Jason S Au1,2, Billy Y S Yiu1,2, Hélène So3, Adrian J Y Chee1,2, Danielle K Greaves1,4, Richard L Hughson1, Alfred C H Yu1,2. 1. Schlegel-University of Waterloo Research Institute for Aging, 250 Laurelwood Dr., Waterloo, N2J0E2, Canada. 2. Department of Electrical and Computer Engineering, University of Waterloo, 200 University Ave West, Waterloo, N2L3G1, Canada. 3. Faculty of Science and Engineering, Sorbonne Université, 75005, Paris, France. 4. University of Caen Normandy, Espl. De la Paix, 14032, Caen, France.
Abstract
PURPOSE: Complex blood flow is commonly observed in the carotid bifurcation, although the factors that regulate these patterns beyond arterial geometry are unknown. The emergence of high-frame-rate ultrasound vector flow imaging allows for noninvasive, time-resolved analysis of complex hemodynamic behavior in humans, and it can potentially help researchers understand which physiological stressors can alter carotid bifurcation hemodynamics in vivo. Here, we seek to pursue the first use of vector projectile imaging (VPI), a dynamic form of vector flow imaging, to analyze the regulation of carotid bifurcation hemodynamics during experimental reductions in cardiac output induced via a physiological stressor called lower body negative pressure (LBNP). METHODS: Seven healthy adults (age: 27 ± 4 yr, 4 men) underwent LBNP at -45 mmHg to simulate a postural hemodynamic response in a controlled environment. Using a research-grade, high-frame-rate ultrasound platform, vector flow estimation in each subject's right carotid bifurcation was performed through a multi-angle plane wave imaging (two transmission angles of 10° and -10°) formulation, and VPI cineloops were generated at a frame rate of 750 fps. Vector concentration was quantified by the resultant blood velocity vector angles within a region of interest; lower concentration indicated greater flow dispersion. Discrete concentration values during peak and late systole were compared across different segments of the carotid artery bifurcation before, and during, LBNP. RESULTS: Vector projectile imaging revealed that external and internal carotid arteries exhibited regional hemodynamic changes during LBNP, which acted to reduce both the subject's cardiac output (Δ - 1.2 ± 0.5 L/min, -19%; P < 0.01) and peak carotid blood velocity (Δ - 6.30 ± 8.27 cm/s, -7%; P = 0.05). In these carotid artery branches, the vector concentration time trace before and during LBNP were observed to be different. The impact of LBNP on flow complexity in the two carotid artery branches showed variations between subjects. CONCLUSIONS: Using VPI, intuitive visualization of complex hemodynamic changes can be obtained in healthy humans subjected to LBNP. This imaging tool has potential for further applications in vascular physiology to identify and quantify complex hemodynamic features in humans during different physiological stressor tests that regulate hemodynamics.
PURPOSE: Complex blood flow is commonly observed in the carotid bifurcation, although the factors that regulate these patterns beyond arterial geometry are unknown. The emergence of high-frame-rate ultrasound vector flow imaging allows for noninvasive, time-resolved analysis of complex hemodynamic behavior in humans, and it can potentially help researchers understand which physiological stressors can alter carotid bifurcation hemodynamics in vivo. Here, we seek to pursue the first use of vector projectile imaging (VPI), a dynamic form of vector flow imaging, to analyze the regulation of carotid bifurcation hemodynamics during experimental reductions in cardiac output induced via a physiological stressor called lower body negative pressure (LBNP). METHODS: Seven healthy adults (age: 27 ± 4 yr, 4 men) underwent LBNP at -45 mmHg to simulate a postural hemodynamic response in a controlled environment. Using a research-grade, high-frame-rate ultrasound platform, vector flow estimation in each subject's right carotid bifurcation was performed through a multi-angle plane wave imaging (two transmission angles of 10° and -10°) formulation, and VPI cineloops were generated at a frame rate of 750 fps. Vector concentration was quantified by the resultant blood velocity vector angles within a region of interest; lower concentration indicated greater flow dispersion. Discrete concentration values during peak and late systole were compared across different segments of the carotid artery bifurcation before, and during, LBNP. RESULTS: Vector projectile imaging revealed that external and internal carotid arteries exhibited regional hemodynamic changes during LBNP, which acted to reduce both the subject's cardiac output (Δ - 1.2 ± 0.5 L/min, -19%; P < 0.01) and peak carotid blood velocity (Δ - 6.30 ± 8.27 cm/s, -7%; P = 0.05). In these carotid artery branches, the vector concentration time trace before and during LBNP were observed to be different. The impact of LBNP on flow complexity in the two carotid artery branches showed variations between subjects. CONCLUSIONS: Using VPI, intuitive visualization of complex hemodynamic changes can be obtained in healthy humans subjected to LBNP. This imaging tool has potential for further applications in vascular physiology to identify and quantify complex hemodynamic features in humans during different physiological stressor tests that regulate hemodynamics.