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(Hypertension. 1995;25:1034-1041.)
© 1995 American Heart Association, Inc.
Articles |
Different Effects of Fosinopril and Atenolol on Wave Reflections in Hypertensive Patients
From the Division of Cardiology, Veterans General Hospital-Taipei (C.-H.C., S.-J.L., T.-L.H., S.-P.W., M.-S.C.); the Veterans General Hospital-Taichung (C.-T.T.), Republic of China; the Division of Cardiology, Johns Hopkins Hospital, Baltimore, Md (F.C.P.Y., C.O.S.); and the Institute of Public Health, National Yang-Ming University, Taipei (P.C.), Republic of China.
Correspondence to Chen-Huan Chen, MD, Division of Cardiology, Department of Medicine, Veterans General Hospital-Taipei, Shih-Pai, Taipei, Taiwan, 11217, ROC.
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Abstract |
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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
.002),
it was lowered by atenolol (-4.8±8.9%, P<.002) but to a
significantly smaller extent (fosinopril versus atenolol effect,
P=.04). Neither drug affected the slightly elevated left
ventricular mass index (fosinopril, 93±13 gm/m2; atenolol,
98±20 gm/m2) compared with normotensive subjects (86±13
gm/m2). At the doses used, fosinopril and atenolol reduced
peripheral blood pressure similarly but had different effects on
central systolic wave reflections, implying a greater effect of
fosinopril than atenolol in reducing central blood pressure than is
apparent from measurements of peripheral pressure. Left ventricular
mass was only slightly elevated in these mild hypertensive patients and
was not altered after 8 weeks of treatment.
Key Words: hypertension, essential • tonometry • fosinopril • atenolol
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Introduction |
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The arterial pressure wave contour differs appreciably from central to peripheral arteries mostly because of superimposition of a reflected wave from the lower body segment on the advancing central arterial wave.1 2 3 4 As the arterial system stiffens with aging, heart failure, or hypertension, the pulse wave velocity increases, and the reflected wave increases in magnitude.5 6 7 8 This combination of a larger, earlier reflection alters the central aortic pulse wave contour to produce an elevated late systolic pressure peak that adds an additional burden to the left ventricle (LV). This additional, long-standing load on the LV may be responsible in part for LV hypertrophy in hypertension,9 10 11 12 which is an independent risk factor for cardiovascular morbidity and mortality.13 14 15 16 17
Recent studies from our laboratory have shown that various classes of antihypertensive agents have different short-term effects on arterial hemodynamics.18 19 20 For example, whereas all the agents were able to decrease blood pressure (BP) into the normal range, only a nonspecific smooth muscle vasodilator (nitroprusside) and a calcium channel antagonist (nifedipine) were able to completely normalize the elevated wave reflections. ß-Adrenergic blockade (propranolol) actually exacerbated the wave reflections. These results, however, are only the manifestation of the short-term effects in the setting of cardiac catheterization. It is not known whether analogous results would be found with long-term administration. In addition, not all antihypertensive agents with equipotent BP-lowering effects are equally effective in preventing or reversing LV hypertrophy.21 22 Although nonhemodynamic factors may partly explain the diversity of effects on the LV,23 some of the diversity may be attributable to the differing hemodynamic actions of these agents.
Depending on the circumstances, the effects of wave reflection may not be appreciated by measurement of peripheral arterial BP.24 The recent demonstration that applanation tonometry on the carotid artery can be used to assess central aortic pressure wave contour and hence the effects of wave reflection2 6 25 26 27 28 now gives us a noninvasive tool that can be used for large-scale, long-term studies. Based on all the above considerations, we performed the present study to compare the effects of fosinopril,29 30 a long-acting angiotensin-converting enzyme inhibitor, and atenolol, a ß-blocker, on peripheral arterial pressure, central arterial wave reflection, and LV mass in patients with mild to moderate hypertension.
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Methods |
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Study Subjects
This was a double-blind, randomized, parallel comparison of the hemodynamic effects of fosinopril versus atenolol in matched groups of patients with mild to moderate essential hypertension. The human investigation committee of the Veterans General Hospital-Taipei approved the study. Over the previous 2 years a mass public health screening of all residents older than 30 years was conducted in Kin-Chen, the largest town on Quemoy Island. From this survey, 474 hypertensive patients (defined as sphygmomanometric BP
160/95 mm Hg)
and 500 normotensive subjects (BP <140/90 mm Hg) divided into roughly
equal numbers in five age decades (30 to 39 years, 40 to 49 years, 50
to 59 years, 60 to 69 years, and 70 years and older) were randomly
selected to participate in a cardiovascular study. Participants were
invited to the local health station for a 2-hour cardiovascular
examination that incorporated a questionnaire seeking details of
previous cardiovascular history, family history, smoking history,
alcohol consumption, and current antihypertensive drug treatment as
well as a physical examination including standard sitting mercury
sphygmomanometer BP measurement, weight, height, waist and hip
circumferences, comprehensive two-dimensional echocardiography, and
carotid tonometry. After the cardiovascular examination was completed,
an ambulatory BP recorder was applied, and the participant was
instructed to return for the removal of the recorder at the same time
the next day.
Protocol
A subgroup of patients identified in the cardiovascular study as
being hypertensive and who were currently on antihypertensive drugs or
who had an average of three sitting diastolic BP values between 95 and
100 mm Hg were eligible for this clinical trial. Those with secondary
hypertension, malignant hypertension, unstable angina, myocardial
infarction within the preceding 6 months, liver or renal function
abnormalities, or contraindications for ß-blockers or
angiotensin-converting enzyme inhibitors were excluded. After giving
informed consent, the candidates stopped previous antihypertensive
medications and received placebos for 2 weeks. Only those with an
average of the three sitting diastolic BP measurements of 95 to 110
mm Hg after 2 weeks of placebo run-in were entered into the 8-week
active treatment period. Study patients were randomly assigned to
receive 10 mg fosinopril daily or 50 mg atenolol daily. The dosage was
doubled if the average sitting diastolic BP was above 90 mm Hg after 2
weeks of active treatment. Dihydrochlorothiazide (25 mg daily) was then
added if the averaged diastolic BP was still above 90 mm Hg after 4
weeks of active treatment. The medication was continued for another 4
weeks. Ambulatory BP, carotid tonometry, and echocardiography (see
below) were performed at the first visit and after 8 weeks of active
treatment. Tonometric recordings before and after treatment were taken
at the same time of day for the same individual although it was not
possible to take measurements at a set time after drug therapy for
every patient. For the purposes of comparison, an age- and sex
distribution–matched normotensive subgroup was identified in whom the
same measurements were made at the time of the visit to the public
health clinic.
Ambulatory BP
To obtain a more representative assessment of each
patient's BP profile than that obtained during a single setting at the
clinic visits, baseline 24-hour ambulatory BP records in all subjects
as well as 24-hour records after completion of the drug treatment in
the hypertensive patients were obtained with the validated SpaceLabs
90207 recorder.31 The recorder was programmed to deflate
in steps of 8 mm Hg at 20-minute intervals during the daytime (from 7
AM to 10 PM) and at 60-minute intervals
during the nighttime (from 11 PM to 6 AM).
Generally, a total of 50 to 60 readings throughout 24 hours could be
obtained in most subjects. A cuff containing a bladder with suitable
dimensions for the arm circumference was selected. Subjects were
advised to work as usual during monitoring but to keep still the arm in
which BP was being measured. The 24-hour readings were not edited
manually, and records with less than 80% successful measurements were
excluded from analysis. Mean 24-hour systolic BP, diastolic BP, and
heart rate, as well as mean hourly BP and heart rate, were obtained
directly from the report generated by a computer software package after
data were retrieved from the recorder through an interface.
Carotid Tonometry
The arterial pressure wave contour was obtained noninvasively
from the right common carotid artery with a pencil-type probe
incorporating a high-fidelity strain-gauge transducer in a
7-mm-diameter flat tip (Millar Instruments Inc).6 25 32
According to the theory of applanation tonometry,33 when
the arterial wall is completely flattened (applanated) by the tip of
the probe, the contact pressure between the probe equals the
intra-arterial pressure. Although there is no direct guide to indicate
optimal applanation, experience has shown that the optimal condition is
approximated when the hold-down force is such that the resulting
waveform has a stable baseline and a nearly maximal
amplitude.6 25 32
The carotid arterial pressure waveform was digitized at a rate of 250 Hz on an IBM-compatible personal computer and saved for off-line analysis. The digitized signals were analyzed with custom software written in our laboratory. Two to 10 consecutive beats were signal averaged. Premature beats and beats immediately after premature beats were excluded. The algorithm displayed the signal-averaged waveform and identified the inflection point on the upstroke or downstroke of the wave by finding the first local minimum of the first derivative of the signal. This inflection is presumed to herald the onset of the reflected wave. The algorithm allowed the operator to override by inspection, if necessary, the computer-identified inflection point. Several different types of waveforms were observed (Fig 1). To specifically assess the effect of wave reflection on the central arterial systolic or pulse pressure and to consistently incorporate two other waveforms (Fig 1B and 1D), which have not been explicitly described previously, we calculated the augmentation index (AI) as follows. The most commonly observed waveforms had an inflection point on the ascending limb (Fig 1A). For this type of wave, the AI (expressed as a percent) was calculated as the ratio of the amplitude from the inflection to the systolic peak to the total pulse pressure. When there were two distinct peaks with the secondary peak higher than the primary peak (Fig 1B), the AI was calculated as the ratio of the difference of these two peaks to the pulse pressure. When the inflection point was on the descending limb and the peak of the secondary wave was less than or equal to the peak of the primary wave (Fig 1C), the AI was considered to be zero. Alternatively, for comparison we also present the results when negative AIs for this type of wave are calculated, as has been done in previous work.1 26 27 28 When two or more inflection points were identified (Fig 1D), the earliest inflection was used for the calculation of AI. To provide an indication of the wave transmission time, the time intervals from the foot of the pressure wave to the first identifiable inflection point for each waveform were measured. The interobserver variability of the carotid AI has been determined from another 62 patients with an intraclass correlation coefficient of .95 and a 95% confidence interval of .88 to .98 between two independent observers.
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t) are calculated for each type of wave. A, For an inflection
point on the ascending limb, the AI (expressed as a percent) is the
ratio of the height of the peak of the carotid wave above its shoulder
(b) to the pulse pressure (a). B, When the inflection point is on the
descending limb and the peak of the secondary wave is higher than the
peak of the primary wave, the AI is the ratio of the difference of
these two peaks to the pulse pressure. C, When the inflection point is
on the descending limb and the peak of the secondary wave is less than
or equal to the peak of the primary wave, AI was calculated in two ways
(see text). D, When more than two inflection points were suspected, the
earliest inflection was used for calculation of AI. The time interval
from the foot of the pressure wave to the first identifiable inflection
point is
Echocardiography
Comprehensive echocardiography including M-mode,
two-dimensional, pulsed Doppler, and color Doppler examinations was
performed with a Hewlett-Packard SONOS 500 echo unit incorporating a
2.5-MHz transducer by one experienced sonographer throughout the study.
The LV mass was measured on-line by application of the truncated
ellipsoid formula.34 Four loops of two-dimensional
echocardiographic images obtained from the parasternal long-axis view,
parasternal short-axis view at the papillary muscle tips, and apical
two-chamber and four-chamber views were stored on-line in a
high-capacity optic disk for analyses of interobserver and
intraobserver variabilities of the LV mass measurement 5 months after
the completion of the cardiovascular survey. The interobserver error
was determined by dividing the difference between observers by the mean
of two observations. The interobserver error calculated from 100
randomly selected cases was 19±15%, and the intraobserver error
calculated likewise from the same random sample was 18±13% for the
present study.
Statistical Analysis
All continuous variables are expressed as mean±SD. The
within-groups and between-groups comparisons of BP, AI, and LV mass
index (LVMI) were performed using paired or unpaired Student's
t tests as appropriate. Statistical significance was
considered to be at the P=.05 level although all probability
values less than .10 are listed.
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Results |
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The normotensive (N) group was composed of 79 subjects (52 men, 27 women; age, 45.8±8.5 years; height, 162±9 cm; weight, 64±9 kg). After 2 weeks of placebo treatment, 79 hypertensive patients who fulfilled the inclusion criteria were entered into the treatment phase. These 79 patients were randomly allocated into two groups: fosinopril (F) and atenolol (A) matched for gender distribution, age, height, and weight (group F: 25 men, 16 women; age, 45.1±8.9 years; height, 163±10 cm; weight, 74±12 kg; group A: 27 men, 11 women; age, 46.6±8.0 years; height, 163±9 cm; weight, 73±12 kg). For group F, the daily regimens at the end of the study were 10 mg fosinopril (2 patients, 5%), 20 mg fosinopril (10 patients, 24%), and 20 mg fosinopril with 25 mg dihydrochlorothiazide (29 patients, 71%). For group A, the daily regimens were 50 mg atenolol (3 patients, 8%), 100 mg atenolol (12 patients, 32%), and 100 mg atenolol with 25 mg dihydrochlorothiazide (23 patients, 60%). Although no subject experienced adverse effects serious enough to warrant discontinuing either drug, some side effects were manifested. Group F patients experienced dry cough (12 patients, 29%), dizziness (3 patients, 7.3%), abnormal taste (2 patients, 4.9%), palpitation (2 patients, 4.9%), and epigastric discomfort (1 patient, 2.4%). Group A patients experienced dizziness (5 patients, 13.2%), headache (2 patients, 5.3%), epigastric discomfort (2 patients, 5.3%), numbness of extremities (1 patient, 2.6%), skin rash (1 patient, 2.6%), blurred vision (1 patient, 2.6%), constipation (1 patient, 2.6%), and cough (1 patient, 2.6%).
Peripheral BP
Table 1 summarizes the results of BP measured
manually during the clinic visits. In both hypertensive groups, after
treatment the significantly elevated systolic and diastolic pressures
were significantly reduced. Table 2 summarizes the
ambulatory BP results. This more comprehensive BP assessment also
revealed that both drugs decreased BP into the normal range to a
similar extent. As expected, both the clinic and ambulatory
measurements showed that atenolol significantly decreased heart rate,
whereas fosinopril slightly increased heart rate.
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Augmentation Index
Illustrative tonometric waveforms in response to the two
drugs in hypertensive patients are shown in Figs 2 and 3, the response for each subject is shown in Fig 4, and the statistical results are summarized in Table 3. The average baseline AI (allowing for zero AI for
waveforms of the type shown in Fig 1C) was not different between the
two groups (15.7±10.9% for group F and 15.9±11% for group A), and
both values were significantly greater than in group N. On average,
after treatment the AI in group F decreased to 6.4±9.3%
(P<.001) and in group A decreased to 11.1±0.9%
(P=.002). The average posttreatment AI was significantly
lower in group F than in group A. When negative AI values were allowed,
the absolute AI values differed slightly from those listed above, but
the differences between the drug effects persisted (Table 3).
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Table 3 also summarizes the effects of the drugs on cardiac cycle length and the timing of the reflected wave. Both the time interval measured from the foot of the carotid pulse to the inflection point and the cycle length increased significantly after treatment in group A, whereas the time interval increased and cycle length decreased in group F.
LV Mass
The LVMI in groups F and A was only slightly but statistically
significantly greater than in group N (Table 3). However, there was no
significant difference before and after treatment with either
fosinopril (93±13 versus 94±17 gm/m2,
respectively) or atenolol (98±20 versus 95±19 gm/m2).
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Discussion |
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The major findings of the present study are (1) peripheral BP response to chronically administered atenolol compared with fosinopril is similar; and (2) despite this similar BP reduction, atenolol has a smaller effect than fosinopril in reducing central wave reflections as manifested in the carotid artery pressure waveform.
The different long-term hemodynamic effects of these two drugs
representing different classes of antihypertensive agents (a
ß-blocker and an angiotensin-converting enzyme inhibitor) are
consistent with but not exactly the same as the differing short-term
hemodynamic effects of the various classes of antihypertensive agents
we reported previously. Those studies indicated that the various major
classes of antihypertensive agents acutely affected arterial
hemodynamics differently, specifically wave reflection properties. A
nonspecific vasodilator (nitroprusside)18 and a calcium
channel antagonist (nifedipine)35 completely normalized
the elevated wave reflections in hypertensive patients, whereas an
angiotensin-converting enzyme inhibitor (captopril)20 only
partially normalized the reflections, and a ß-antagonist
(propranolol)18 exacerbated the reflections. Although it
is difficult to directly compare the short- and long-term studies, the
increase in wave reflections observed earlier with propranolol and the
smaller decrease observed here with atenolol compared with fosinopril
may be attributable to the lack of a direct sympathomimetic effect of
propranolol on the large arteries. Propranolol may acutely be unmasking
some degree of 
-mediated vasoconstriction, accounting for both the
increase in wave reflections and the slight increase in BP that are not
observed with atenolol.
The present findings are also in agreement with previous findings5 24 that the peripheral actions of a vasodilating antihypertensive agent may underestimate its central hemodynamic effects. Therefore, it is becoming clear that, with some knowledge of the detailed hemodynamic actions of a particular antihypertensive agent, one can more specifically target therapy toward a desired goal (eg, reducing the vascular load and hence LV hypertrophy) rather than merely attempting to control BP alone. How specific one may need to get is further exemplified by previous results comparing the effects of two types of ß-blockers, dilevalol and atenolol. Both drugs reduced pulse wave velocity and peripheral BP to the same extent, but only dilevalol reduced the carotid artery AI.5 Why that study found no change in AI with atenolol compared with the small but statistically significant reduction found in the present study is not entirely clear.
The above conclusions are based on the premise that the AI obtained from the carotid artery pressure waveform is, in fact, a measure of the effect of arterial wave reflection. Before one can definitively conclude that, however, several issues need to be considered. First, an assumption of the tonometric method is that the height of the pressure wave above the first inflection point (the portion labeled b in Fig 1) is the reflected wave. Although this may be true in most instances, the other examples in Fig 1 demonstrate the difficulty in identifying the actual reflected wave because it is superimposed on the forward-traveling wave. More importantly, extracting an absolute value of the reflected wave from the tonometer signal is fraught with uncertainty because a direct calibration of the tracing is unreliable because of varying effects of the hold-down force on the transducer. Despite this inability to directly quantify the magnitude of the wave reflections, the fact that the late systolic portion of the carotid waveform decreased during treatment with both drugs is suggestive evidence that the magnitude of wave reflections decreased in both groups. Although no large-scale studies have directly compared carotid waveforms obtained with tonometry with simultaneously recorded central pressures, several studies suggest that waveforms obtained with carotid tonometry systematically underestimate aortic augmentation.5 25 28
Second, the AI is affected by the timing and magnitude of the reflected wave as well as by the duration of ventricular ejection (which was not measured in this study but was indirectly indexed by the cardiac cycle length). Although ejection duration may be more important than cycle length in determining AI, both tend to change in the same direction. A reflected wave appearing early in ejection will produce an early inflection point in the arterial pressure waveform, resulting in a larger AI than if the same wave appeared later in ejection. The time of appearance of the reflected wave in the arterial system depends on the pulse wave velocity, which is, in turn, directly related to the BP level. In the present study since both drugs lowered pressure, the reflected wave appeared later in both groups of patients. In the atenolol group, however, this potentially beneficial effect was counterbalanced to some extent by the longer ejection duration that would cause the peak of the forward wave to also appear later and cause AI to be higher than if ejection were not affected. Therefore, the changes in magnitude of wave reflections notwithstanding, the effects of these drugs on BP, wave speed, and ejection duration would be to produce a larger decrease in AI with fosinopril than with atenolol, as was observed.
When carotid waveforms are of the type shown in Fig 1C, there is an ambiguity in how AI can be defined; therefore, we used alternative means to estimate AI. If one considers the effect of wave reflection solely on the basis of augmentation of the central peak systolic pressure, when the peak of the reflected wave falls after and below the peak forward systolic pressure wave, it no longer influences the measured peak systolic pressure, and its effect can be considered to be zero. Alternatively, if one considers wave reflections as comprising ventricular afterload (eg, systolic pressure–time product), then it is logical to consider the downstroke of the wave in the same manner as the upstroke, that is, to quantify negative AIs. Despite the obvious quantitative differences in AI values and, in particular, the underestimation of the effect of each drug if the former method is used to estimate AI (see Table 3), the conclusions regarding the different drug effects were the same.
Despite the decrease in central wave reflections and hence presumably also in the central aortic pressures in both groups, we found no change in LVMI in either group after 8 weeks of treatment. There are several possibilities for the lack of LV mass regression. First, our patients had only mild hypertension and consequently probably only a small decrease in central pressures. Second, although statistically significant, our patient groups had only a mild amount of LV hypertrophy (LVMI of 93 to 98 g/m2 compared with other studies in hypertensive patients in which LVMI values >100 g/m2 are reported21 ). This combination of very mild hypertrophy and a small decrease in pressure may not have been a sufficient stimulus for LV mass regression. Third, the 8-week duration of our treatment may have been too short to induce regression. Although this could be a factor in the response to fosinopril, it is unlikely for atenolol because a previous study using 6 months of atenolol in an elderly population with more LV hypertrophy than in our study also found no LV mass regression despite an average fall in systolic pressure of 31 mm Hg.21 That study, however, found clear evidence that a calcium channel antagonist was able to regress LV mass. Finally, there is always the possibility that, like atenolol, fosinopril is not effective in regressing LV mass. If future studies support this contention, this would be additional evidence that not all antihypertensive agents are equally effective in producing LV mass regression.
In summary, this double-blind, randomized study of atenolol and fosinopril in mild hypertensive patients demonstrates that, at the doses used, atenolol decreases peripheral BP as effectively as fosinopril but decreases carotid AI less than fosinopril. This implies a greater effect on central aortic BP reduction with fosinopril than with atenolol than is apparent from measurements of peripheral BP. LVMI does not change with either drug. Although the AI cannot definitively address the specifics of how wave reflections are altered by a particular antihypertensive agent, the results are strongly suggestive that this is the case. In addition, the results of this long-term study, which encompasses a wider age range than previously examined, generally confirm results from our earlier short-term studies18 19 20 indicating that various classes of antihypertensive drugs affect arterial wave reflections differently.
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Acknowledgments |
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This work was supported in part by contracts NSC 81-0412-B-010-534-Y and NSC 82-0412-B-010-117-Y from the National Science Council, Taiwan, ROC; contract NO1-AG-1-2118 from the National Institutes of Aging, National Institutes of Health, Bethesda, Md; and a grant from the Tzong-Jen Foundation.
Received May 2, 1994; first decision June 15, 1994; accepted January 13, 1995.
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