- and nanoplastics (MNPs) are emerging risk factors for cardiovascular diseases. The present study aimed to evaluate the burden of MNPs in coronary blood across the spectrum of coronary artery disease (CAD), and their association with air pollution exposure and inflammation. Methods. Cross-sectional study, including 61 consecutive patients undergoing coronary angiography for suspected CAD, stratified into: ST-segment elevation myocardial infarction (STEMI, n=19), chronic coronary syndromes (CCS, n=20), and controls with normal coronary arteries (n=22). MNPs were quantified in coronary and peripheral blood using pyrolysis-gas chromatography-mass spectrometry and laser direct infrared spectroscopy. Air pollution exposure data were collected on the day of the invasive procedure (acute exposure) and over the preceding two years (chronic exposure). Results. MNPs were detected significantly more frequently in STEMI patients (84.2%) than in CCS (40%) and controls (31.8%) (p=0.002), with higher concentration and greater polymer diversity [median of 3 polymers (IQR: 2–4), p<0.001]. Polyethylene was the predominant polymer (97%). The same polymers were consistently identified in peripheral and coronary blood samples from individual patients, with the highest concentrations in coronary blood (p<0.001). STEMI patients showed higher levels of IL-6 and TNF-α (p0.006) and were exposed to higher levels of PM2.5 (p0.012). MNP detection was more frequent among smokers and patients exposed to PM2.5>15 µg/m³ (p=0.006), with all patients presenting both factors showing detectable MNPs (p<0.001). In multivariable analysis, smoking history emerged as the only independent predictor of MNP presence (OR 5.69, 95%CI 1.33-26.63, p=0.023). Conclusions. STEMI patients exhibited a greater burden of MNPs in coronary blood than CCS and controls. MNPs detection frequently co-occurred with elevated inflammatory biomarkers, greater PM2.5 exposure, and smoking, suggesting a potential association between environmental exposure and CAD.