The pervasive presence of microplastics and nanoplastics (MNPs) in the environment has raised growing concerns regarding their potential health impacts. While research has progressively revealed the toxicological effects of MNPs, limited attention has been given to their specific influence on the cardiovascular system, particularly in human models. This systematic review synthesizes current evidence on MNP-induced cardiotoxicity, highlighting both physiological outcomes and underlying mechanisms.

A total of 72 studies—including in vivo experiments on aquatic species and rodents, and in vitro assays on human cardiovascular cells—were analyzed. The findings consistently demonstrate that MNPs can impair cardiac function by altering heart rate, inducing pericardial edema, and promoting myocardial fibrosis. These effects are mediated by mechanisms such as oxidative stress, inflammation, apoptosis, and disruptions in cellular signaling pathways.

Toxicity outcomes vary based on particle characteristics (type, size, and surface chemistry), exposure dose and duration, organismal factors (age, sex, species), and co-exposure to other pollutants. Notably, smaller particles (< 100 nm) exhibit greater bioaccumulation and systemic penetration, correlating with higher cardiovascular toxicity.

Despite growing evidence, standardized protocols for evaluating MNP cardiotoxicity remain lacking, and human-based data are scarce. This review underscores the urgent need for long-term, mechanistic studies and regulatory frameworks to assess cardiovascular risks posed by environmental MNPs. Advancing this research frontier is critical to understanding the public health implications of chronic plastic particle exposure.