Full text of DOI:10.1345/aph.10104

Spironolactone in the Treatment of
Congestive Heart Failure
Stanley J Lloyd and Vincent F Mauro
OBJECTIVE: To evaluate evidence supporting the use of spironolactone in managing congestive heart failure.
DATA SOURCES: Literature accessed through MEDLINE (January 1966–December 1999) and cross-referencing of selected articles.
Search terms included spironolactone and heart failure.
DATA SYNTHESIS: Heart failure is a leading cause of morbidity and mortality. Through aldosterone antagonism, spironolactone may
be an effective pharmacotherapeutic addition to patients not responding to standard drug therapy for heart failure.
RESULTS: Clinical trials have demonstrated that, in patients with heart failure, spironolactone improves laboratory indices, quality of
life, and morbidity. Recently, spironolactone has been demonstrated to improve the survival of patients with New York Heart
Association (NYHA) III or IV heart failure.
CONCLUSIONS: Spironolactone use should be considered in patients with NYHA Class III or IV heart failure.
KEY WORDS: spironolactone, heart failure, aldosterone.
Ann Pharmacother 2000;34:1336-40.
REQUEST
line measured after four to six weeks of ACE-inhibitor
therapy dissipated after three to 12 months of therapy even
What evidence supports the use of spironolactone in man-
though angiotensin II concentrations remained suppressed.
aging congestive heart failure?
Explanations for this observation include enhanced sensi-
tivity to angiotensin II, increased release of adrenocorti-
cotropic hormone, and/or a compensatory physiologic re-
action, possibly related to the electrolyte shifts resulting
from the initial lack of aldosterone. The inability of ACE
inhibition to provide lasting suppression of aldosterone
concentrations has led to speculation that a role may exist
for the use of a direct aldosterone antagonist, such as spir-
onolactone, in the treatment of patients with heart failure.
RESPONSE
BACKGROUND
The pathogenesis of heart failure involves several sig-
nificant neurohormonal components. Failure of the my-
ocardial tissue to adequately propel blood throughout the
body results in increased release of compensatory neuro-
hormones, including two products resulting from the acti-
vation of the renin–angiotensin system: angiotensin II and
aldosterone. Although increased release of aldosterone
may improve cardiac function in the short term, persistent-
ly elevated aldosterone concentrations are thought to cause
or contribute to many of the adverse changes in heart fail-
ure, including water retention,1 electrolyte abnormalities,1
myocardial fibrosis,2 decreased baroreceptor responses,3
decreased large artery compliance,4 and increased arrhyth-
mogenicity.5
Angiotensin-converting enzyme (ACE) inhibitors, agents
proven to decrease the mortality of patients with heart fail-
ure,6 lower serum aldosterone concentrations by decreas-
ing the production of angiotensin II. However, small trials7,8
evaluating aldosterone concentrations during ACE-inhib-
itor therapy have shown a lack of sustained suppression.
Initial reductions of aldosterone concentrations from base-
CLINICAL TRIALS
A review of the diuretic effects of spironolactone in
heart failure has appeared elsewhere.9 Historically, the role
of spironolactone in heart failure has been to provide syn-
ergistic diuresis in patients who are refractory to combined
ACE-inhibitor and loop diuretic therapy.10,11 One early re-
port10 described three patients with marked congestive
heart failure whose symptoms worsened despite treatment
with digoxin, a loop diuretic, and an ACE inhibitor. Each
patient’s regimen was supplemented with spironolactone
50 or 100 mg/d and, after one to four weeks, resulted in
improved diuresis, weight loss, and resolution of pulmo-
nary and peripheral edema. The authors attributed these re-
sults to the diuretic effects of spironolactone.
An early clinical trial11 involved 21 patients with New
York Heart Association (NYHA) Class III or IV heart fail-
ure with marked edema that was unresponsive to loop di-
Author information provided at the end of the text.
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Drug Information Rounds
uretics. Patients initially received a five-day regimen of an
ACE inhibitor at the highest tolerated dosage plus bumeta-
nide 5 mg twice daily. Five patients experienced diuresis
quickly, achieving a 25% reduction in excess body weight
relative to prior measurements. The other 16 patients had
spironolactone 100 mg/d added to their regimen. Within
seven days of this therapy, improved diuresis occurred in
all but three patients. The mean daily weight loss increased
from 0.08 to 0.61 kg. The authors concluded that adding
spironolactone appears beneficial in patients unresponsive
to loop diuretic and ACE-inhibitor therapy and speculated
that increased suppression of the renin–angiotensin–aldos-
terone pathway may have been responsible for the improved
diuresis.
Evidence now exists supporting the thought that spirono-
lactone can be beneficial in the treatment of heart failure in
ways other than its diuretic effect.12-14 In a trial12 monitor-
ing clinical symptoms, 35 patients with NYHA Class IV
heart failure receiving thiazide and/or loop diuretics were
randomized to receive captopril alone or with spirono-
lactone 20–40 mg three times daily. After four weeks of
therapy, the spironolactone/captopril group experienced
significantly greater improvement (from 4.3 to 8.1) in
mean dyspnea–fatigue rating score (0 = lowest; 12 = high-
est possible score) than patients in the captopril monother-
apy group (from 4.2 to 6.0; p < 0.01). The scores improved
prior to the achievement of spironolactone-induced diure-
sis, thus affirming the thought that spironolactone could
contribute to the treatment of heart failure patients apart
from its diuretic effects.
an ACE inhibitor, to additionally receive either spironolac-
tone 50 mg/d or placebo. Based on patient tolerance, spiro-
nolactone dosages were as high as 100 mg/d. At eight-
week assessments, patients receiving spironolactone (n =
28) had significantly greater reductions (p < 0.05) from
baseline in premature ventricular contractions compared
with placebo patients (>20% vs. ~10% reduction; p <
0.05). The impact spironolactone had on transient ventric-
ular tachycardias could not be fully determined since their
occurrence rate was too low for statistical evaluation. The
initial results of this study suggested that spironolactone
might have suppressed arrhythmias by elevating serum
magnesium and intracellular potassium concentrations. In
an attempt to confirm this finding, further assessments
were conducted in six patients from each group. Myocar-
dial 123I-metaiodobenzylguanidine uptake, a measure of
catecholamine uptake by myocardial cells, was increased
within the spironolactone patients (from 1.31 to 1.47); it
was decreased (from 1.42 to 1.35) within the placebo
group (p < 0.01). Catecholamines appear to be broken
down once inside the myocardial tissue14; thus, spironolac-
tone may indirectly reduce circulating catecholamine con-
centrations, decreasing the potential for cardiac arrhyth-
mias.
Although improvements in cardiac rhythms and bio-
chemical measurements are of interest, standard therapies
should also improve patients’ quality of life and mortality
rates. The recently published Randomized Aldactone Eval-
uation Study (RALES)16 was the first large-scale, random-
ized, double-blind, placebo-controlled trial conducted to
assess the impact of low-dose spironolactone therapy on
hospitalization and mortality rates in patients with heart
failure. The researchers enrolled 1663 patients with pri-
marily NYHA Class III (70.5% of patients) or IV (29%)
heart failure who were already being treated with a loop di-
uretic (100% of patients) and/or an ACE inhibitor (~95%).
The majority of patients were also receiving digoxin
(~73%); about 10% of the patients were receiving a β-
blocker. The average age of the patients was 65 years; 73%
of the patients were men and 87% were white. The mean
ejection fraction of the subjects was 25%, and heart failure
was due to ischemic causes in 55% of the patients. Patients
were permitted to receive vasodilator therapy in addition to
ACE inhibitors or as alternative therapy when ACE in-
hibitors were not tolerated. Patients with renal insufficien-
cy (serum creatinine >2.5 mg/dL) or elevated potassium
concentrations (>5 mEq/L) were not permitted into the tri-
al.
MacFayden et al.13 assessed the impact of spironolac-
tone on heart rate variability, a reflection of the capacity of
the myocardium to support the varying metabolic demands
of daily living. Thirty-one patients with heart failure al-
ready receiving an ACE inhibitor and diuretic were ran-
domized to receive spironolactone 50 mg/d or placebo.
The spironolactone dosage was titrated, depending on tol-
erability, to dosages up to 100 mg/d. Heart-rate variability
was assessed after eight weeks in 24 of these patients by
measurement of their electrocardiogram R–R interval
lengths. The change from baseline in standard deviation of
normal-to-normal intervals was 9.1 msec within the spir-
onolactone group compared with –1.2 msec within the
placebo group (p < 0.05). Other heart-rate variability pa-
rameters were also increased. The concentrations of serum
procollagen type III amino terminal peptide, an indicator
of myocardial fibrosis, were also measured. Fibrosis of
myocardial tissue, a process facilitated by aldosterone,2 has
been found in patients having arrhythmias of no apparent
etiology.15 Spironolactone, due to its aldosterone antago-
nistic properties, could theoretically reduce the incidence
of cardiac dysrhythmias by impairing the myocardial fi-
brosis process. In this investigation, although reductions in
serum procollagen type III amino terminal peptide concen-
trations were observed, the difference was not significant.13
The antiarrhythmic effects of spironolactone were stud-
ied in a trial14 that randomized 42 NYHA Class II or III
heart-failure patients, already receiving a loop diuretic and
Eligible patients were randomized to additionally re-
ceive daily placebo (n = 841) or spironolactone 25 mg (n =
822). The groups were similar with regard to demograph-
ics, heart disease severity, and the use of traditional cardiac
medications (ACE inhibitors, loop diuretics, digoxin, β-
blockers, aspirin). The investigators had previously17 deter-
mined that a 25-mg daily dose of spironolactone was well
tolerated and likely to be effective. The dosages of spiro-
nolactone were reduced to 25 mg every other day in pa-
tients who became hyperkalemic with the initial dose if
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modification of concurrent medications could not alleviate
this electrolyte disorder. Eight weeks into the trial, the dos-
age was increased to 50 mg/d, if tolerated, in patients who
were experiencing a worsening of their heart failure but
had not developed hyperkalemia. The average daily dose
ultimately used in the investigation was approximately 25
mg. All-cause mortality was the primary end point; sec-
ondary end points included mortality of cardiac cause, hos-
pitalization, and changes in NYHA functional class. The
trial was terminated prematurely (average 24-mo length of
follow-up) due to the magnitude of improvement observed
in the patients receiving spironolactone.16
continuation more often than do dosages ≤25 mg/d. A
greater risk of hyperkalemia is associated with using spir-
onolactone in patients with baseline serum creatinine con-
centrations >1.6 mg/dL, or potassium concentrations ≥4.2
mEq/L, or in patients receiving higher dosages of ACE in-
hibitors.17 In RALES,16 spironolactone induced a median
increase of 0.3 mEq/L in potassium concentrations, which
was statistically significant (p < 0.001) but clinically unre-
markable. Some patients who developed hyperkalemia
subsequently achieved acceptable potassium concentra-
tions after decreasing their spironolactone dose,14 but oth-
ers, especially those with preexisting renal disease, re-
quired discontinuation of the agent.14,18
The incidence of overall death was decreased within the
spironolactone group compared with the placebo group
(34.5% vs. 45.9%, respectively). The authors reported that
this was a 30% reduction in the risk of overall deaths (rela-
tive risk [RR] 0.70; 95% CI 0.60 to 0.82; p < 0.001) and an
11.4% absolute reduction in the incidence of death. Spiro-
nolactone reduced the incidence of cardiac death from
37.3% to 27.5%, representing a 31% reduction (RR 0.69;
95% CI 0.58 to 0.82; p < 0.001). Spironolactone was also
associated with significant decreases in the incidences of
sudden death (13.1% vs. 10.0%; p < 0.02) and death from
worsening heart failure (22.5% vs. 15.5%; p = 0.001). In
addition to mortality benefit, spironolactone was associat-
ed with a significant decrease (30%) in the risk of cardiac-
related hospitalizations compared with placebo (515 vs.
753 hospitalizations, respectively; RR 0.70; 95% CI 0.59
to 0.82; p < 0.001) compared with placebo. This primarily
reflected the significant decrease in hospitalizations for
worsening heart failure (413 vs. 663, respectively; RR
0.65; 95% CI 0.54 to 0.77; p < 0.001).16
Gynecomastia and breast pain (combined incidence:
10% spironolactone vs. 1% placebo) were the only signifi-
cant adverse events (p < 0.001) associated with spironolac-
tone use reported in RALES.16 These effects were not re-
ported in the other trials reviewed above; however, the du-
ration of these trials was much shorter. Although digoxin,
by virtue of its steroid-like structure, is also known to in-
duce gynecomastia, its use in RALES was equally dis-
tributed among placebo and spironolactone patients.
Dehydration has been reported10,11 when spironolactone
was used in conjunction with high-dose loop diuretics.
Complete recovery occurred with fluid replacement and/or
drug discontinuation. Renal dysfunction has developed
when spironolactone was coadministered with ACE in-
hibitors, particularly with daily spironolactone dosages of
≥50 mg.10,11,17,18 Renal function returned to baseline upon
withdrawing and/or adjusting the dosages of both medica-
tions.10,11
Forty-one percent of patients receiving spironolactone
improved their NYHA classification compared with only
33% of those receiving placebo (p < 0.001). Subgroup
analysis indicated that age (≥ vs. <67 y), gender, ejection
fraction (≥ vs. <26%), or cause of heart failure (ischemic
vs. nonischemic) did not impact the effects of spironolac-
tone therapy. However, spironolactone did not significantly
benefit patients with heart failure who were not concur-
rently receiving either digoxin or ACE-inhibitor therapy,
although a beneficial trend was present. The absence of β-
blocker therapy did not preclude patients from receiving
any benefit from spironolactone; however, the concurrent
use of β-blocker therapy did further magnify the favorable
effects of spironolactone.16
PRACTICAL ISSUES
Two practical issues need to be further delineated with
respect to the use of spironolactone in patients with heart
failure. The first is to identify patients who would benefit
from spironolactone therapy. RALES16 primarily investi-
gated patients with NYHA Class III or IV heart failure. At
present, it is not known whether these findings can be ex-
trapolated to patients with less severe forms of heart fail-
ure. It may be reasonable to surmise that patients with
higher serum aldosterone concentrations may benefit more
from aldosterone antagonism, and it has been shown11 that
higher plasma aldosterone concentrations correlate with a
weaker response to loop diuretics and ACE inhibitors. Un-
fortunately, cost and other procedural factors limit the rou-
tine assessment of plasma aldosterone concentrations.
Clinical trials11,12 have shown that commonly available uri-
nary Na+:K+ concentration ratios are inversely proportional
to serum aldosterone concentrations, and a urinary Na+:K+
ratio <1.0 may be a useful marker for initiating spironolac-
tone therapy in patients with heart failure.11
ADVERSE EFFECTS
Although the evidence presented here suggests that us-
ing spironolactone in heart failure is likely beneficial, pa-
tients’ ability to tolerate this agent is an important issue to
consider. A primary concern with using this drug in pa-
tients with heart failure is the potential for inducing hyper-
kalemia. Published reports,14,16-18 have described hyper-
kalemia occurring in patients receiving spironolactone
even in the absence of renal disease or other risk factors for
hyperkalemia. Spironolactone dosages ≥50 mg/d cause hy-
perkalemia severe enough to require dose reduction or dis-
Once a patient who can benefit from spironolactone
therapy has been identified, the second issue is to define
when spironolactone should be initiated in relation to other
medications proven to be beneficial in heart failure. Given
the abundance of clinical supportive data, ACE-inhibitor
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Drug Information Rounds
SUMMARY
therapy or, when patients become intolerant to ACE in-
hibitors, another form of vasodilator therapy (e.g., hy-
dralazine/isosorbide dinitrate or angiotensin II receptor
blocker) should be considered first-line therapy. Diuretics
are indicated in patients with congestion. Once these thera-
pies have been initiated and the dosages have been titrated
to appropriate levels, clinicians should consider adding
other pharmacologic modalities, including spironolactone.
The routine use of β-blocker therapy has most recently
become established in the therapy of heart failure.19 Wheth-
er or not spironolactone should be added prior to β-blocker
therapy or vice versa in patients eligible to receive β-block-
er therapy is not definitively known at present. The results
of RALES16 indicated that spironolactone significantly
benefited patients regardless of the presence of β-blocker
therapy; however, the benefit associated with spironolac-
tone was more pronounced in patients receiving concurrent
β-blocker therapy. This suggests that the ultimate goal of
therapy for heart failure should be to initiate both medica-
tions; however, it should be noted that β-blocker therapy is
not advocated in patients who are clinically unstable or
have severe symptoms (i.e., NYHA Class IV).19
A compilation of results from clinical trials imply that
appropriately dosed spironolactone is a well-tolerated
agent that improves the laboratory indices, quality of life,
and morbidity of patients with heart failure. More recently,
spironolactone also has been demonstrated to improve the
survival of patients with more serious degrees of heart fail-
ure. These data, along with current knowledge of the mech-
anisms of action of spironolactone and the pathophysiolo-
gy of heart failure, indicate that spironolactone can benefit
patients with NYHA Class III or IV heart failure.
Stanley J Lloyd PharmD, at time of writing, PharmD Student, Col-
lege of Pharmacy, University of Toledo, Toledo OH; now, Assistant
Editor, Harvey Whitney Books
Vincent F Mauro PharmD FCCP, Associate Professor of Clinical
Pharmacy, College of Pharmacy, University of Toledo; and Adjunct
Associate Professor of Medicine, Department of Medicine, Medical
College of Ohio, Toledo, OH
Reprints: Vincent F Mauro PharmD FCCP, University of Toledo,
2801 W. Bancroft St., Toledo, OH 43606, FAX 419/530-1950, E-mail
vmauro@utnet.utoledo.edu
References
In RALES,16 although a favorable trend was observed,
spironolactone did not significantly benefit patients who
were not receiving concurrent digoxin. Digoxin has been
demonstrated19 to reduce morbidity of heart failure and its
use is encouraged, especially in symptomatic patients.
Digoxin, however, has not been demonstrated to improve
survival of patients with heart failure; it therefore is often
avoided due to concerns for possible toxicity.20 An issue
that requires further investigation is whether patients re-
ceiving spironolactone should receive concurrent digoxin
to maximize the beneficial attributes of spironolactone.
When spironolactone therapy is going to be initiated, it
has been recommended17 that patients receiving concurrent
ACE-inhibitor therapy should first receive spironolactone
25 mg/d if the serum potassium concentration is within
normal limits. The spironolactone dosage should be de-
creased if hyperkalemia or renal dysfunction develops. In
addition, clinicians should consider titrating the dosage up
to 50 mg/d, if tolerated, in patients whose heart failure is
progressing despite the initiation of spironolactone. Pa-
tients receiving spironolactone, especially in conjunction
with ACE inhibitors, should have their serum potassium
and creatinine concentrations monitored after seven days
of treatment and then frequently (weekly–monthly) for the
first few months, and routinely (every 3–6 mo) thereafter.
The drug should be avoided in patients with renal insuffi-
ciency or high baseline serum potassium concentrations.
Patients with serum baseline potassium concentrations
>5.0 mEq/L were excluded from RALES.16 Potassium
supplements or potassium-retaining or -containing medica-
tions should be used cautiously, if at all, in patients receiv-
ing spironolactone, especially if ACE inhibitors or an-
giotensin II receptor blockers, medications also known to
increase serum potassium concentrations, are being used
concurrently.
1. Weber KT, Villarreal D. Aldosterone and antialdosterone therapy in con-
gestive heart failure. Am J Cardiol 1993;71(suppl):3A-11A.
2. Weber KT, Brilla CG. Pathological hypertrophy and cardiac interstitium:
fibrosis and renin–angiotensin–aldosterone system. Circulation 1991;83:
1849-65.
3. Wang W. Chronic administration of aldosterone depresses baroreceptor
reflex function in the dog. Hypertension 1994;24:571-5.
4. Duprez DA, De Buyzere ML, Rietzschel ER, Taes Y, Clement DL, Mor-
gan D, et al. Inverse relationship between aldosterone and large artery
compliance in chronically treated heart failure patients. Eur Heart J 1998;
19:1371-6.
5. Packer M. Neurohormonal interactions and adaptations in congestive
heart failure. Circulation 1988;77:721-30.
6. Hailemeskel B, Mauro VF. Use of angiotensin-converting enzyme in-
hibitors in heart failure. J Pharm Technol 1994;10:156-63.
7. Staessen J, Lijnen P, Fagard R, Verschueren LJ, Amery A. Rise in plas-
ma concentration of aldosterone during long-term angiotensin II sup-
pression. J Endocrinol 1981;91:457-65.
8. Cleland JGF, Dargie HJ, Hodsman GP, Ball SG, Robertson JIS, Morton
JJ, et al. Captopril in heart failure: a double-blind controlled trial. Br
Heart J 1984;52:530-5.
9. Muller J. Spironolactone in the management of congestive heart failure:
a review. Clin Ther 1986;9:63-76.
10. Ikram H, Webster MWI, Nicholls MG, Lewis GRJ, Richards AM,
Crozier IG. Combined spironolactone and converting-enzyme inhibitor
therapy for refractory heart failure. Aust N Z J Med 1986;16:61-3.
11. van Vliet AA, Donker AJM, Nauta JJP, Verheugt FWA. Spironolactone
in congestive heart failure refractory to high-dose loop diuretic and low-
dose angiotensin-converting enzyme inhibitor. Am J Cardiol 1993;71
(suppl):21A-8A.
12. Han YL, Tong M, Jing QM, Hu XL, Liu JQ. Combined therapy of cap-
topril and spironolactone for refractory congestive heart failure. Chin J
Med (Engl) 1994;107:688-92.
13. MacFayden RJ, Barr CS, Struthers AD. Aldosterone blockade reduces
vascular collagen turnover, improves heart rate variability and reduces
early morning rise in heart rate in heart failure patients. Cardiovasc Res
1997;35:30-4.
14. Barr CS, Lang CC, Hanson J, Arnott M, Kennedy N, Struthers A. Ef-
fects of adding spironolactone to an angiotensin-converting enzyme in-
hibitor in chronic congestive heart failure secondary to coronary artery
disease. Am J Cardiol 1995;76:1259-65.
15. Sugrue DD, Holmes DR Jr, Gersh BJ, Edwards WD, McLaran CJ, Wood
DJ, et al. Cardiac histologic findings in patients with life-threatening
ventricular arrhythmias of unknown origin. J Am Coll Cardiol 1984;4:
952-7.
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16. Pitt B, Zannad F, Remme W, Cody R, Castaigne A, Oerez A, et al. The
effect of spironolactone on morbidity and mortality in patients with se-
vere heart failure. N Engl J Med 1999;341:709-17.
17. The RALES Investigators. Effectiveness of spironolactone added to an
angiotensin-converting enzyme inhibitor and a loop diuretic for severe
chronic congestive heart failure (The Randomized Aldactone Evaluation
Study [RALES]). Am J Cardiol 1996;78:902-7.
pacientes con fallo cardíaco. Recientemente se demostró que el uso de
espironolactona mejora la supervivencia de pacientes con fallo cardíaco
clase III ó IV de la Asociación del Corazón de New York (NYHA, por
sus siglas en inglés).
CONCLUSIÓNES: El uso de espironolactona debiera ser considerado en
pacientes con fallo cardíaco clase III ó IV de la NYHA.
Juan Francisco Feliú
18. Dahlström U, Karlsson E, Captopril and spironolactone therapy for re-
fractory congestive heart failure. Am J Cardiol 1993;71(suppl):29A-
33A.
RÉSUMÉ
19. Packer M, Cohn JN. Consensus recommendations for the management
of chronic heart failure. Am J Cardiol 1999;83(suppl):1A-38A.
20. Digoxin Investigator Group. The effect of digoxin on mortality and mor-
bidity in patients with heart failure. N Engl J Med 1997;336:525-33.
OBJECTIF: Évaluer la littérature concernant l’utilisation de la
spironolactone dans le traitement de l’insuffisance cardiaque.
DEVIS EXPERIMENTAL: Une recherche via MEDLINE a été effectuée au
cours de la période de janvier 1966 à décembre 1999. Les termes
spironolactone et insuffisance cardiaque ont été utilisés.
RÉSUMÉ: L’insuffisance cardiaque représente une cause importante de
mortalité et de morbidité. La spironolactone peut être ajoutée dans le
traitement pharmacologique de l’insuffisance cardiaque chez les patients
ne répondant pas au traitement conventionnel.
EXTRACTO
OBJETIVO: Evaluar la evidencia que apoya el uso de espironolactona en
el manejo de fallo cardíaco congestivo.
RÉSULTATS: Les études cliniques ont démontré que chez les patients
présentant une insuffisance cardiaque, la spironolactone améliore la
qualité de vie, les tests de laboratoire, et la morbidité. Récemment, une
étude a démontré que la spironolactone améliorait la survie des patients
avec insuffisance cardiaque de la NYHA classe III ou IV.
FUENTES DE INFORMACIÓN: Literatura accesada a través de MEDLINE
(enero de 1966 a diciembre 1999) y referencia cruzada de articulos
selectos. Espironolacona y fallo cardíaco fueron incluídos como
términos de búsqueda.
SÍNTESIS: Fallo cardíaco es una causa principal de morbilidad y
mortalidad. Espironolactona, a través de su antagonismo de aldosterona,
puede ser una adición farmacoterapéutica efectiva para pacientes que no
han respondido a la terapia farmacológica estándar de fallo cardíaco.
CONCLUSIONS: La spironolactone devrait être utilisée chez les patients en
insuffisance cardiaque de la NYHA classe III ou IV.
Louise Mallet
RESULTADOS: Estudios clínicos han demostrado que espironolactona
mejora los parámetros de laboratorio, la calidad de vida, y morbilidad en
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