Plastic use dramatically increased over the past few years. Besides obvious benefits, the consequent plastic waste and mismanagement in disposal have caused ecological problems. Plastic abandoned in the environment is prone to segregation, leading to the generation of microplastics (MPs) and nanoplastics (NPs), which can reach aquatic and terrestrial organisms. MPs/NPs in water can access fish’s bodies through the gills, triggering an inflammatory response in loco. Furthermore, from the gills, plastic fragments can be transported within the circulatory system altering blood biochemical parameters and hormone levels and leading to compromised immunocompetence and angiogenesis. In addition, it was also possible to observe an unbalanced ROS production, damage in vascular structure, and enhanced thrombosis. MPs/NPs led to cardiotoxicity, pericardial oedema, and impaired heart rate in fish cardiac tissue. MPs/NPs effects on aquatic organisms pose serious health hazards and ecological consequences because they constitute the food chain for humans. Once present in the mammalian body, plastic particles can interact with circulating cells, eliciting an inflammatory response, with genotoxicity and cytotoxicity of immune cells, enhanced haemolysis, and endothelium adhesion. The interaction of MPs/NPs with plasma proteins allows their transport to distant organs, including the heart. As a consequence of plastic fragment internalisation into cardiomyocytes, oxidative stress was increased, and metabolic parameters were altered. In this scenario, myocardial damage, fibrosis and impaired electrophysiological values were observed. In summary, MPs/NPs are an environmental stressor for cardiac function in living organisms, and a risk assessment of their influence on the cardiovascular system certainly merits further analysis.

The liver and other organs are connected to each other through the bloodstream. Therefore, the connection between tissues is generally mediated by soluble molecules able to cross the endothelial wall of capillaries. We developed a multicompartmental device, multicompartmental bioreactor (MCB), designed to mimic the connection between different tissues in which crosstalk is mediated by soluble molecules transported through the blood. A comparative study of the crosstalk between hepatocytes (HepG2) and endothelial cells (human umbilical vein endothelial cells) in connected culture in the MCB and in a traditional static coculture system was performed by analyzing glucose consumption and secretion of albumin, urea, and nitric oxide. When hepatocytes and endothelial cells were cultured together, the production of albumin and urea increased, and the increase was higher in the MCB than in traditional static coculture. In spite of this enhanced metabolic activity, the crosstalk between hepatocytes and endothelial cell leads to decreased glucose consumption with respect to hepatocytes alone, both in static and in dynamic conditions. However, the dynamic connected culture has a higher rate of metabolite synthesis and secretion with respect to cocultures. This means a more efficient use of energetic substrates and enhanced hepatocyte function in the MCB.

Computational fluid dynamics methods based on in vivo 3-D vessel reconstructions have recently been identified the influence of wall shear stress on endothelial cells as well as on vascular smooth muscle cells, resulting in different events such as flow mediated vasodilatation, atherosclerosis, and vascular remodeling. Development of image-based modeling technologies for simulating patient-specific local blood flows is introducing a novel approach to risk prediction for coronary plaque growth and progression. In this study, we developed 3-D model of plaque formation and progression that was tested in a set of patients who underwent coronary computed tomography angiography (CTA) for anginal symptoms. The 3-D blood flow is described by the Navier-Stokes equations, together with the continuity equation. Mass transfer within the blood lumen and through the arterial wall is coupled with the blood flow and is modeled by a convection-diffusion equation. The low density lipoprotein (LDL) transports in lumen of the vessel and through the vessel tissue (which has a mass consumption term) are coupled by Kedem-Katchalsky equations. The inflammatory process is modeled using three additional reaction-diffusion partial differential equations. A full 3-D model was created. It includes blood flow and LDL concentration, as well as plaque formation and progression. Furthermore, features potentially affecting plaque growth, such as patient risk score, circulating biomarkers, localization and composition of the initial plaque, and coronary vasodilating capability were also investigated. The proof of concept of the model effectiveness was assessed by repetition of CTA, six months after the baseline evaluation. Besides the low values of local shear stress, plaque characteristics, risk profile, pattern of circulating adhesion molecules, and reduced coronary flow reserve at baseline appeared to affect plaque progression toward flow-limiting lesions at follow-up evaluation. Although preliminary, our multidisciplinary approach to a “personalized” prediction of coronary plaque progression suggests that incorporation in atherosclerotic models of systemic and local hemodynamic features may better predict evolution of plaques in coronary artery disease stable patients.