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1 Heart Institute, School of Medicine, University of São Paulo, São Paulo 05403-000, Brazil; and 2 Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Arterial compliance is
determined by structural factors, such as collagen and elastin, and
functional factors, such as vasoactive neurohormones. To determine
whether angiotensin II contributes to decreased arterial compliance in
patients with heart failure, this study tested the hypothesis that
administration of an angiotensin-converting enzyme inhibitor improves
arterial compliance. Arterial compliance and stiffness were determined
by measuring carotid artery diameter, using high-resolution duplex
ultrasonography, and blood pressure in 23 patients with heart failure
secondary to idiopathic dilated cardiomyopathy. Measurements were made
before and after intravenous administration of enalaprilat (1 mg) or
vehicle. Arterial compliance was inversely related to both baseline
plasma angiotensin II (r = 
0.52; P = 0.015) and angiotensin-converting enzyme concentrations (r = 0.45; P = 0.041). During
isobaric conditions, enalaprilat increased carotid artery compliance
from 3.0 ± 0.4 to 5.0 ± 0.4 × 10
10
N1 · m4 (P = 0.001)
and decreased the carotid artery stiffness index from 17.5 ± 1.8 to 10.1 ± 0.6 units (P = 0.001), whereas the
vehicle had no effect. Thus angiotensin II is associated with reduced carotid arterial compliance in patients with congestive heart failure,
and angiotensin-converting enzyme inhibition improves arterial elastic
properties. This favorable effect on the pulsatile component of
afterload may contribute to the improvement in left ventricular
performance that occurs in patients with heart failure treated with
angiotensin-converting enzyme inhibitors.
carotid arteries; angiotensin-converting enzyme inhibitors
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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THE ELASTIC BEHAVIOR of conduit arteries contributes importantly to left ventricular function and aortic flow (17, 21, 25, 39, 41, 43). Increased pulse pressure, an index of the pulsatile hemodynamic load, is a risk factor for the development of congestive heart failure (CHF) (11, 12). The increased pulsatile load that results from a decrease in arterial compliance reduces left ventricular stroke volume more so when the contractile state is depressed than in the normally functioning ventricle (31). Therefore, impaired arterial elasticity is particularly deleterious in patients with congestive heart failure.
Elasticity of conduit arteries is determined by both structural and functional factors. Both sets of factors are governed by the tunica media, which constitutes a large part of the arterial wall and is the principal determinant of the vessel's mechanical properties (45). Structural factors that passively alter arterial elastic properties include degeneration of elastic fibers, increased collagen content, and calcium deposition. Functional factors actively reduce distensibility of arteries by constricting vascular smooth muscle. These factors, which include vasoconstrictive substances related to increased activity of sympathetic nervous and renin-angiotensin systems, may be particularly relevant to abnormal elasticity in patients with heart failure. Arterial compliance in vitro is reduced by norepinephrine and angiotensin II (6, 14). In addition, exogenous administration of norepinephrine and angiotensin II reduces arterial compliance when administered to animals and normal subjects in vivo (8, 13, 29). Endothelium-derived nitric oxide may also contribute to the regulation of arterial smooth muscle tone of the large arteries and influence the mechanical properties of conductance vessels (23, 30).
We and others (1, 10, 18, 21, 28, 33) have demonstrated previously that arterial compliance is reduced in patients with heart failure. Because angiotensin II is frequently elevated in these patients, we reasoned that it may contribute to decreased arterial distensibility. We utilized a technique that uses high-resolution ultrasonography to directly visualize the common carotid artery and determine its elastic properties by relating changes in arterial diameter to changes in pressure generated with each heartbeat. Our aim was to test the hypothesis that acute administration of an angiotensin-converting enzyme inhibitor would improve arterial compliance in patients with CHF.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Subjects.
The subject population included 23 patients with CHF secondary to
idiopathic dilated cardiomyopathy. Primary valvular heart disease and
systemic arterial hypertension were excluded by history and physical
examination. Coronary artery disease was excluded by coronary
angiography, which was performed in all patients. All participants were
in sinus rhythm and clinically stable for 
3 wk before the study.
Fourteen patients were in New York Heart Association class II, 6 were
in class III, and 3 were in class IV. Medical treatment included
digoxin in 21 patients, diuretics in 22, angiotensin-converting enzyme
(ACE) inhibitors in 21, and other vasodilators in 4 patients. ACE
inhibitors and vasodilators were withheld 72 h before the
investigation. The protocol was approved by the Committee for the
Protection of Humans from Research Risk at the Heart Institute of the
University of São Paulo, and each subject gave written informed consent.
Experimental protocol.
All studies were performed in a temperature-controlled (22-24°C)
cardiovascular research laboratory. An indwelling venous catheter was
placed in an arm vein of each patient for blood collection and drug
administration. All subjects rested in the supine position for 20 min
before acquisition of hemodynamic measurements and drug infusion.
Carotid artery image acquisition. An ultrasound scanner (Ultramark-8, ATL, Bothell, WA) equipped with a high-resolution transducer (7.5 MHz) was used to image the carotid artery. A longitudinal image of the cephalic portion of the common carotid artery, 1 cm below the bifurcation, was acquired with the transducer positioned at 90° to the vessel so that the near- and far-wall interface were clearly discernible. These images, as well as an electrocardiographic signal, were recorded on a super VHS videotape recorder. Videotape images were selected at time points that corresponded with systolic expansion of the carotid artery (within 60 ms of the electrocardiographic T wave) and with diastolic relaxation (concurrent with the onset of the electrocardiographic R wave). These images were digitized with a video-frame grabber (Willow Publishers VGA, Willow Peripherals; Bronx, NY) and stored on a microcomputer.
Image analysis was performed with the aid of a dedicated image workstation to determine carotid artery diameter. The operator identified and traced the posterior wall boundary (far wall), corresponding to the interface between the lumen and intima, and the anterior wall boundary (near wall), corresponding to the interface of the adventitia and media. An automated algorithm then determined the average distance between corresponding points along both arterial walls. Carotid artery diameter was then calculated in millimeters using a calibration factor derived from the real-time ultrasound image. An average of three measurements of carotid artery diameter was obtained in each patient. The repeatability of carotid artery diameter in systole and diastole is r = 0.95, P = 0.0001, and r = 0.96, P = 0.0001, respectively. The interobserver and intraobserver variability of the method is 1.5 ± 1.0% and 1.0 ± 0.8%, respectively (27).Arterial elastic properties determination.
Blood pressure was determined during carotid artery image acquisition
by upper arm sphygmomanometry using an automated oscillometric method
(Dinamap 1466, Critikon; Tampa, FL). The two measurements of carotid
artery elastic properties described in this report include compliance
(C) and stiffness index (
). Arterial compliance was calculated using
the following equation (42)
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, a measurement of rigidity of the vessel, was calculated
according to the equation (22)
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Carotid artery blood flow.
Carotid artery blood flow velocity curves were obtained using the
pulsed Doppler system (Ultramark-8, ATL) equipped with a 7.5-MHz
transducer. The carotid artery blood flow velocity image acquisition
uses the same computer system as described above for the carotid artery
image acquisition, and the blood flow velocity curve analysis was
performed with the aid of the same dedicated image workstation. The
operator identified the contour of the curve, and an automated
algorithm was used to calculate carotid artery blood flow velocity
(m/s). The repeatability of carotid artery blood flow velocity is
r = 0.90, P = 0.001, and the
variability of this method is 0.2 ± 2.7%. An average of five
measurements of carotid artery blood flow velocity was obtained in each
patient. Carotid artery blood flow was calculated as the product of
carotid artery blood flow velocity and carotid artery cross-sectional area (during systole) according to the equation
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Carotid and brachial arteries tonometry. To ascertain that carotid and brachial artery blood pressure were comparable, carotid and brachial artery pressure waves were recorded noninvasively in five patients using a micromanometer-tipped probe (model SPR-428, Millar Instruments; Houston, TX) by the technique of applanation tonometry (26). This technique yields an analog output, which is digitized and recorded on a personal computer. Pulse recordings were performed consecutively from the right common carotid and right brachial arteries. Sphygmomanometric measurements of right brachial artery systolic and diastolic pressures were made with an oscillometric recorder (Dinamap 1466, Critikon). The brachial artery pressure wave was assigned peak and minimal amplitudes determined by the sphygmomanometric measurement of systolic and diastolic pressures. Carotid artery pressure was then calibrated by equating the carotid mean and end-diastolic pressures to the brachial artery measurements (26).
Five patients (age, 47 ± 4 y) with dilated cardiomyopathy and heart failure class III or IV were analyzed. The protocol was the same as the one employed in the primary study. Carotid and brachial artery pressure waves were recorded at baseline and at 1, 2, and 3 h after the infusion of vehicle or 1 mg of enalaprilat intravenously on two separate occasions.Neurohormonal assays.
Venous blood samples were collected in 22 patients from the indwelling
catheter for determination of plasma angiotensin II, plasma ACE, and
plasma norepinephrine levels. Samples were immediately placed on ice
and centrifuged at 2°C. Plasma samples were stored at 70°C before
assay. Plasma concentration of norepinephrine was quantified by
high-performance liquid chromatography (6). Plasma
angiotensin II was quantified by a radioimmunoassay method (5) and plasma ACE by a fluorometric assay
(37).
Statistical analysis. All values are presented as means ± SE. The proportionality of sex distribution in each group was compared by the Fisher exact test. Between-group comparison of age, left ventricle ejection fraction, plasma norepinephrine, plasma angiotensin II and plasma ACE concentration, basal arterial compliance, arterial stiffness, mean blood pressure, carotid artery blood flow velocity, carotid artery blood flow, and carotid artery cross-sectional area employed a t-test for unpaired data. The effect of enalaprilat and saline within and between each group on arterial compliance, arterial stiffness, carotid artery blood flow velocity, carotid artery blood flow, mean blood pressure, and carotid artery cross-sectional area was analyzed by analyses of variance for repeated measures and F-Wilks post hoc testing for statistical significance. Brachial artery pressure and tonometry-estimated carotid artery pressure were compared by using a Wilcoxon test. Univariate linear regression analysis was used to determine the relation between selected continuous variables, including arterial compliance, mean blood pressure, plasma angiotensin II, plasma ACE concentrations, and diameter repeatability. Independence of association was assessed by stepwise multiple regression. Statistical significance was accepted at the 95th percentile (P < 0.05).
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Clinical characteristics and baseline compliance and neurohormonal
measurements of each group of subjects are shown in Table 1. There were no significant differences
between the two groups for any of these baseline measurements.
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Effects of vehicle.
The hemodynamic and arterial elastic properties at baseline and 1, 2, and 3 h after vehicle are presented in Table
2. There were no statistical changes in
any of the variables after saline (vehicle) administration (Fig.
1).
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Effects of enalaprilat.
The hemodynamic and arterial elastic measurements at baseline and 1, 2, and 3 h after drug administration are presented in Table
3. The changes in compliance
(P < 0.01), stiffness index (P < 0.01), and blood pressure (P < 0.01) were
significantly greater following enalaprilat administration compared
with vehicle. Enalaprilat increased carotid artery compliance from
3.0 ± 0.4 at baseline to a maximum of 5.0 ± 0.4 × 1010 N1 · m4 and
decreased arterial stiffness from 17.5 ± 1.8 to a nadir of 10.1 ± 0.6 three hours after drug administration (each
P < 0.01) (Fig. 1). Enalaprilat significantly reduced
mean blood pressure from 85 ± 3 to 78 ± 3 mmHg at the 1-h
time point (P < 0.01). Blood pressure returned to
baseline values by 3 h after drug administration. Thus changes in
compliance and stiffness at 3 h are under isobaric conditions.
After adjustment of both the compliance and stiffness index for mean
blood pressure, the changes in each variable remain statistically
significant.
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Carotid and brachial arteries tonometry.
There was no significant difference in systolic or diastolic blood
pressure between the carotid and brachial arteries whether measured at
baseline or after drug or vehicle administration (Table 4). The relationship between the carotid
and brachial artery systolic blood pressure (SBP) was defined as
SBPcarotid = 0.82 × SBPbrachial + 21.17 (r = 0.74, standard error of estimate = 6.81), and that between carotid and brachial diastolic blood pressure (DBP) was defined as DBPcarotid = 0.84 × DBPbrachial + 13.63 (r = 0.87, standard error of estimate = 4.30).
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Neurohormonal measurements.
Plasma angiotensin II was 11.7 ± 0.8 pg/ml at baseline and
decreased to 6.6 ± 0.5 pg/ml 3 h after enalaprilat
administration (P < 0.01). Plasma ACE was
53.9 ± 5.8 nmol · min1 · ml1 at
baseline and decreased to 21.5 ± 5.8 nmol · min1 · ml1 after
enalaprilat (P < 0.01). There were no statistical
changes in plasma angiotensin II and plasma ACE after vehicle.
0.52; P = 0.015 and
r = 0.45; P = 0.041, respectively).
Mean blood pressure was not related to plasma angiotensin II
(r = 0.26; P = 0.26) or plasma ACE
concentrations (r = 0.26; P = 0.27).
A stepwise multiple regression analysis, where plasma angiotensin II,
plasma ACE, and mean blood pressure were included in the model, found
that only plasma angiotensin II correlated with carotid arterial
compliance (P = 0.043).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The new findings from this study are that plasma angiotensin II is associated with decreased carotid artery compliance and increased carotid arterial stiffness in patients with CHF and that ACE inhibition improves these arterial elastic properties. These results implicate angiotensin II as an important functional determinant of arterial elasticity in patients with heart failure.
Determinants of arterial compliance. Previous studies have demonstrated an impairment of arterial elastic properties in CHF (1, 10, 18, 21, 28, 33). Using methodology identical to that employed in this study, we found previously that arterial compliance is reduced 56% in patients with CHF compared with normal subjects (28). The mechanism, however, responsible for modifications of the arterial elastic properties in CHF is not entirely known, and several factors may be involved. Structural factors associated with an increase in the sodium and water content of the arterial wall and a decrease in elastin:collagen ratio may participate. We previously determined that carotid artery wall thickness averaged 19.5% more in patients with CHF secondary to idiopathic dilated cardiomyopathy (28) than in healthy age-matched subjects. Yet, even though carotid artery wall thickness was greater in patients with CHF, it does not appear to contribute to distensibility (28).
Functional factors that modify arterial smooth muscle tone may be particularly important in patients with CHF once there is an increase in neurohormonal activity in these patients. Indeed, mechanical properties of large arteries can be modified by neurohormonal mechanisms, particularly the sympathetic nervous system and renin-angiotensin system (20, 34). Dobrin and Rovick (14) and Barra et al. (4) showed that norepinephrine decreased arterial incremental elastic modulus under isobaric conditions. In addition, both norepinephrine and angiotensin II have been shown to reduce arterial compliance in vitro (16). Wilson et al. (44) demonstrated that arterial compliance of conductance arteries in pigs can decrease in response to acute infusion of norepinephrine in vivo. Further support for an active or functional component of arterial compliance comes from Bank et al. (3), who, using intravascular ultrasound in normal human subjects, demonstrated that administration of nitroglycerin and norepinephrine significantly shifted the brachial artery stress-strain curve in opposite directions. Boutouyrie et al. (7) showed that sympathetic activation induced by cold pressor test or mental stress test reduced arterial compliance in healthy humans; however, Joannides et al. (24) showed an opposite result. Previously, Creager's laboratory (28) found a significant positive relationship between plasma norepinephrine concentration and Young's modulus of elasticity in patients with CHF.Effect of ACE inhibition. Activation of renin-angiotensin-aldosterone system is intrinsic to the pathophysiology of CHF (15, 19, 40). To assess the role of angiotensin II in modulating arterial elasticity, we measured the effects of ACE inhibition on carotid artery compliance in patients with CHF secondary to dilated cardiomyopathy. We observed a substantial increase in arterial compliance (59.5%) and decrease in arterial stiffness (57.8%) after administration of enalaprilat. These changes of arterial elastic properties were independent of blood pressure, which had returned to baseline levels 3 h after drug administration, at which time the effect of enalaprilat on compliance was maximal. Moreover, arterial compliance correlated inversely with pretreatment plasma angiotensin II and plasma ACE levels. Giannattasio et al. (21) found similarly that radial artery compliance improved in patients with CHF after 4-8 wk of treatment with benazepril. Important features that distinguish the two studies include the acuity of treatment, the techniques used to assess arterial compliance and stiffness, and the administration of vehicle as a control for time and conditions in our experimental procedures.
Inhibition of ACE has been shown to enhance peripheral endothelium-dependent vasodilation in patients with mild heart failure (32). Because flow stimulates release of endothelium-derived nitric oxide and vasodilation (35), we considered the possibility that enalaprilat-induced increase in carotid artery blood flow would provoke endothelium-dependent relaxation and alter compliance. However, we did not observe changes in arterial cross-sectional area or carotid blood flow. Thus flow-mediated factors cannot satisfactorily explain the improvement of arterial elastic properties after ACE inhibition. Our findings are comparable to those observed in hypertensive patients in whom the compliance and diameter of large (brachial and carotid) arteries are increased by ACE inhibition, even at doses that do not produce a systemic hypotensive response (2, 36, 38). Therefore, the local effect of angiotensin II in conduit vessels is a potential mechanism to explain the arterial elastic properties in CHF. This can be modified by ACE inhibition.Study limitations. The formulas used to calculate arterial compliance and stiffness assume that there is a constant linear, rather than curvilinear, relation between changes in arterial diameter and pressure. This limitation should be acceptable in clinical studies, because the changes in arterial diameter and blood pressure are usually <25% and occur over the linear portion of the curve (9). Also, the arterial elastic properties were calculated by measuring carotid artery diameter and brachial artery pressure. In a subset of five patients, we measured both carotid artery and brachial artery pressure and found them to be comparable, lending credibility to using brachial artery pressure in the calculations. Also, we did not assess the effect of ACE inhibition on arterial compliance in healthy subjects and therefore do not discount the possibility that angiotensin contributes to arterial compliance under normal physiological conditions.
In conclusion, the findings in this study enable us to conclude that angiotensin II adversely affects compliance of conduit vessels in patients with CHF. Moreover, ACE inhibition improves arterial elastic properties. This favorable effect on the pulsatile component to the afterload may contribute to the improvement in left ventricular performance that occurs in patients with heart failure treated with ACE inhibitors.| |
ACKNOWLEDGEMENTS |
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This study was supported in part by Grant Fundação de Amparo a Pesquisa do Estado de São Paolo 2445-1 and CNPq 403570-91-3, S. G. Lage is a recipient of a Fulbright Fellowship 13378.
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FOOTNOTES |
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Address for reprint requests and other correspondence: S. G. Lage, Heart Institute, School of Medicine, Univ. of São Paulo, Av. Dr. Enéas de Carvalho Aguiar 44, São Paulo 05403-000, Brazil (E-mail: sglage{at}incor.usp.br).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
May 23, 2002;10.1152/ajpheart.00820.2001
Received 18 September 2001; accepted in final form 20 May 2002.
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REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Arnold, JMO,
Marchiori GE,
Imrie JR,
Burton GL,
Plugfelder PW,
and
Kostuk WJ.
Larger artery function in patients with chronic heart failure. Studies of brachial artery diameter and hemodynamics.
Circulation
84:
2418-2425,
1991
2.
Asmar, RG,
Pannier B,
Santoni J,
Laurent S,
London GM,
Levy BI,
and
Safar ME.
Reversion of cardiac hypertrophy and reduced arterial compliance after converting enzyme inhibition in essential hypertension.
Circulation
78:
941-950,
1988
3.
Bank, AJ,
Wilson RF,
Kubo SH,
Holte JE,
Dresing TJ,
and
Wang H.
Direct effects of smooth muscle relaxation and contraction on in vivo human brachial artery elastic properties.
Circ Res
77:
1008-1016,
1995
4.
Barra, JG,
Armentano RL,
Levenson J,
Fischer EIC,
Pichel RH,
and
Simon A.
Assessment of smooth muscle contribution to descending thoracic aortic elastic mechanics in conscious dogs.
Circ Res
73:
1040-1050,
1993
5.
Barret, JD,
Eggena P,
and
Sambhi MP.
Extraction and measurement of circulating angiotensin II in blood by radioimmunoassay.
Clin Chem
23:
464-468,
1977
6.
Bouloux, P,
Perrett D,
and
Bresser GM.
Methodological considerations in the determination of plasma cathecholamines by high-performance liquid chromatography with electrochemical detection.
Ann Clin Biochem
22:
194-203,
1985.
7.
Boutouyrie, P,
Lacolley P,
Girerd X,
Beck L,
Safar M,
and
Laurent S.
Sympathetic activation decreases medium-sized arterial compliance in humans.
Am J Physiol Heart Circ Physiol
267:
H1368-H1376,
1994
8.
Cabrera, E,
Levenson J,
Armentano R,
Barra J,
Pichel R,
and
Simon AC.
Aortic pulsatile pressure and diameter response to intravenous perfusions of angiotensin, norepinephrine, and epinephrine in conscious dogs.
J Cardiovasc Pharmacol
12:
643-649,
1988[Web of Science][Medline].
9.
Caro, CG,
Pedley TJ,
Schroder RC,
and
Seed WA.
The Mechanics of the Circulation. Oxford: Oxford University Press, 1978, p. 86-105.
10.
Carrol, JD,
Shroff S,
Wirth P,
Halstead M,
and
Rajfer SI.
Arterial mechanical properties in dilated cardiomyopathy: aging and the response to nitroprusside.
J Clin Invest
87:
1002-1009,
1991[Web of Science][Medline].
11.
Chae, CU,
Pfeffer MA,
Glynn RJ,
Mitchell GF,
Taylor JO,
and
Hennekens CH.
Increased pulse pressure and risk of heart failure in the elderly.
JAMA
281:
634-639,
1999
12.
Chen, YT,
Vaccarino V,
Williams CS,
Butler J,
Berkman LF,
and
Krumholz HM.
Risk factors for heart failure in the elderly: a prospective community-based study.
Am J Med
106:
605-612,
1999[Web of Science][Medline].
13.
Cox, RH.
Pressure dependence of the mechanical properties of arteries in vivo.
Am J Physiol
229:
1371-1375,
1975
14.
Dobrin, PB,
and
Rovick AA.
Influence of vascular smooth muscle on contractile mechanics and elasticity of arteries.
Am J Physiol
217:
1644-1651,
1969
15.
Dzau, VJ,
Colucci WS,
Hollenberg NK,
and
Williams GH.
Relation of the renin-angiotensin-aldosterone system to clinical state in congestive heart failure.
Circulation
63:
645-651,
1981
16.
Dzau, VJ,
and
Safar ME.
Large conduit arteries in hypertension: role of the vascular renin-angiotensin system.
Circulation
77:
947-954,
1988
17.
Elzinga, G,
and
Westerhof N.
Pressure and flow generated by the left ventricle against different impedance.
Circ Res
32:
178-186,
1973
18.
Finkelstein, SM,
Cohn JN,
Ross Collins V,
Carlyle PF,
and
Shelley WJ.
Vascular hemodynamic impedance in congestive heart failure.
Am J Cardiol
55:
423-427,
1985[Web of Science][Medline].
19.
Gavras, H,
Flessas A,
Ryan TJ,
Brunner HR,
Faxon DP,
and
Gavras I.
Angiotensin II inhibition: treatment of congestive heart failure in a high-renin hypertension.
JAMA
238:
880-882,
1977
20.
Gerova, M,
and
Gero J.
Range of the sympathetic control of the dog femoral artery.
Circ Res
24:
349-359,
1969
21.
Giannattasio, C,
Failla M,
Stella ML,
Mangoni AA,
Turrini D,
Carugo S,
Pozzi M,
Grassi G,
and
Mancia G.
Angiotensin-converting enzyme inhibition and radial artery compliance in patients with congestive heart failure.
Hypertension
26:
491-496,
1995
22.
Hirai-Tadakazu, H,
Sasayama S,
Kawasaki T,
and
Yagi S.
Stiffness of systemic arteries in patients with myocardial infarction. A noninvasive method to predict severity of coronary atherosclerosis.
Circulation
80:
78-86,
1989
23.
Joannides, R,
Richard V,
Haefeli WE,
Benoist A,
Linder L,
Lüscher TF,
and
Thuillez C.
Role of nitric oxide in the regulation of the mechanical properties of peripheral conduit arteries in humans.
Hypertension
30:
1465-1470,
1997
24.
Joannides, R,
Richard V,
Moore N,
Godin M,
and
Thuillez C.
Influence of sympathetic tone on mechanical properties of muscular arteries in humans.
Am J Physiol Heart Circ Physiol
268:
H794-H801,
1995
25.
Kass, DA,
Shapiro EP,
Kawaguchi M,
Capriotti AR,
Scuteri A,
deGroof RC,
and
Lakatta EG.
Improved arterial compliance by a novel advanced glycation end-product crosslink breaker.
Circulation
104:
1464-1470,
2001
26.
Kelly, R,
and
Fitchett D.
Noninvasive determination of aortic input impedance and external left ventricular power output: a validation and repeatability study of a new technique.
J Am Coll Cardiol
20:
952-963,
1992[Abstract].
27.
Lage Polak, JF SG,
O'Leary DH,
and
Creager MA.
Relationship of arterial compliance to baroreflex function in hypertensive patients.
Am J Physiol Heart Circ Physiol
265:
H232-H237,
1993
28.
Lage, SG,
Kopel L,
Monachini MC,
Medeiros CJ,
Pileggi F,
Polak JF,
and
Creager MA.
Carotid arterial compliance in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy.
Am J Cardiol
74:
691-695,
1994[Web of Science][Medline].
29.
Levenson, JA,
Safar ME,
Simon AC,
Kheder AI,
Daou JN,
and
Levi BI.
Systemic arterial compliance and diastolic runoff in essential hypertension.
Angiology
32:
402-413,
1981
30.
Levy, BI,
Benessiano J,
Poitevin P,
and
Safar ME.
Endothelium-dependent mechanical properties of the carotid artery in WKY and SHR. Role of angiotensin converting enzyme inhibition.
Circ Res
66:
321-328,
1990
31.
Maruyama, Y,
Nishioka O,
Nozaki E,
Kinoshita H,
Kyono H,
Koiwa Y,
and
Takishima T.
Effects of arterial distensibility on left ventricular ejection in the depressed contractile state.
Cardiovasc Res
27:
182-187,
1993
32.
Nakamura, M,
Funakoshi T,
Arakawa N,
Yoshida H,
Makita S,
and
Hiramori K.
Effect of angiotensin-converting inhibitors on endothelium-dependent peripheral vasodilation in patients with chronic heart failure.
J Am Coll Cardiol
24:
1321-1327,
1994[Abstract].
33.
Pepine, CJ,
Nicholas WW,
and
Conti CR.
Aortic input impedance in heart failure.
Circulation
58:
460-465,
1978
34.
Pieper, HP,
and
Paul LT.
Responses of aortic smooth muscle studied in intact dog.
Am J Physiol
217:
154-160,
1969
35.
Rubanyi, GM,
Romero JC,
and
Vanhoutte PM.
Flow-induced release of endothelium-derived relaxing factor.
Am J Physiol Heart Circ Physiol
250:
H1145-H1149,
1986
36.
Safar, ME,
Van Bortel LMAB,
and
Struijker-Boudier HAJ
Resistance and conduit arteries following converting enzyme inhibition in hypertension.
J Vasc Res
34:
67-81,
1997[Web of Science][Medline].
37.
Santos, RAS,
Krieger EM,
and
Grune LJ.
An improved fluorometric assay of rat serum and plasma converting enzyme.
Hypertension
7:
244-252,
1985
38.
Schartl, M,
Bocksch WG,
Dreysse S,
Beckman S,
Franke O,
and
Hünten U.
Remodeling of myocardium and arteries by chronic angiotensin converting enzyme inhibition in hypertensive patients.
J Hypertens
4:
537-542,
1994.
39.
Sunagawa, K,
Maugham WL,
and
Sagawa K.
Stroke volume effect of changing arterial input impedance over selected frequency ranges.
Am J Physiol Heart Circ Physiol
248:
H477-H484,
1985
40.
Swedberg, K,
Eneroth P,
Kjekshus J,
and
Wilhelmsen L.
Hormones regulating cardiovascular function in patients with severe congestive heart failure and their relation to mortality.
Circulation
82:
1730-1736,
1990
41.
Urschel, CW,
Covell JW,
Sonnenblick EH,
Ross J,
and
Braunwald E.
Effects of decreased aortic compliance on performance of the left ventricle.
Am J Physiol
214:
298-304,
1968
42.
Van Merode, T,
Hick PJJ,
Hoeks APG,
Rahn KH,
and
Reneman RS.
Carotid artery wall properties in normotensive, and borderline hypertensive subjects of various ages.
Ultrasound Med Biol
14:
563-569,
1988[Web of Science][Medline].
43.
Weber, KT,
Janicki JS,
Hunter WC,
Shroff S,
Pearlman ES,
and
Fishman AP.
The contractile behavior of the heart and its functional coupling to the circulation.
Prog Cardiovasc Dis
24:
375-400,
1982[Web of Science][Medline].
44.
Wilson, RA,
Di Mario C,
Krams R,
Soei LK,
Wenguang L,
Laird AC,
The SHK,
Gussenhoven E,
Verdouw P,
and
Roelandt JRTC
In vivo measurement of regional large artery compliance by intravascular ultrasound under pentobarbital anesthesia.
Angiology
46:
481-488,
1995[Web of Science][Medline].
45.
Wolinsky, H,
and
Glagov S.
Structural basis for the static mechanical properties of the aortic media.
Circ Res
14:
400-413,
1964
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P < 0.01 for enalaprilat versus vehicle as
determined by post hoc testing.