Micro- and Nanoplastics in Cardiovascular Toxicology: Human Tissue Detection, Clinical Phenotypes, and Adverse Outcome Signals.

Micro- and nanoplastics (MNPs) have emerged from a diffuse environmental concern to a plausible cardiovascular exposure with potential clinical relevance. The current evidence base is heterogeneous: human observational and tissue-detection studies have identified MNPs in blood, thrombi, atherosclerotic plaques, arterial tissue, and cardiac surgical specimens, whereas cell, organoid, and animal studies provide mechanistic plausibility for vascular inflammation, thrombosis, myocardial injury, remodeling, and electrophysiological disturbance. Key clinical signals now include polyethylene detection in 58.4% of carotid plaques and a reported 4.53-fold higher risk of myocardial infarction, stroke, or all-cause death among patients with MNP-positive plaques in the landmark carotid plaque cohort. Accordingly, the central question is no longer only whether MNPs can induce oxidative stress or inflammation in isolated systems, but whether they may contribute to clinically recognizable cardiovascular phenotypes and adverse outcomes. In this review, we reframe the field from a mechanism-dominant narrative toward a clinically oriented synthesis integrating human specimen evidence, disease phenotypes, evidence calibration, analytical limitations, and translational implications. We summarize current human evidence for MNPs presence in circulation and diseased vascular tissues, examine phenotype-specific evidence for atherosclerosis, thrombosis and coagulation disturbance, myocardial injury and fibrotic remodeling, contractile dysfunction, electrophysiological abnormalities, and developmental cardiovascular toxicity, and distinguish these clinical signals from preclinical mechanistic support. Across these phenotypes, the most reproducible mechanisms involve endothelial injury, immunoinflammatory activation, oxidative stress, mitochondrial dysfunction, and prothrombotic signaling. Overall, current evidence supports biological plausibility and clinically relevant associations rather than definitive causality, but the convergence of human tissue detection, phenotype-oriented experiments, and emerging clinical associations justifies considering MNPs as emerging cardiovascular risk modifiers.