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(Hypertension. 1995;26:491-496.)
© 1995 American Heart Association, Inc.

Articles

Angiotensin-Converting Enzyme Inhibition and Radial Artery Compliance in Patients With Congestive Heart Failure

Cristina Giannattasio; Monica Failla; Maria L. Stella; Arduino A. Mangoni; Davide Turrini; Stefano Carugo; Massimo Pozzi; Guido Grassi; Giuseppe Mancia

From Cattedra di Medicina Interna, Università di Milano and Ospedale S. Gerardo di Monza; Centro Auxologico Italiano, Milano; and Centro di Fisiologia Clinica e Ipertensione, Ospedale Maggiore, Milano, Italy.

	Abstract

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Abstract Congestive heart failure is characterized by a clear-cut impairment of arterial compliance of medium-sized arteries, but whether this alteration is irreversible or can be favorably affected by cardiovascular drugs currently used in congestive heart failure treatment is unknown. We studied 9 congestive heart failure patients (New York Heart Association class II; age, [mean±SEM] 60.7±3.3 years) receiving diuretic and digitalis treatment in whom arterial compliance was assessed at the level of the radial artery by an echotracking device capable of measuring the arterial diameter along the entire cardiac cycle. Beat-to-beat arterial blood pressure was concomitantly measured by a Finapres device that allowed diameter-pressure curves and compliance-pressure curves (Langewouters' formula) to be calculated for the entire systolic-diastolic blood pressure range. Arterial compliance was expressed as the area under the compliance-pressure curve normalized for pulse pressure (compliance index). Data were collected before and after 4 and 8 weeks of oral administration of benazepril (10 mg/day). Ten healthy subjects were studied before and after an observational period of 4 weeks (5 subjects) or 8 weeks (5 subjects), and 9 age-matched mildly essential hypertensive subjects studied before and after 4 to 12 weeks of benazepril administration served as control subjects. In congestive heart failure patients, baseline compliance index was significantly less than in normotensive and hypertensive subjects. However, the compliance index showed a marked increase after 4 weeks of benazepril administration (+95.7±24.9%, P<.05); the increase was also marked after 8 weeks of angiotensin-converting enzyme inhibitor treatment (+77.7±4.2%, P<.05). At this time the compliance values of the congestive heart failure patients were not different from those of the healthy and hypertensive groups, in which the observational period and angiotensin-converting enzyme inhibitor administration, respectively, had brought no change in compliance. Similar results were observed when compliance index was calculated for the blood pressure range shared by the three groups (isobaric compliance). These data provide the first evidence that the impairment of arterial compliance occurring in congestive heart failure can be favorably affected by the addition of an angiotensin-converting enzyme inhibitor to the treatment regimen. This has favorable implications for the cardiovascular functions adversely affected by a reduced arterial compliance (eg, cardiac work and oxygen consumption, coronary perfusion, and arterial baroreflex).

Key Words: arteries • heart failure, congestive • circulation • angiotensin-converting enzyme inhibitors

	Introduction

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Arterial compliance is markedly reduced in severe congestive heart failure (CHF), and a less pronounced but clear-cut compliance abnormality occurs also in mild CHF.^{1 2} This has important pathophysiological implications because a reduction in arterial compliance leads to an increase in arterial impedance and cardiac afterload^{3 4} as well as to a reduction in diastolic pressure and coronary blood flow. It may also cause an impaired responsiveness of stretch sensors, such as the arterial baroreceptors, to pressure stimuli, thereby participating in the baroreflex impairment and prognostically adverse sympathetic activation that occurs in CHF.^{5 6 7 8 9 10 11 12 13 14 15 16}

No information is available as to whether drugs used in the treatment of CHF increase arterial compliance, thereby improving the balance between cardiac demand and perfusion and restoring reflex sympathetic inhibition. In the present study we examined the effects of angiotensin-converting enzyme (ACE) inhibition on radial artery compliance in patients with CHF. Radial artery compliance was measured by a method that allowed its continuous estimate over the existing systolic-diastolic blood pressure range. Measurements were performed before and after 4 and 8 weeks of benazepril administration.

	Methods

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Subjects
We investigated 28 outpatients of either sex (21 men, 7 women). Ten patients (52.4±1.2 years [mean±SEM]) had no clinical or laboratory evidence of cardiovascular disease and thus served as normotensive control subjects. Nine patients (62.7±0.7 years) had untreated mild or moderate essential hypertension; ie, their diastolic pressure (fifth Korotkoff sound by sphygmomanometry) was between 91 and 104 mm Hg at repeated visits in the outpatient clinic, and there was no history or clinical evidence of cardiovascular events or major target-organ damage. Patients with mild arterial hypertension were selected because of the evidence that radial artery compliance is not reduced in the baseline condition.^{17 18} The remaining 9 patients (60.7±3.3 years) had class II CHF (New York Heart Association) caused by primary cardiomyopathy (n=5) or coronary heart disease (n=4). The CHF patients were included in the study if they had (1) no history of a myocardial infarction in the previous 6 months, (2) no clinical or laboratory evidence of major atherosclerotic lesions of the aorta and carotid and femoral arteries, (3) no prior hypertension or diabetes mellitus, and (4) no atrial fibrillation or other major arrhythmias. All CHF patients were under long-term treatment with oral furosemide (25 to 50 mg daily) and digoxin (0.125 to 0.250 mg daily), which were continued throughout the study. Informed consent was obtained from each subject, and the study protocol was approved by the review ethic committees of the institutions involved.

Measurements
Arterial compliance was measured in the left radial artery by a new echotracking device (NIUS 02, Asulab and Capital Medical Services).¹⁹ The device consisted of a 10-MHz focalized transducer that was stereotaxically positioned over the radial artery 2 to 3 cm above the wrist, direct contact with the skin (and arterial deformation) being prevented by the use of a gel medium. With the subject supine and the arm immobile at the heart level, the transducer was switched to the Doppler mode and oriented perpendicularly to the longitudinal axis of the artery, thus focusing its largest cross section. After the device was switched to A mode, the backscattered echoes from the inner anterior and posterior walls were visualized on an oscilloscope, and the related electric signals were picked up by an electronic tracer whose displacement allows one to evaluate the vessel diameter several thousand times per second. Continuous assessment of radial artery diameter was coupled with continuous recording of blood pressure by a photoplethysmographic device (Finapres 2300, Ohmeda, BOC Group Inc) positioned on the middle finger of the ipsilateral hand and capable of providing blood pressure values similar to the ones taken invasively from the radial artery.^{20 21} Arterial diameter and blood pressure signals were directed to a computer that was programmed (1) to provide diameter-pressure curves over the range of blood pressure values obtained by finger recording, (2) to calculate cross-sectional compliance based on the arctangent model of Langewouters et al,²² and (3) to derive compliance-pressure curves over the blood pressure range obtained by the finger pressure recording. The echotracking device resolution allowed the identification of diameter changes greater than 125 µm,²³ and the finger pressure device resolution allowed identification of blood pressure changes greater than 2 mm Hg.²⁰ Data were collected by a single operator. The coefficient of variation of two radial artery diameter measurements performed by the same operator in two different sessions was 4%.

Radial artery diameter, radial artery compliance, and blood pressure measurements were coupled with heart rate measurements, which were obtained via the finger pressure signal as the reciprocal of the interval between consecutive systolic beats. Measurements included left ventricular end-diastolic diameter and left ventricular ejection fraction, which were obtained from an echocardiogram in M-mode after the measurement section had been selected in B-mode. The echocardiogram was performed the day before each study (see below). The coefficient of variation of two left ventricular end-diastolic diameter measurements performed by the same operator in two different sessions was 6%.

In CHF patients plasma renin activity was measured by radioimmunoassay²⁴ from blood samples taken from an antecubital vein at the end of the first and last experimental periods.

Protocol and Data Analysis
Each subject was brought to the laboratory in the afternoon, placed in the supine position, and fitted with the blood pressure measuring and echotracking devices. After a 20-minute interval, blood pressure, heart rate, radial artery diameter-pressure curves, and radial artery compliance-pressure curves were measured continuously for 15 minutes. These procedures were repeated after (1) a 4-week (five subjects) or 8-week (five subjects) observational period in control subjects, (2) a 4- to 12-week period of benazepril administration at the single daily dose of 10 mg in hypertensive patients, and (3) both 4 and 8 weeks of 10 mg daily of benazepril in CHF patients. Blood samples for plasma renin activity measurements were withdrawn before and after the 8 weeks of oral administration of benazepril. Benazepril was always taken in the morning, and adherence to treatment was ensured by (1) pill counting at the time of the on-treatment studies and (2) measuring the increase in plasma renin activity values in CHF patients as a result of the blockade of angiotensin II formation (see "Results").

In each subject hemodynamic data were averaged over five 30-second periods obtained at 3-minute intervals. For statistical comparisons, radial artery diameter and compliance were expressed as single values. For diameter this was obtained by averaging the diameter values existing at diastolic pressure for the five 30-second periods. For compliance it was obtained by taking the area under the curve relating compliance to arterial blood pressure divided by pulse pressure. This was referred to as the compliance index. We also calculated the compliance index for the common blood pressure range existing between the three groups in the different conditions to overcome possible differences in compliance simply caused by differences in absolute blood pressure values. This was referred to as the isobaric compliance index. The compliance index values were averaged as described for arterial diameter.

Data were analyzed by an investigator who was unaware of the clinical and echocardiographic findings. Data from individual subjects were averaged and are expressed as mean±SEM separately for control subjects, hypertensive subjects, and CHF patients. The statistical significance of the differences in average values was assessed by two-way ANOVA. The two-tailed t test for paired observations was used to locate the differences between pretreatment and treatment, and the two-tailed t test for unpaired observations was used to locate differences between groups with Bonferroni correction. A value of P<.05 was taken as the minimal level of statistical significance.

	Results

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As shown in the Table baseline heart rate and body weight values were similar in control subjects, hypertensive subjects, and CHF patients. Baseline blood pressure was greater in hypertensive than control subjects and CHF patients, whereas left ventricular end-diastolic diameter was greater and left ventricular ejection fraction smaller in CHF patients compared with the subjects of the other two groups. In control subjects none of the above variables showed any significant alteration 4 to 8 weeks later, whereas in hypertensive subjects benazepril administration for 4 to 12 weeks significantly reduced blood pressure. In CHF patients benazepril administration caused a slight but not significant reduction in blood pressure after 4 and 8 weeks. In contrast, left ventricular ejection fraction was slightly but significantly increased at week 8 of treatment with the drug. The 8-week administration of benazepril also caused a marked increase in plasma renin activity, from 2.6±0.7 to 5.0±0.6 ng/mL per hour. The increase was observed in all patients, and the difference between pretreatment and treatment values was statistically significant (P<.05).

View this table: [in this window] [in a new window]   Table 1. Echocardiographic, Blood Pressure, and Heart Rate Values in Control and Hypertensive Subjects and Congestive Heart Failure Patients

Fig 1 shows that in control subjects, hypertensive subjects, and CHF patients radial artery diameter increased slightly and radial artery compliance decreased markedly from diastolic to systolic pressure. Baseline radial artery diastolic diameter was similar in the three groups (Fig 2, top), whereas baseline radial artery compliance was less in patients with CHF than in the other two groups, the reduction in compliance index being statistically significant (Fig 2, middle). In control and hypertensive subjects diameter and compliance values were unchanged after the 4-week and 8-week observational periods and the 4 to 12-week ACE inhibitor treatments, respectively. In contrast, in CHF patients arterial diameter was unchanged, and arterial compliance was increased after both the 4 and 8 weeks of benazepril administration. After ACE inhibitor administration the compliance-pressure curves and compliance index values of the CHF patients were no longer significantly different from those of the other two groups (Figs 1 and 2). Similar results were obtained when arterial compliance was analyzed under isobaric conditions, ie, for the blood pressure range common to the three groups (Fig 2, bottom).

View larger version (20K): [in this window] [in a new window]   Figure 1. Line graphs show radial artery compliance-pressure curves in 10 control subjects (C), 9 hypertensive subjects (H), and 9 patients with mild congestive heart failure (CHF). Data are mean±SEM. C and H subjects were studied at baseline and after an observational period of 4 or 8 weeks and 4 to 12 weeks of benazepril (B) treatment, respectively. CHF patients were studied at baseline and after 4 and 8 weeks of benazepril administration. BP indicates blood pressure.

View larger version (40K): [in this window] [in a new window]   Figure 2. Bar graphs show diastolic diameter, compliance index, and isobaric compliance index of 10 control subjects (C), 9 hypertensive subjects (H), and 9 patients with mild congestive heart failure (CHF). Data are mean±SEM of baseline (open bars [left open bars in C subjects]), observational period of 4 or 8 weeks in C subjects (right open bars), 4 to 12 weeks of benazepril treatment in H subjects (hatched bars), 4 weeks of benazepril treatment in CHF patients (hatched bars), and 8 weeks of benazepril treatment in CHF patients (shaded bars). *P<.05.

	Discussion

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Our study shows that in patients with mild CHF radial artery compliance was less than in control normotensive and hypertensive subjects. However, it also shows that in these patients 4- and 8-week administrations of benazepril at a dose that clearly interfered with the renin-angiotensin system were accompanied by an increase in arterial compliance that made its values similar to those of the two control groups, in which an observational period or ACE inhibitor treatment of similar duration had no effect. This provides the first evidence that the reduction of radial artery compliance occurring in mild CHF^{1 2} is not irreversible. On the contrary, this reduction is improved by ACE inhibitor treatment, and the improvement can be such as to quickly, completely, and persistently reverse the compliance alteration characterizing this condition.^{1 2}

The mechanisms responsible for the impairment of radial artery compliance in CHF patients are not known. However, it can be suggested that the impairment may originate from one or more of the following mechanisms: (1) an increased contraction of arterial smooth muscle, leading to an increased vessel elastic modulus²⁵ and originating from the neurohumoral activation typical of CHF^{10 11 12 13} ; (2) an increased contraction of vascular smooth muscle because of an impaired secretion of endothelium-derived relaxing factors caused by a reduction in cardiac output, tissue blood flow, and endothelial shear stress^{26 27 28} ; (3) an increase in the sodium and water contents of the arterial wall^{29 30} ; and (4) an increase in arterial wall collagen at the expense of more distensible tissues such as elastin.^{31 32} Our present findings are useful for furthering discussion of these mechanisms. For example, the observation that in our patients treatment modified radial artery compliance within only 4 weeks argues against the possibility that the compliance reduction in CHF is caused by a structural modification of the arterial wall, such as an increase in tissue collagen. Furthermore, our data also argue against a relationship between the impaired compliance and a waterlogging phenomenon because (1) retention of sodium and water is not a prominent feature of mild CHF and (2) the increase in arterial compliance seen during ACE inhibition was not associated with any reduction in body weight. A more likely explanation is that radial artery compliance was improved by ACE inhibition via a reduction of an excessive vascular smooth muscle contraction and that therefore this contraction represents the main mechanism for the impairment of radial artery compliance in mild CHF. It can be presumed that ACE inhibition achieves the effect via blockade of angiotensin II production,³³ reduction of sympathetic influences,^{34 35 36 37 38 39 40 41} and direct or indirect (through an increase in cardiac output) secretion of endothelium-derived relaxing factors,^{42 43} ie, by opposing vasomotor influences that are enhanced in mild CHF.^{28 44} However, an additional vasomotor influence brought about by ACE inhibition may be increased production of bradykinin and prostaglandins,⁴⁵ which could make the favorable effect of ACE inhibition on radial artery compliance the result of removal of vasoconstrictor influences and enhancement of vasodilator influences.

The demonstration that benazepril improves radial artery compliance in patients with mild CHF raises three questions. First, is the improvement in compliance specific for ACE inhibitors or common to all drugs used in the treatment of CHF, eg, diuretics, digitalis, and all vasodilators? Second, is the more marked impairment of radial artery compliance associated with severe CHF also improved by treatment, or does it rather represent a partial or totally irreversible phenomenon? And third, is the increase in arterial compliance limited to middle-sized arteries, or does it occur to the same extent in large elastic arteries? The first two questions will be difficult to answer because background treatment with diuretics and digitalis cannot be easily withdrawn in patients with CHF.^{46 47} Furthermore, ACE inhibitors are now commonly regarded as preferable to vasodilators, except in the presence of serious side effects or contraindications. It will also be difficult to answer the third question because in large arteries (eg, aorta, common carotid artery) a precise estimate of diameter changes cannot be easily coupled with precise noninvasive blood pressure measurements from nearby sides to obtain reliable compliance-pressure curves.^{48 49 50 51}

Finally, because an increase in arterial compliance implies a reduction in arterial impedance on cardiac afterload,^{3 4 26} our results add to the data that ACE inhibition has favorable hemodynamic effects in CHF. More interestingly, they offer a mechanism to account for the sympathetic deactivation that follows ACE inhibitor administration in CHF.^{34 35 36 37 38 39 40 41 52} Given the evidence that ACE inhibitor treatment potentiates the arterial baroreflex in hypertension⁵³ and myocardial infarction,⁵⁴ we can speculate that a similar phenomenon occurs in CHF and is responsible for the sympathetic deactivation, similar to what has been suggested for digitalis.^{55 56} We can also speculate that given the stretch-receptive nature of the baroreceptors,⁵⁷ baroreflex potentiation originates from the improved arterial compliance associated with ACE inhibitor treatment. This is supported by recent evidence that there is a relationship between the sensitivity of the baroreflex, arterial compliance, and sympathetic nerve traffic in CHF.⁵⁸

	Footnotes

 
Reprint requests to Prof Giuseppe Mancia, Divisione Medicina Interna I, Ospedale S. Gerardo dei Tintori, via Donizetti, 106, Monza, Mi, Italy.

Received January 25, 1995; first decision February 21, 1995; accepted March 30, 1995.

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