Arterial Stiffness and Wave Reflections Following Acute Calcium Blockade in Essential Hypertension

Antihypertensive agents are routinely studied in terms of changes in the level of systolic, diastolic, and mean arterial pressure. Pulse pressure may be independently modified from these parameters as a consequence of specific changes in the mechanical properties of the large arteries and in the timing of incident and reflected pressure waves. The aim of this study was to evaluate the changes in pulse pressure produced by acute calcium blockade by the dihydropiridine derivative, lacidipine, in a double-blind design versus placebo in 18 subjects with mild to moderate hypertension. Carotid and femoral pressure waveforms were recorded noninvasively by applanation tonometry using a Millar micromanometer-tipped probe. Early (Pi) and midto-late (Ppk) systolic peaks of carotid pressure waveform were evaluated, enabling the effect of incident pressure wave to be quantified as the ratio of Pi to the total height of carotid pulse wave (PP) (Pi/PP) and the effect of wave reflections as the ratio (Ppk - Pi)/PP. Travel time of the reflected wave (Δtp) was timed from the foot of the pressure wave to the foot of the late systolic peak. Pulsatile changes in diameter were studied using noninvasive echo-tracking techniques. Whereas mean arterial pressure significantly decreased following lacidipine, pulse pressure measured at three different sites (brachial, carotid, and femoral arteries) was unchanged. Carotid-femoral pulse wave velocity, carotid and femoral arterial stiffness, and Δtp were not modified, whereas the (Ppk - Pi)/PP ratio and left ventricular ejection time were significantly reduced and the Pi/PP ratio was significantly increased. The study provides evidence that the unchanged pulse pressure following acute calcium blockade involves both an increase in ventricular ejection and incident pressure wave and a significant modification in the timing between ventricular ejection and the return of arterial wave reflections. During antihypertensive therapy by acute calcium blockade, unchanged pulse pressure in the presence of reduced mean arterial pressure may contribute to maintaining or even increasing the pulsatile component of the cardiac work in the early phase of treatment. Am J Hypertens 1994;7:168–176