Neel D. Jani’s research while affiliated with University of California, Berkeley and other places

Deciphering the source of an embolism is a common challenge encountered in stroke treatment. Carotid stenosis is a key source of embolic strokes. Carotid interventions can be indicated when a patient has greater than 50% stenosis in the carotid ipsilateral to the cerebral infarction, which is designated as the symptomatic carotid. However, there are often significant number of cases where carotid emboli travel contralaterally leading to ambiguity regarding which carotid is symptomatic. We use a patient-specific computational embolus-hemodynamics interaction model developed in prior works to conduct an in silico experiment spanning 30 heart-to-brain arterial models with differing combinations of bilateral severe and mild stenosis degrees. We used these models to study source-to-destination transport of thromboemboli released from left/right carotid disease sites, and cardiogenic sources. Across all cases considered, thromboemboli from left and right carotid sources showed non-zero contralateral transport. We also found that cardiogenic thromboemboli do not have an altered hemisphere distribution or distinct transport preference dependent on stenosis degree, thus potentially making the underlying etiology more cryptic. In patients with carotid stenosis or chronic occlusion ipsilateral to the area affected by stroke, we have demonstrated that the presence of contralateral stenosis can cause emboli that travel across the Circle of Willis (CoW) which can potentially lead to ambiguity when deciding which carotid is truly symptomatic.

We describe a patient-specific simulation based investigation on the role of Circle of Willis anatomy in cardioembolic stroke. Our simulation framework consists of medical image-driven modeling of patient anatomy including the Circle, 3D blood flow simulation through patient vasculature, embolus transport modeling using a discrete particle dynamics technique, and a sampling based approach to incorporate parametric variations. A total of 24 (four patients and six Circle anatomies including the complete Circle) models were considered, with cardiogenic emboli of varying sizes and compositions released virtually and tracked to compute distribution to the brain. The results establish that Circle anatomical variations significantly influence embolus distribution to the six major cerebral arteries. Embolus distribution to MCA territory is found to be least sensitive to the influence of anatomical variations. For varying Circle topologies, differences in flow through cervical vasculature are observed. This incoming flow is recruited differently across the communicating arteries of the Circle for varying anastomoses. Emboli interact with the routed flow, and can undergo significant traversal across the Circle arterial segments, depending upon their inertia and density ratio with respect to blood. This interaction drives the underlying biomechanics of embolus transport across the Circle, explaining how Circle anatomy influences embolism risk.

We describe a patient-specific simulation based investigation on the role of Circle of Willis anatomy in cardioembolic stroke. Our simulation framework consists of medical image-driven modeling of patient anatomy including the Circle, 3D blood flow simulation through patient vasculature, embolus transport modeling using a discrete particle dynamics technique, and a sampling based approach to incorporate parametric variations. A total of 24 (four patients and six Circle anatomies including the complete Circle) models were considered, with cardiogenic emboli of varying sizes and compositions released virtually and tracked to compute distribution to the brain. The results establish that Circle anatomical variations significantly influence embolus distribution to the six major cerebral arteries. Embolus distribution to MCA territory is found to be least sensitive to the influence of anatomical variations. For varying Circle topologies, differences in flow through cervical vasculature are observed. This incoming flow is recruited differently across the communicating arteries of the Circle for varying anastomoses. Emboli interact with the routed flow, and can undergo significant traversal across the Circle arterial segments, depending upon their inertia and density ratio with respect to blood. This interaction drives the underlying biomechanics of embolus transport across the Circle, explaining how Circle anatomy influences embolism risk.

Stroke caused by an embolism accounts for about a third of all stroke cases. Understanding the source and cause of the embolism is critical for diagnosis and long-term treatment of such stroke cases. The complex nature of the transport of an embolus within large arteries is a primary hindrance to a clear understanding of embolic stroke etiology. Recent advances in medical image-based computational hemodynamics modeling have rendered increasing utility to such techniques as a probe into the complex flow and transport phenomena in large arteries. In this work we present a novel, patient-specific, computational framework for understanding embolic stroke etiology, by combining image-based hemodynamics with discrete particle dynamics and a sampling-based analysis. The framework allows us to explore the important question of how embolism source manifests itself in embolus distribution across the various major cerebral arteries. Our investigations illustrate prominent numerical evidence regarding (i) the size/inertia dependent trends in embolus distribution to the brain, (ii) the relative distribution of cardiogenic versus aortogenic emboli amongst the anterior, middle, and posterior cerebral arteries, (iii) the left versus right brain preference in cardio-emboli and aortic-emboli transport, and (iv) the source-destination relationship for embolisms affecting the brain.