Hypertension‐induced alterations in hemodynamics and wave dynamics are important pathological mechanisms for cerebrovascular diseases, vascular cognitive impairment and dementia. However, fundamental understanding of hemodynamics and wave dynamics in hypertension remains… Click to show full abstract
Hypertension‐induced alterations in hemodynamics and wave dynamics are important pathological mechanisms for cerebrovascular diseases, vascular cognitive impairment and dementia. However, fundamental understanding of hemodynamics and wave dynamics in hypertension remains limited due to the restricted temporal and spatial resolution of current medical devices. To address the gap, this study developed a closed‐loop multiscale computational modeling framework for the entire cardiovascular system. A novel “parameter assignment method” designed for diverse 0D peripheral vascular bed models across the entire cardiovascular system was proposed. Additionally, a mathematical modeling strategy was introduced to characterize cardiovascular parameters associated with hypertension across varying degrees of severity. Key findings from model‐based studies indicated that in hypertension, there was early arrival and increased magnitudes of forward compression wave intensity and power (FCWI and FCWP), forward expansion wave intensity and power (FEWI and FEWP), and back compression wave intensity and power (BCWI and BCWP) in extra‐intracranial cerebral arteries. The proximal aorta, however, exhibited delayed arrival of FCWI and FCWP but early arrival of BCWI and BCWP, along with negligible change in FCWI magnitudes and slightly increased BCWI magnitudes, significantly increased FEWI, FCWP, FEWP and BCWP magnitudes. Moreover, parametric studies demonstrated that progressively enlarging central large elastic arteries, increasing passive myocardial stiffness, and raising peripheral vascular resistance led to reduced magnitudes of FCWI, BCWI, FCWP and BCWP in cerebral arteries. Conversely, stiffening of central large elastic arteries and increasing myocardial contractility had opposite effects. The proposed computational modeling framework will serve as a powerful tool for elucidating the complex mechanisms underlying hypertension‐associated hemodynamics and wave dynamics.
               
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