Large Artery Compliance in Essential Hypertension: Effects of Calcium Antagonism and  -Blocking

Abstract

This study used 2D Doppler flowmetry to assess the effects on peripheral hemodynamics of effective treatment with nicardipine or atenolol in 40 patients with mild or moderate essential hypertension. Two groups of 20 patients received treatment with nicardipine or atenolol, respectively, for 8 months. Consequently, those patients considered to be responders (blood pressure less than 150/90 mm Hg) were monitored for another 4 weeks after the therapy was suspended in order to determine whether the changes, if any, in arterial compliance persisted. Following the 8-month therapy, four patients from each group were excluded from the study because of unsatisfactory blood pressure levels. After the treatment, there was a decrease in blood pressure in both groups (P less than .01). In the nicardipine group, there was a significant increase in diameter and compliance (P less than .01), whereas pulse wave velocity and resistance decreased (P less than .01). In the atenolol group, these parameters did not change significantly. After therapy was ended, blood pressure returned to baseline values in both groups. However, in the nicardipine group, the observed improvement in forearm hemodynamics persisted. This result may indicate that nicardipine is able to induce a regression of functional and/or structural changes in the large arteries of hypertensive patients.

Association between arterial stiffness and platelet activation

“…[13][14][15][17][18][19] Increased PWV has also been reported to be an independent predictor of cardiovascular events in patients with hypertension or renal failure, and in elderly subjects. 22,23 The association between increased arterial stiffness and high incidence of cardiovascular events may be explained by the existence of atherosclerosis.…”

“…2,3 Increased platelet activation is observed in patients with coronary risk factors and cardiovascular events. [4][5][6][7][8][9][10][11][12] Increased arterial stiffness, measured with pulse wave velocity (PWV), has been shown to be associated with atherosclerosis and risk factors of atherosclerotic cardiovascular disease, [13][14][15][16][17][18][19][20][21] and is an independent predictor of cardiovascular events, 22,23 Therefore, although platelets are likely to be activated in patients with atherosclerotic disease who exhibit increased arterial stiffness, little is known about the relation of arterial stiffness itself to platelet activation.…”

Isolated Systolic Hypertension

“…In contrast, ␤-blockers, as monotherapy, have been shown to increase conduit vessel stiffness and the magnitude of the reflected wave. 40,41 Results with calcium channel blockers have been mixed. [42][43][44] Additional longterm studies with direct, repeated measurements of conduit vessel stiffness are needed to further refine the role of therapy targeted to reducing conduit vessel stiffness.…”

Pulse waveform analysis of arterial compliance: relation to other techniques, age, and metabolic variables

“…Second, HiBP-Rx subjects were on various drug therapies, including diuretics, ␤-blockers, calcium channel blockers, ␣-blockers, converting enzyme inhibitors, and angiotensin II receptor blockers; and not enough subjects were on each drug to determine whether compliance was differentially affected by any one class. [27][28][29] Thus, the possibility that studying more hypertensive patients would have revealed compliance differences between unmedicated and medicated subjects, and the fact that isobaric compliance was not measured, make it difficult to distinguish the effect of lower BP itself versus pressure-independent drug effects on the vasculature. Third, data reported here demonstrating the physiologic correlates of compliance were obtained in relatively few subjects.…”