Arterial dilation and reduced wave reflection. Benefit of dilevalol in hypertension.

Abstract

We compared dilevalol (an isomer of labetalol), 200-400 mg daily, against atenolol, 50-100 mg daily, in a double-blind, crossover, placebo-controlled trial with respect to effects on arterial distensibility (measured as pulse wave velocity [FVW]) and wave reflection (assessed from carotid pressure wave contour). Twelve patients of mean age 58 years (range 44-73 years) with essential hypertension (supine diastolic blood pressure 95-114 mm Hg) took active therapy for 12 weeks, separated by a 2-4-week placebo period. Carotid pressure waveforms were recorded noninvasively by applanation tonometry with a Millar micromanometer-tipped probe. PVW was measured between carotid and femoral arteries (aortic PWV), carotid and radial arteries (arm PVW), and femoral and pedal arteries (leg PWV). Early wave reflection was calculated from the ratio of the height of the peak of the carotid wave above its shoulder to the pulse pressure and was expressed as an augmentation index. Both drugs were equally effective in reducing brachial sphygmomanometric pressure and PWV in all three regions (active vs. placebo, p<0.001), but there was no significant difference between the two active therapies. However, the augmentation index (averaged during the treatment period) was significantly lower with dilevalol (19%) than with atenolol (28%, /;<0.01), corresponding to a greater decrease of 5-8 mm Hg in carotid systolic pressure compared with the brachial artery. Although both drugs were equally effective in reducing arterial distensibility, the vasodilating action of dilevalol gave added benefit in reducing wave reflection, presumably through its vasodilatory effect on peripheral conduit arteries. (Hypertension 1989;14:14-21)

Favourable effects on arterial wave reflection and pulse pressure amplification of adding angiotensin II receptor blockade in resistant hypertension

“…There has been a recent surge in interest in drugs that not only reduce blood pressure but also modify the blood pressure curve. In this setting, nitrates, 27 calcium-channel blockers, 15 vasodilating beta-blockers 10 and ACE inhibitors [12][13][14] have all been shown to decrease AWR in the ascending aorta. This is in contrast to drugs that have no effect on AWR and arterial stiffness despite the same extent of blood pressure reduction.…”

“…9 Early wave reflection certainly has adverse haemodynamic consequences and delaying it would be logical therapy in the management of hypertension and left ventricular hypertrophy. [10][11][12][13][14][15] Attention is being directed at drugs that reduce early AWR and arterial stiffness, as not all antihypertensives have a beneficial effect on arterial stiffness and AWR despite the same level of blood pressure reduction. 16,17 Angiotensin-converting enzyme (ACE) inhibitors, in particular, have been shown to delay AWR and increase the pulse pressure gradient between the central and peripheral circulation in both animal 18 and human studies.…”

Carotid Intimal-Medial Thickness and Stiffness Are Not Affected by Hypercholesterolemia in Uncomplicated Essential Hypertension

“…The systolic portion of the carotid waveform was analyzed to calculate the augmentation index, 35,36 a means of quantifying the contribution of reflected pressure waves to the central pulse pressure. After identification of the early and late systolic peaks and the inflection that separates them, pressures were determined at peak systolic pressure (P pk ) and at the inflection point (P i ) by using the previously described calibrated computer system.…”

Increased systolic pressure in chronic uremia. Role of arterial wave reflections.

“…11 -13 -18 - 21 Sphygmomanometric measurements of brachial artery blood pressure may underestimate blood pressure and PP alterations in central arteries and do not provide information about the shape of pressure waves. Recent developments in high fidelity applanation tonometry allow noninvasive recording of the arterial pressure waveform and magnitude in both peripheral and central arteries and allow the effects of aging and disease states to be more accurately evaluated.…”