Background: The human bioaccumulation of micro- and nano-plastics (MNPs) is increasingly being recognised in the aetiology and pathophysiology of human disease. Objective: This systematic scoping review aims to provide a comprehensive investigation of studies examining the impacts of MNPs on the human cardiovascular system. Methods: Five databases (PubMed, SCOPUS, CINAHL, Web of Science and EMBASE) were systematically searched. Results: Forty-six articles were identified, 13 of which investigated the presence of MNPs within the human cardiovascular system, including atherosclerotic plaques, saphenous vein tissue, thrombi and venous blood. The effect of MNPs on cell lines suggest MNPs are cytotoxic, immunotoxic, and genotoxic. Significance: The findings of this review, when evaluated together with additional studies utilising animal models, suggest MNPs may contribute to global cardiovascular morbidity and mortality. In particular, the ability of MNPs to induce endothelial damage, oxy-LDL formation, foam cell development and apoptosis, as well as to alter the clotting cascade, has potential implications for vascular diseases. In addition, MNPs may play a role in the aetiology and progression of congenital heart abnormalities, infective pathologies and cardiomyopathies. Despite an increasing awareness of the ability for MNPs to result in cardiovascular disease and dysfunction, a limited amount of research has been conducted to date characterising the presence of MNPs in the human cardiovascular system. Reseach is required to understand the extent of this rapidly emerging issue and to develop strategies that will support clinicians to appropriately manage and educate their patients in the future.

Classic features of polycystic ovary syndrome (PCOS) include derangement of metabolic and cardiovascular health, and vascular dysfunction is commonly reported. These comorbidities indicate impaired blood flow; however, other than limited reports of increased plasma viscosity, surprisingly little is known regarding the physical properties of blood in PCOS. We aimed to investigate whether haemorheology was impaired in women with PCOS. We thus measured a comprehensive haemorheological profile, in a case-control design, of lean women with PCOS and age-matched healthy controls. A clinical examination determined similar cardiovascular risk for the two groups. Whole blood and plasma viscosity was measured using a cone-plate viscometer. The magnitude and rate of red blood cell (RBC) aggregation was determined using a light-transmission aggregometer, and the degree of RBC deformability was measured via laser-diffraction ektacytometry. Plasma viscosity was significantly increased in women with PCOS. Blood viscosity was also increased for PCOS at lower-to-moderate shear rates in both native and standardised haematocrit samples. The magnitude of RBC aggregation–a primary determinant of low-shear blood viscosity–was significantly increased in PCOS at native and 0.4 L·L^-1 haematocrit. No difference was detected between PCOS and CON groups for RBC deformability measurements. A novel measure indicating the effectiveness of oxygen transport by RBC (i.e., the haematocrit-to-viscosity ratio; HVR) was decreased at all shear rates in women with PCOS. In a group of young and lean women with PCOS with an unremarkable cardiovascular risk profile based on clinical data, significant haemorheological impairment was observed. The degree of haemorheological derangement observed in the present study reflects that of overt chronic disease, and provides an avenue for future therapeutic intervention in PCOS.