The Haemodynamic Genesis of Hypertension

Abstract

Hypertension has classically been attributed to an increase in peripheral vascular resistance. Such an increase in peripheral vascular resistance would increase mean and diastolic blood pressure but have little influence on pulse pressure. However, hypertension in our ageing society occurs mainly as a result of an increase in pulse pressure and hence in systolic blood pressure. Haemodynamic mechanisms leading to increased pulse pressure are complex and are best understood using a combination of detailed haemodynamic profiling in epidemiological studies, theoretical analyses, and experimental interventions. These underscore the importance of arterial stiffness, pressure dependence of arterial stiffness as a link between diastolic and systolic pressure and ventricular ejection characteristics as determinants of pulse pressure and pulse wave morphology. From the perspective of therapeutic interventions to prevent a rise in pulse pressure, it is key to understand the degree to which conventional anti-hypertensive agents may prevent or reverse arterial stiffening or whether this will be largely dependent on the development of agents that have specific anti-stiffening effects. Ventricular ejection characteristics may depend on loading conditions, both pre-load and after-load, on central cardiac drive and on the intrinsic properties of the myocardium. As with arterial stiffness the relative importance of these factors and the degree to which they may be manipulated by conventional anti-hypertensive agents will determine future approaches to prevent or reverse systolic hypertension and its complication such heart failure. Tailoring the therapeutic approach to target individual haemodynamic determinants of hypertension may provide the best use of current and future treatments.