High arterial blood pressure (BP) is one of the most important causes of global morbidity and mortality. We are using haemodynamics to characterise and quantify individual cardiovascular contributions to arterial BP and its amplification to the periphery
-- where it is normally measured -- and to uncover the underlying physical mechanisms leading to increased BP.
We have shown that:
- Central pulse pressure (cPP; i.e. the amplitude of the aortic BP wave) is mainly determined by total arterial compliance (inversely associated with central arterial stiffness) and ventricular dynamics (Hypertension, 2017);
- Heart dynamics contribute by more than 50% to the increase in cPP in hypertension (the major cause of incident hypertension in middle-aged to older persons), suggesting that cardiac dynamics are more important than vascular properties, contrary to the common knowledge. Pressure reflection from the vasculature may be less important in raising cPP than previously thought and, hence, cardiac properties should be involved in the treatment strategy (Hypertension, 2017);
- The age-related increase in cPP is driven mainly by an increase in aortic stiffness, sustained ventricular ejection, and an increase in stroke volume that parallels that in BMI. Consequently, conditions and drugs that influence cardiac function may influence pulse wave morphology independent of arterial function. Since drugs with a specific action to reduce arterial stiffness are not yet available, interventions to decrease stroke volume (e.g. weight reduction) and modulate ventricular dynamics might be useful in preventing/treating systolic hypertension (Hypertension, 2019);
- Cardiac contractility plays a crucial role in amplifying the peripheral BP wave, both theoretically (Frontiers Physiol, 2021) and experimentally using the model shown below (Am J Physiol, 2017). This offers opportunity for noninvasive assessment of ventricular health; e.g. using the PPG signal measured in the periphery;
- Peripheral systolic BP is mainly determined by cardiac and aortic properties that are different from the determinants of central systolic BP (Am J Physiol, 2021). This may be a potential mechanism why BP-lowering drugs like β-blockers may have differential effects on central and peripheral BP. It potentially explains why in very elderly subjects, low peripheral BP and low peripheral amplification may be associated with increased cardiovascular events.
These results have been obtained using haemodynamics-based algorithms developed by us, including
- A three-element Windkessel model to calculate cPP from aortic blood flow and examine cPP dependence on cardiac and vascular properties (Hypertension, 2017);
- A method for estimating cPP from non-invasive measurements of aortic flow and peripheral PP, based on a comprehensive understanding of the main cardiovascular properties that determine PP augmentation along the aortic-brachial arterial path (Frontiers Physiol, 2021);
- A method to create populations of thousands of virtual subjects for in silico evaluation of pulse wave indices and algorithms (Symmetry, 2021; Am J Physiol, 2015 and 2019; J Biomech, 2016).