And Long-Acting Loop Diuretics in Outpatients with Chronic Heart Failure

Home , Azosemide

Journal of Cardiology (2012) 59, 352—358

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Original Article

Comparative study of therapeutic effects of short-

and long-acting loop diuretics in outpatients with

chronic heart failure (COLD-CHF)

Masaaki Miyata (MD, FJCC), Takeshi Sasaki (MD), Yoshiyuki Ikeda (MD),

Takuro Shinsato (MD), Takuro Kubozono (MD), Yuko Furusho (MD),

Atsushi Kusumoto (MD), Shuichi Hamasaki (MD, FJCC),

∗

Chuwa Tei (MD, FJCC) , COLD-CHF Investigators

Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine, Kagoshima University,

Kagoshima, Japan

Received 23 September 2011; received in revised form 7 December 2011; accepted 28 December 2011

Available online 24 February 2012

KEYWORDS Summary

Background: Loop diuretics have two different classes with different duration of activity: short-

Chronic heart failure;

Diuretic; acting such as furosemide (duration of activity, 6 h) and long-acting such as azosemide (duration

of activity, 10—12 h). We conducted a multicenter, randomized, controlled trial in order to

Brain natriuretic

peptide; compare the therapeutic effects of azosemide, a long-acting loop diuretic, and furosemide,

a short-acting one, on neurohumoral factors and cardiac function in outpatients with chronic

Atrial natriuretic

peptide heart failure (CHF).

Methods: We enrolled 98 patients with CHF who were receiving furosemide and an angiotensin-

converting enzyme inhibitor, and they were randomly divided into furosemide (n = 49) and

azosemide (n = 49) groups. The furosemide group continued furosemide at the same dosage,

and the azosemide group switched from furosemide to azosemide. At baseline and after 3

months, we measured body weight, and levels of brain natriuretic peptide (BNP), atrial natri-

uretic peptide (ANP), norepinephrine, active renin, creatinine, blood urea nitrogen, sodium,

potassium, and hematocrit. Chest X-ray and echocardiography were also performed.

Results: Body weight and plasma levels of BNP and ANP signiﬁcantly decreased after 3 months

in the azosemide group compared to the furosemide group. There were no signiﬁcant differ-

ences in changes of levels of creatinine, blood urea nitrogen, sodium, potassium, hematocrit,

norepinephrine, and active renin after 3 months between the furosemide and azosemide groups.

∗

Corresponding author at: Department of Cardiovascular, Respiratory and Metabolic Medicine, Graduate School of Medicine,

Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima 890-8520, Japan. Tel.: +81 99 275 5316; fax: +81 99 275 5322.

E-mail address: [email protected] (C. Tei).

Short- and long-acting diuretics in CHF 353

Echocardiography and chest X-ray did not demonstrate signiﬁcant differences between the two

groups.

Conclusions: Long-acting azosemide is suggested to be useful for the improvement of neurohu-

moral factors compared with short-acting furosemide in patients with CHF.

Introduction

Study design

Heart failure is a major and growing public health prob-

This randomized multicenter clinical trial was conducted at

lem, and the number of heart failure deaths has increased

16 hospitals in Japan from October, 2005 to January, 2008.

steadily despite advances in treatment [1]. Diuretics have

The patients were randomly divided into furosemide and

been shown to improve cardiac function, symptoms, and

azosemide groups by an envelope method. The furosemide

exercise tolerance in patients with chronic heart failure

group was assigned to continue receiving furosemide, and

(CHF) [2—4]. Loop diuretics with strong diuretic effects are

the azosemide group was assigned to switch from furosemide

essential for the treatment of pulmonary congestion and

to azosemide. Regarding the doses of both drugs, 20 and

symptoms in heart failure patients [1]. The loop diuretics

40 mg furosemide was equivalent to approximately 30 and

are categorized into short- and long-acting groups based on

60 mg azosemide, respectively, based on the results of a clin-

their duration of action. Furosemide with rapid action is a

ical pharmacology study [5]. Examinations were conducted

potent diuretic representing the short-acting group, while

3 months after registration, and all clinical parameters were

azosemide with a mild and long-lasting effect is representa-

examined before and 3 months after assignment. Readers of

tive of the long-acting group [5].

chest X-ray and echocardiography were blinded to the inves-

Despite their hypotensive effects, short-acting calcium

tigation in the treatment allocation, although the grouping

channel blockers were reported to increase mortality in

was open to physicians and patients.

patients with cardiovascular disease, while long-acting cal-

Concomitant ACE inhibitors already being used at enroll-

cium channel blockers were not associated with increased

ment were continued as prescribed. Other drugs were

mortality in hypertensive patients [6,7]. This hypothesis

also allowed to continue without making further changes

can also be applied theoretically to diuretics with differ-

after registration. Cases requiring any changes in medica-

ent durations of action in patients with CHF. Azosemide,

tion, including other heart failure drugs, were deﬁned as

a long-acting loop diuretic, was associated with a better dropouts.

outcome in Dahl rat heart-failure models compared with

The study design complied with the Declaration of

short-acting furosemide, partly through attenuation of the

Helsinki and was unanimously approved by the Ethics Com-

reﬂex increase in cardiac sympathetic neuronal activity

mittee of Kagoshima University. Written informed consent

caused by the development of heart failure [8]. Further-

was obtained before enrolment from all of the patients who

more, the comparative effects of long-acting azosemide and

participated in the present study.

short-acting furosemide on neurohumoral factors, and the

usefulness of azosemide for improving quality of life were

Physical examination and chest X-ray

shown in a clinical study [9,10]. However, these studies were

only performed in a small number of patients in a single hos-

pital, and thus the usefulness of long-acting diuretics has not The NYHA functional class, body weight, systolic blood

yet been validated. Therefore, we conducted a multicenter pressure (SBP), diastolic blood pressure (DBP), and cardio-

randomized controlled trial, and compared the effects of thoracic ratio (CTR) on chest radiography were determined

azosemide on neurohumoral factors and cardiac function to before and 3 months after commencing the study.

those of furosemide in outpatients with CHF of New York

Heart Association (NYHA) class I—III. Laboratory examinations

Methods

A fasting blood sample was taken in the morning. The plasma

Patients levels of BNP, atrial natriuretic peptide (ANP), norepineph-

rine (NE), and renin activity, the serum levels of creatinine,

blood urea nitrogen, sodium, potassium, and chloride, and

We enrolled 98 consecutive CHF outpatients with NYHA class

hematocrit were measured before and 3 months after assign-

I—III whose brain natriuretic peptide (BNP) level was greater

ment.

than 20 pg/ml, who had been receiving an angiotensin-

converting enzyme (ACE) inhibitor and furosemide for at

least 1 month and were in a stable condition. They were Echocardiography

not administered any angiotensin II type 1 receptor blocker

(ARB). The diagnosis of heart failure was deﬁned by symp- Cardiac function was evaluated by echocardiography

toms, clinical signs, and BNP levels more than 100 pg/ml before and 3 months after the start of the clinical trial.

before medication [11]. Standard two-dimensional and Doppler echocardiographic

354 M. Miyata et al.

Tei index

Mitral

= (ICT + IRT) / ET

(Tricuspid )

ICT ET

inflow IRT = (a –b) / b

Aortic

(Pulmonary )

ICT: isovo lumic contraction time

ejection flo w

IRT: isovolumic relaxation time

bbc ET : ejection time

ECG c d

IRT

Figure 1 Scheme and principle of measurement of Tei index.

examinations were performed in all subjects using 1- to

Figure 2 Changes in body weight (A) and cardiothoracic

5-MHz phased array transducers and commercially available

ratio (CTR) on chest X-ray (B) after 3 months. White bars are

scanners [12]. Left ventricular systolic dimension (LVDs) and

furosemide group; black bars are azosemide group.

diastolic dimension (LVDd), and left atrial dimension (LAD)

were determined. Left ventricular ejection fraction (LVEF)

Results

was obtained by modiﬁed biplane Simpson’s method from

apical 2- and 4-chamber views. LV mass was calculated by

the American Society of Echocardiography-recommended Patient characteristics

× {

formula [13]: LV mass (g) = 0.8 1.04[(LVDd + posterior

wall thickness + interventricular septum Ninety-eight patients were enrolled and randomly divided

3 − 3 }

thickness) (LVDd) ] + 0.6 g. LV mass was divided by into furosemide and azosemide groups. One patient in the

body surface area to obtain LV mass index (LVMI). azosemide group was excluded from the trial, because she

Doppler time intervals were measured from the left ven- complained of frequent urination and refused the continu-

tricular (LV) inﬂow and outﬂow velocities, and Tei index was ation of study. There were no other adverse drug effects

determined as shown in Fig. 1. Interval ‘‘a’’ was measured in either group. As shown in Table 1, there were no sig-

from the cessation of LV inﬂow to the onset of the next niﬁcant differences in patient background characteristics

inﬂow. Interval ‘‘b’’, ejection time, was measured from the between the furosemide (n = 49) and azosemide groups

onset of LV outﬂow velocity to its cessation. LV isovolumic (n = 48). The dose of furosemide 3 months after enroll-

relaxation time (IRT) was calculated by subtracting interval ment was 26.3 ± 10.5 mg/day, and that of azosemide was

‘‘d’’, between the R wave on the electrocardiogram and the 39.9 ± 25.3 mg/day.

cessation of LV ejection ﬂow, from interval ‘‘c’’, between

the R wave and the onset of LV inﬂow. LV isovolumic contrac-

Symptoms and physical examination ﬁndings

tion time (ICT) was obtained by subtracting IRT from (a − b).

All measurements were performed from three consecutive

We assessed the symptoms and physical ﬁndings at the start-

beats, and average values were determined. LV Tei index,

ing point and 3 months after enrolment, and compared the

deﬁned as the sum of the isovolumic contraction and relax-

changes between the furosemide and azosemide groups.

ation times divided by the ejection time, was calculated

There were no signiﬁcant differences in NYHA class, SBP,

as (a − b)/b [14—16]. In addition, right ventricular (RV) Tei

and DBP between the two groups. Fig. 2A shows the changes

index was also calculated from Doppler time intervals, which

in body weight after 3 months (Table 2).

were determined from RV inﬂow and RV outﬂow velocities.

In comparison with the azosemide group, patients who

LV and RV Tei indices represent a composite of systolic and

received furosemide gained weight while administration of

diastolic function of the LV and RV, respectively.

azosemide induced a reduction of body weight, resulting in a

signiﬁcant difference in the change of body weight between

Statistical analysis

the two groups (p < 0.05). Chest X-ray showed no signiﬁcant

difference in the change of CTR between the two groups

Values are expressed as mean ± SD, except for ANP and BNP

(Fig. 2B).

which are shown as median (25th and 75th percentiles).

Paired t-test and test were used for intra-group com-

Laboratory measurements

parison (prior to and 3 months after initiation of the

trial), and unpaired t-test was performed for inter-group

comparison (comparison of changes in parameters after Over the 3 months of the study, there were no signiﬁcant

administration between furosemide and azosemide groups). differences in changes of creatinine, blood urea nitrogen,

Non-parametric Mann—Whitney U test was used for non- sodium, potassium, and chloride levels, and hematocrit

normally distributed variables, such as ANP and BNP. A between the furosemide and azosemide groups, although

p-value less than 0.05 was considered to indicate signiﬁcant the creatinine levels were signiﬁcantly increased after 3

difference. months in both groups (Table 2).

Short- and long-acting diuretics in CHF 355

Table 1 Patient characteristics.

Parameter Furosemide group (n = 49) Azosemide group (n = 48) p-value

Age (year) 75.7 ± 7.9 75.8 ± 9.6 0.957

Sex

Male 30 (61.2%) 21 (43.7%) 0.129

Female 19 (38.8%) 27 (56.3%)

Body weight (kg) 53.7 ± 11.1 56.3 ± 12.1 0.267

Height (cm) 154.0 ± 9.6 154.5 ± 11.3 0.807 NYHA

Class I1414 0.882

Class II 33 31

Class III 2 3

± ±

CTR (%) 54.6 5.5 55.7 6.6 0.405

LVEF (%) 58.0 ± 16.2 59.8 ± 13.7 0.554

LVDd (mm) 51.2 ± 7.9 48.2 ± 9.7 0.092

LVDs (mm) 35.2 ± 9.7 33.3 ± 8.0 0.314

LAD (mm) 42.7 ± 8.1 41.9 ± 7.1 0.621

LVMI (g/m ) 137.1 ± 35.5 130.1 ± 43.5 0.392

LV Tei index 0.49 ± 0.20 0.46 ± 0.16 0.369

RV Tei index 0.33 ± 0.13 0.32 ± 0.13 0.687

BNP (pg/ml) 90.2 (51.2, 160.0) 102.5 (58.7, 211.5) 0.218

ANP (pg/ml) 31.0 (21.0, 53.0) 48.0 (28.0, 61.0) 0.139

Etiology of heart failure

Valvular disease 29 26

Ischemic heart disease 12 13 0.966

Dilated cardiomyopathy 6 7

Hypertensive heart disease 2 2

ACE inhibitors

Enalapril 29 25

Imidapril 20 21 0.236 Delapril 0 2

␤

blocker 99 0.832 Spironolactone 7 8 0.785 Statin 10 12 0.634 Digitalis 12 13 0.819 Nitrate 11 13 0.644

Values are mean SD except for ANP and BNP which are shown as median (25th and 75th percentiles); NYHA, New York Heart Association;

CTR, cardiothoracic ratio; LVEF, left ventricular ejection fraction; LVDd, left ventricular end-diastolic dimension; LVDs, left ventricular

end-systolic dimension; LAD, left atrial dimension; LVMI, left ventricular mass index; LV, left ventricular; RV, right ventricular; BNP, brain

natriuretic peptide; ANP, atrial natriuretic peptide; ACE, angiotensin converting enzyme; NS, not signiﬁcant.

Neurohumoral factors changes between the groups (Fig. 4A). Although RV Tei index

signiﬁcantly increased after 3 months in the furosemide

With regard to plasma levels of BNP and ANP, the azosemide group, there was no signiﬁcant difference in changes in RV

group showed a decline in these two factors whereas the Tei index between the groups (Fig. 4B). There were no sig-

furosemide group showed an increase in both parameters, niﬁcant differences in changes in LVDd, LVDs, LVEF, LAD, and

demonstrating signiﬁcant differences in the changes in these LVMI after 3 months between the furosemide and azosemide

two markers between the two groups (p < 0.05, Fig. 3A and groups.

B). In contrast, there were no signiﬁcant differences in

changes of plasma levels of norepinephrine and renin activ- Discussion

ity after 3 months between the furosemide and azosemide

groups (Table 2).

Loop diuretics are regarded as suitable for improving pul-

monary congestion and heart failure symptoms by reducing

Echocardiography preload, as described in the guidelines for treatment of CHF

[17]. Loop diuretics have two different classes with differ-

LV Tei index tended to increase after 3 months in the ent duration of activity: short-acting such as furosemide

furosemide group, while it decreased in the azosemide (duration of activity, 6 h) and long-acting such as azosemide

group; however, there was no signiﬁcant difference in the (duration of activity, 10—12 h) [5]. In the present study,

356 M. Miyata et al.

Table 2 Changes in blood pressure, PRA, NE, BUN, Cr, K, Na, Cl, and hematocrit.

Furosemide group (n = 49) Azosemide group (n = 48)

Baseline After 3 months Baseline After 3 months

SBP (mmHg) 136.1 ± 26.2 133.2 ± 23.6 135.3 ± 27.9 133.4 ± 23.6

DBP (mmHg) 71.9 ± 14.4 71.7 ± 12.3 71.5 ± 12.0 73.9 ± 10.0

PRA (ng/ml/h) 4.3 ± 5.4 4.1 ± 5.3 4.5 ± 6.1 4.7 ± 6.2

NE (pg/ml) 513.0 280.3 519.3 361.8 472.2 ± 267.6 479.6 ± 432.1

± ± ±

BUN (mg/dl) 23.0 8.2 22.5 8.5 21.1 9.0 21.6 ± 9.3

* **

± ±

± ± Cr (mg/dl) 0.97 0.42 1.02 0.42 1.03 0.33 1.09 0.35

± ± ±

K (mmol) 4.3 0.5 4.4 0.5 4.4 0.5 4.3 0.5

Na (mmol) 142.0 ± 3.5 141.4 ± 2.9 142.8 ± 3.3 142.2 ± 2.4

Cl (mmol) 106.6 ± 12.6 102.8 ± 14.1 104.4 ± 3.7 105.0 ± 3.0

Ht (%) 37.2 ± 5.7 36.9 ± 5.0 36.1 ± 5.4 35.9 ± 4.9

SBP, systolic blood pressure; DBP, diastolic blood pressure; PRA, plasma renin activity; NE, norepinephrine; BUN, blood urea nitrogen;

Cr, creatine; Ht, hematocrit.

p < 0.05 vs baseline in furosemide group.

p < 0.01 vs baseline in azosemide group.

we compared the effect on neurohumoral factors between

furosemide and azosemide, and found that long-acting

azosemide signiﬁcantly decreased plasma BNP and ANP lev-

els compared with short-acting furosemide.

ANP and BNP are secreted mainly from the atria and

ventricles, respectively, and these markers are predictors

of LV dysfunction. The plasma ANP and BNP levels are

considered a particularly useful predictive biomarker for

prognosis and cardiovascular events in patients with CHF

[18—20] and acute myocardial infarction [21]. In the SAVE

study, where neurohumoral factors were measured 12 days

after myocardial infarction in 534 patients, multivariate

analysis revealed that only plasma ANP level and plasma

renin activity on day 12 after disease onset were associated

with outcome in patients with acute myocardial infarction

[22]. In the Val-HeFT study, plasma levels of norepineph-

rine, aldosterone, and BNP were measured in 4300 patients

Figure 3 Changes in brain natriuretic peptide (BNP) (A) and

with moderate to severe heart failure, and the plasma BNP

atrial natriuretic peptide (ANP) (B) after 3 months. White bars

level showed the greatest prognostic value [23]. In the

are furosemide group; black bars are azosemide group.

present study, these parameters signiﬁcantly decreased in

the azosemide group compared to those in the furosemide

group, suggesting that long-acting diuretics may be useful

for improving cardiac function and prognosis in CHF.

McCurley et al. conducted a placebo-controlled com-

parative study to investigate the effect of furosemide on

progression of LV dysfunction in a heart failure model,

and reported that furosemide signiﬁcantly accelerated the

progression of LV systolic dysfunction [24]. In addition,

Starklint et al. reported that administration of furosemide

did not induce any signiﬁcant change in plasma ANP

and BNP levels in CHF patients [25]. The present study

also demonstrated that neurohumoral factors and car-

diac function assessed by echocardiography were not fully

improved by furosemide. Several investigators reported

that the furosemide causes excessive volume loss and

electrolyte disturbances due to its strong and rapid diuretic

Figure 4 Changes in left ventricular (LV) Tei index (A) and effect, and the response to the rapid volume reduction

right ventricular (RV) Tei index (B) after 3 months. White bars may lead to activation of the sympathetic nervous system

are furosemide group; black bars are azosemide group. *p < 0.05 and the renin—angiotensin—aldosterone system, resulting

for comparison between baseline and after 3 months. in increased plasma ANP and BNP levels [26,27], although

Short- and long-acting diuretics in CHF 357

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