학술논문

In-silico modelling of the impact of hypertension on the mean transvalvular gradients in aortic stenosis.
Document Type
Article
Source
PLoS ONE. 6/8/2023, Vol. 17 Issue 6, p1-12. 12p.
Subject
*AORTIC stenosis
*BLOOD pressure
*CARDIOVASCULAR system
*SINUS of valsalva
*HYPERTENSION
*AORTIC valve
*MITRAL valve
*CONTRACTILITY (Biology)
*PULMONARY valve
Language
ISSN
1932-6203
Abstract
Introduction: The influence of hypertension on the diagnostic assessment of aortic stenosis (AS) severity is unclear, yet clinically relevant. To clarify the effect of hypertension on transvalvular gradients, requires a better understanding of the impact that blood pressure change has on mean flow rate. Also, the effect of various degrees of AS severity, the valve geometry and intrinsic left ventricular contractile function (elastance) on this interaction, needs to be clarified. The current work aims to assess this interaction and the magnitude of these effects. Methods: A validated, zero-dimensional electro-hydraulic analogue computer model of the human cardiovascular circulatory system was generated. It was used to assess the impact of blood pressure changes on left ventricular pressure and transvalvular gradients at various flow rates, left ventricular elastances, a range of aortic valve areas and for different aortic valve morphologies. Results and discussion: The magnitude of the impact of hypertension induced changes on the mean gradient (MG) is influenced by the mean flow rate, the AS severity, the hydraulic effective valve orifice area and the left ventricular elastance. Generally, for a given change in systemic arterial pressure, the impact on MG will be the most marked for lower flow rate states such as is expected in more severe degrees of AS, for worse intrinsic left ventricular (LV) contractility, shorter ejection times and lower end diastolic LV volumes. Given the above conditions, the magnitude of the effect will be more for a larger aortic sinus diameter, and also for a typical degenerative valve morphology compared to a typical rheumatic valve morphology. Conclusion: The interaction between hypertension and mean gradients in AS is complex. The current work places previous recommendations in perspective by quantifying the magnitude of the effect that the changes in blood pressure has on mean gradient in various pathophysiological states. The work creates a framework for the parameters that should be considered in future clinical research on the topic. [ABSTRACT FROM AUTHOR]