Arterial Stiffness - The Pathophysiology of Arterial Stiffness

The Pathophysiology of Arterial Stiffness

The primary site of damage following an increase in arterial stiffness is the heart. Moreover, the means by which arterial stiffness causes damage to the heart are several-fold.

Firstly, stiffened arteries interrupt the Windkessel effect of the arteries. This function describes how arteries can be exposed to pulsatile ejections of blood from the heart at one end and convert it into a steady, even flow at the other end. This function is made possible because arteries are compliant and are readily able to expand due to pressure, but they also possess the ability to recoil.

Thus, stiffened arteries require a greater amount of force to cause them to expand and take up the blood ejected from the heart. This increased force requirement is provided by the heart, which begins to contract harder to accommodate the artery. Over time, this increased load placed on the heart causes left ventricular hypertrophy and eventually left ventricular failure. Causing further damage is the increased time required for systole and the reduction of diastole. This reduction in both time and pressure during diastole decreases the amount of perfusion for cardiac tissue. Thus the heart, which is becoming hypertrophic (and with therefore a greater oxygen demand) is starved of oxygen and nutrition, adding to cardiac damage.

Arterial stiffness also repositions the site of pulse wave reflections. These reflections are an inevitable phenomenon of any conduit system with geometric discontinuity. As pressure waves travel down and through a tube of decreasing diameter, a reflected wave of energy is created. Within a young person, these reflected waves arrive at the heart during late systole to diastole, thus contributing to the magnitude of diastole via constructive wave interference. However, stiffened arteries equate to an earlier reduction in the diameter of the artery, thus establishing the point of wave reflection at an earlier point along the arterial tree. Therefore, the reflected wave arrives at the heart closer to systole, increasing its magnitude through constructive wave interference. Once again, this increase in systole places a greater load on the heart, causing it to become hypertrophic.