The need to optimize the thrombogenic performance of blood recirculating cardiovascular devices, e.g., prosthetic heart valves (PHV) and ventricular assist devices (VAD), is accentuated by the fact that most of them require lifelong anticoagulation therapy that does not eliminate the risk of thromboembolic complications. The formation of thromboemboli in the flow field of these devices is potentiated by contact with foreign surfaces and regional flow phenomena that stimulate blood clotting, especially platelets. With the lack of appropriate methodology, device manufacturers do not specifically optimize for thrombogenic performance. Such optimization can be facilitated by formulating a robust numerical methodology with predictive capabilities of flow-induced platelet activation. In this study, a phenomenological model for platelet cumulative damage, identified by means of genetic algorithms (GAs), was correlated with in vitro experiments conducted in a Hemodynamic Shearing Device (HSD). Platelets were uniformly exposed to flow shear representing the lower end of the stress levels encountered in devices, and platelet activity state (PAS) was measured in response to six dynamic shear stress waveforms representing repeated passages through a device, and correlated to the predictions of the damage accumulation model. Experimental results demonstrated an increase in PAS with a decrease in "relaxation" time between pulses. The model predictions were in very good agreement with the experimental results.A recognized feature of the complex interplay regulating the pathogenesis of thrombosis is the effect of blood flow-induced mechanical forces on platelets. Physical agonists, such as these flow-induced forces, and chemical agonists, such as adenosine diphosphate and serotonin, trigger platelet activation. This process commences with the secretion of procoagulant and selfstimulating substances from granules, 1 which catalyze thrombin production. 2 As a direct consequence of activation, the platelets undergo a change in shape, marked by pseudopod extension. This increases the strength of adhesion to exogenous surfaces and decreases the resistance to aggregation.One of the major culprits in blood recirculating devices is the emergence of nonphysiologic (pathologic) flow patterns that enhance the hemostatic response. Elevated flow stresses that are present in the nonphysiologic geometries of blood recirculating devices enhance their propensity to initiate thromboembolism. In recent years, it has been demonstrated that flow induced thrombogenicity, caused by chronic platelet activation and the initiation of thrombus formation, is the salient aspect of mechanically induced blood trauma in devices. 3 This lends itself to the hypothesis that thromboembolism in prosthetic blood recirculating devices is

The hemodynamics within the aorta of five healthy humans were investigated to gain insight into the complex helical flow patterns that arise from the existence of asymmetries in the aortic region. The adopted approach is aimed at (1) overcoming the relative paucity of quantitative data regarding helical blood flow dynamics in the human aorta and (2) identifying common characteristics in physiological aortic flow topology, in terms of its helical content. Four-dimensional phase-contrast magnetic resonance imaging (4D PC MRI) was combined with algorithms for the calculation of advanced fluid dynamics in this study. These algorithms allowed us to obtain a 4D representation of intra-aortic flow fields and to quantify the aortic helical flow. For our purposes, helicity was used as a measure of the alignment of the velocity and the vorticity. There were two key findings of our study: (1) intra-individual analysis revealed a statistically significant difference in the helical content at different phases of systole and (2) group analysis suggested that aortic helical blood flow dynamics is an emerging behavior that is common to normal individuals. Our results also suggest that helical flow might be caused by natural optimization of fluid transport processes in the cardiovascular system, aimed at obtaining efficient perfusion. The approach here applied to assess in vivo helical blood flow could be the starting point to elucidate the role played by helicity in the generation and decay of rotating flows in the thoracic aorta.

The mechanics of blood flow in arteries plays a key role in the health of individuals. In this framework, the role played by the presence of helical flow in the human aorta is still not clear in its relation to physiology and pathology. We report here a method for quantifying helical flow in vivo employing time-resolved cine phase contrast magnetic resonance imaging to obtain the complete spatio-temporal description of the three-dimensional pulsatile blood flow patterns in aorta. The method is applied to data of one healthy volunteer. Particle traces were calculated from velocity data: to them we applied a Lagrangian-based method for helical flow quantification, the Helical Flow Index, which has been developed and evaluated in silico in order to reveal global organization of blood flow. Our results: (i) put in evidence that the systolic hemodynamics in aorta is characterized by an evolving helical flow (we quantified a 24% difference in terms of the content of helicity in the streaming blood, between mid and early systole); (ii) indicate that in the first part of the systole helicity is ascrivable mainly to the asymmetry of blood flow in the left ventricle, joined with the laterality of the aorta. In conclusion, this study shows that the quantification of helical blood flow in vivo is feasible, and it might allow detection of anomalies in the expected physiological development of helical flow in aorta and accordingly, could be used in a diagnostic/prognostic index for clinical practice.

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Theme Issue Article Biomechanics in vascular biologyand CVD SummaryAtherosclerotic plaques are found at distinct locations in the arterial system, despite the exposure to systemic risk factors of the entire vascular tree. From the study of arterial bifurcation regions, emerges ample evidence that haemodynamics are involved in the local onset and progression of the atherosclerotic disease. This observed co-localisation of disturbed flow regions and lesion prevalence at geometrically predisposed districts such as arterial bifurcations has led to the formulation of a 'haemodynamic hypothesis', that in this review is grounded to the most current research concerning localising factors of vascular disease. In particular, this review focuses on carotid and coronary bifurcations because of their primary relevance to stroke and heart attack. We highlight reported relationships between atherosclerotic plaque location, progression and composition, and fluid forces at vessel's wall, in particular shear stress and its 'easier-tomeasure' surrogates, i.e. vascular geometric attributes (because geometry shapes the flow) and intravascular flow features (because they mediate disturbed shear stress), in order to give more insight in plaque initiation and destabilisation. Analogous to Virchow's triad for thrombosis, atherosclerosis must be thought of as subject to a triad of, and especially interactions among, haemodynamic forces, systemic risk factors, and the biological response of the wall.

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