Different Effects of Fosinopril and Atenolol on Wave Reflections in Hypertensive Patients

Abstract

We conducted this study to compare the effects of fosinopril versus atenolol on peripheral blood pressure, central arterial wave reflection, and left ventricular mass in a group of patients with essential hypertension. We conducted a double-blind, randomized trial of fosinopril and atenolol in 79 hypertensive patients (52 men, 27 women; mean age, 45.8 +/- 8.5 years; range, 30 to 68 years). Carotid pressure waveforms were recorded noninvasively by applanation tonometry with a Millar micromanometer-tipped probe. The extent of wave reflection was estimated by the augmentation index defined as the ratio of the amplitude of pressure wave above its systolic shoulder to the pulse pressure. The augmentation index, left ventricular mass index by two-dimensional echocardiography, and 24-hour ambulatory blood pressures were determined before and after 8 weeks of daily treatment with fosinopril (10 to 20 mg) or atenolol (50 to 100 mg) with or without diuretics and compared with those values in 79 normotensive control subjects. After 8 weeks of treatment, both drugs lowered 24-hour ambulatory peripheral systolic and diastolic pressures into the normal range to a similar extent (fosinopril, -18/-13 mm Hg; atenolol, -23/-17 mm Hg, both P = NS). On the other hand, whereas the elevated augmentation index in hypertensive patients compared with normotensive subjects (16 +/- 11% versus 10 +/- 8%) was completely normalized by fosinopril (-9.3 +/- 9.8%, P < or = .002), it was lowered by atenolol (-4.8 +/- 8.9%, P < .002) but to a significantly smaller extent (fosinopril versus atenolol effect, P = .04).(ABSTRACT TRUNCATED AT 250 WORDS)

Macro and microvasculature in hypertension: therapeutic aspects

“…1,2,16 Second, ACEI, but not atenolol, is known to reduce reflection coefficients (Table 1). [21][22][23] In conclusion, there is hardly any doubt that CV events are the consequences of vascular damage at both the macro and microvascular level. Possible interrelationships between alterations in the macro and microvasculature and mechanisms possibly involved represent an extremely interesting topic, which deserve further and thorough investigation, also considering its relevant clinical impact, especially in terms of possible prevention or regression of the concerned alterations.…”

“…[21][22][23] Herein, the major factors to consider are not only the distensibility and the diameter of each arteriolar branch of the bifurcation, but also their exact location. With age, the reflection sites are closer to vital organs, such as the heart, brain and kidney, and even wave reflections may contribute particularly to organ damage.…”

“…29 The difference between Per/Ind and atenolol could be due exclusively to the atenolol-induced heart rate reduction, thereby causing the maintenance of disturbed wave reflections. [21][22][23][24][25][26][27] However, this result was observed only within the first 6 months of treatment. 25 After this period, the Reason Study showed that the mechanism of SBP reduction under Per/Ind was highly modified.…”

Cardiovascular prevention: relationships between arterial aging and chronic drug treatment

“…7 Because the carotid PP is known to be physiologically lower than brachial PP for the same mean blood pressure (MBP), common carotid artery and radial artery pressure waveforms were recorded non-invasively by applanation tonometry with the SphygmoCor system (AtCor Medical, Sydney, Australia). [8][9][10] Although SBP and PP are known to increase physiologically and significantly (8-12 mm Hg) from central to peripheral arteries, falls in DBP or MBP from the ascending aorta to the radial artery do not exceed 2-3 mm Hg. [9][10][11] Therefore, the carotid pressure wave was calibrated assuming that radial and carotid DBP and MBP were nearly equal.…”

“…[8][9][10] Although SBP and PP are known to increase physiologically and significantly (8-12 mm Hg) from central to peripheral arteries, falls in DBP or MBP from the ascending aorta to the radial artery do not exceed 2-3 mm Hg. [9][10][11] Therefore, the carotid pressure wave was calibrated assuming that radial and carotid DBP and MBP were nearly equal. The MBP of the carotid pressure wave, computed from the area measurement of the wave in the corresponding heart period, was taken as equal to brachial MBP.…”