Abstract
The global spread of micro- and nanoplastics (MNPs) has emerged as an environmental and medical concern, with growing evidence of their role in cardiovascular disease (CVD). These particles, originating from the degradation of larger plastics and consumer products, can be ingested or inhaled, cross biological barriers, and accumulate in human tissues, including blood, myocardium, and atherosclerotic plaques. Experimental and clinical studies suggest that MNPs contribute to CVD through multiple mechanisms: activation of systemic inflammation and inflammasomes, oxidative stress, endothelial dysfunction, prothrombotic activity, and direct myocardial injury, ultimately promoting fibrosis and impaired contractility. Epidemiological data further indicate that populations exposed to higher plastic pollution or with pre-existing cardiovascular risk factors may be particularly vulnerable. Taken together, these findings identify MNPs as a potential novel environmental cardiovascular risk factor. Advancing detection methods, mechanistic research, and public health strategies will be essential to mitigate their impact and reduce plastic-related cardiovascular burden.