The time to return of the reflected wave (Tr) was calculated as the time from the beginning of the derived aortic systolic pressure waveform to the inflection point.
Arterial stiffness causes an early return of the reflected pressure wave to the aorta, with subsequently augmented central systolic pressure.
Stiffer vessels produce an earlier return of the reflected wave from vascular branching points to the ascending aorta.
The loss of vasodilator potential results in increased amplitude and early return of the reflected wave, causing high pulse pressure.
However, progressive stiffening of the arterial walls (as occurs in most people with longstanding diabetes) accelerates the return of the reflected wave causing its earlier arrival during late systole.
In adults with hypertension, early return of the reflected wave may lead to increasing LV afterload and central pulse pressure (PP), which in turn promote LV hypertrophy and subendocardial ischemia.
The lesser decrease in systolic blood pressure on the old-drug combination (18) is probably the consequence of the beta blocker-induced reduction of heart rate, which is responsibeta blocker-inducedreduction reflected waves in the central arteries during systofe and more pronounced systolic augmentation (24, 25).
The pathophysiological correlation between arterial stiffness and HTN is that the increased arterial stiffness reduces the lumen diameter, for a given smooth muscle tone and blood pressure, leading to a premature return of the reflected wave in late systole, thereby increasing the central pulse pressure and SBP, and decreasing DBP [ 17].
From a mechanistic standpoint, excessive arterial stiffness is responsible for a premature return of the reflected pulse wave in the late phase of systole, which causes an increase in central pulse pressure and thus an excess of workload and oxygen demand for the left ventricle.
Increased arterial stiffness, due to increased intima-media thickness and collagen accumulation produced by invading vascular smooth muscle cells (VSMCs), results in an increase in aortic pulse wave velocity and thus, early return of the reflected pressure wave and elevation in systolic pressure.
