Are Central Hemodynamic Parameters Better Prognostic Markers than Peripheral Blood Pressure in Stroke?

Abstract

The complex pathophysiological mechanisms involved in stroke confound the associative and causal role of blood pressure. This is particularly relevant in monitoring changes in blood pressure with respect to treatment efficacy and stroke outcome, which is highly dependent on the both patient and stroke characteristics. However, whereas blood pressure may have a variable prognostic role in both the underlying causes of stroke as well as stroke outcome due to modifications of intracranial pressure and autoregulation of cerebral blood flow, particularly in the elderly, measures of pulsatile phenomena, such as arterial stiffness affecting wave propagation have been shown to be strong independent predictors of overall cardiovascular events. Aortic stiffness has been shown to be related to cognitive decline, cerebral small vessel disease and acute hypertensive response and outcome following ischemic stroke.

In this debate, a case will be made that measures associated with arterial stiffness (pulse wave velocity, magnitude of forward and backward waves, intensity of wave reflection), pulsatility of arterial pressure and flow and central aortic pressure are better prognostic markers than conventional brachial blood pressure for assessment of stroke outcome. Specifically, this will involve measurement of arterial stiffness gradient to assess the amount of pulsatile energy generated by central hemodynamics and that is transmitted to the peripheral cerebral tissue leading to potential microvascular damage. These measures can provide additional information beyond brachial blood pressure to enable better alignment of patient and stroke characteristics and so improve management of stroke and mitigate cerebrovascular risk.

The effects of aortic pulsatility impact on the heart, brain, kidneys and other vascular beds, particularly in the elderly with elevated blood pressure, in who pulsatility is enhanced due to large vessel stiffness and is transmitted further distally along blood vessels into smaller arteries, affecting target organs to a greater degree. The brain, like the heart and the kidney, “sees” central blood pressure more directly than peripheral, brachial, blood pressure. Thus, central blood pressure could be a more accurate and direct reflection of the pathophysiological effects of elevated blood pressure on the brain than peripheral blood pressure. Indeed, central blood pressure appears to have a closer correlation with risk of stroke or other target organ damage than peripheral blood pressure. However, peripheral blood pressure has been the subject of millions person-years studies, many of them with hard end-points such as stroke, myocardial infarction, renal failure, death, compared to a few thousand patient studies for central pressure and some measure of target organ damage. Brachial pressure is measured around the world, and definitions, thresholds and goals have been established on the basis of huge numbers of data. Beyond controversies on the accuracy and reliability of central pressure measurements, there are nowhere equivalent numbers available for central pressure or the data needed to provide evidence-based directives for treatment of elevated blood pressure based on central pressure. Thus, a small advantage in risk prediction does not justify the adoption of measurement of central pressure over a proven method that is cheaper and generalized across the world, including in low-and middle-income countries with financially constrained health care systems.