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Acute Precipitants of Congestive Heart Failure Exacerbations
Ross T. Tsuyuki, BSc(Pharm), PharmD, MSc;
Robert S. McKelvie, MD, PhD;
J. Malcolm O. Arnold, MD;
Álvaro Avezum, Jr, MD;
Antônio C. P. Barretto, MD;
Antonio C. C. Carvalho, MD;
Debra L. Isaac, MD;
Allan D. Kitching, MD, MSc;
Leopoldo S. Piegas, MD, PhD;
Koon K. Teo, MB, PhD;
Salim Yusuf, DPhil, FRCPC
Arch Intern Med. 2001;161:2337-2342.
ABSTRACT
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Background Few studies have prospectively and systematically explored the factors
that acutely precipitate exacerbation of congestive heart failure (CHF) in
patients with left ventricular dysfunction. Knowledge of such factors is important
in designing measures to prevent deterioration of clinical status. The objective
of this study was to prospectively describe the precipitants associated with
exacerbation of CHF status in patients enrolled in the Randomized Evaluation
of Strategies for Left Ventricular Dysfunction Pilot Study.
Methods We conducted a 2-stage, multicenter, randomized trial in 768 patients
with CHF who had an ejection fraction of less than 40%. Patients were randomly
assigned to receive enalapril maleate, candesartan cilexetil, or both for
17 weeks, followed by randomization to receive metoprolol succinate or placebo
for 26 weeks. Investigators systematically documented information on clinical
presentation, management, and factors associated with the exacerbation for
any episode of acute CHF during follow-up.
Results A total of 323 episodes of worsening of CHF occurred in 180 patients
during 43 weeks of follow-up; 143 patients required hospitalization, and 5
died. Factors implicated in worsening of CHF status included noncompliance
with salt restriction (22%); other noncardiac causes (20%), notably pulmonary
infectious processes; study medications (15%); use of antiarrhythmic agents
in the past 48 hours (15%); arrhythmias (13%); calcium channel blockers (13%);
and inappropriate reductions in CHF therapy (10%).
Conclusions A variety of factors, many of which are avoidable, are associated with
exacerbation of CHF. Attention to these factors and patient education are
important in the prevention of CHF deterioration.
INTRODUCTION
DESPITE MANY advances in congestive heart failure (CHF) therapy, worsening
of clinical status, often to the point of requiring hospitalization, remains
a common occurrence.1 It is estimated that
there are 700 000 hospitalizations for CHF per year in the United States.
In the Studies of Left Ventricular Dysfunction registry of 6273 consecutive
patients with CHF,2 19% were hospitalized 1
or more times for CHF and 27% died or were hospitalized for CHF within 1 year.
In 2 large CHF trials, the Studies of Left Ventricular Dysfunction Treatment
Trial3 and the Digitalis Investigation Group
Trial,4 26% and 27%, respectively, of patients
in the active treatment groups were hospitalized at least once during the
3 to 4 years of follow-up. Indeed, approximately two thirds of the economic
burden of CHF is due to hospitalizations for worsening clinical status.5
Clinical and lifestyle factors associated with deterioration of patients
with CHF have not been systematically addressed. Most studies that have explored
the prognostic importance of CHF have relied on historical, clinical, or investigational
data obtained at "entry" into the study. The impact of these prognostic indicators
on later deterioration of clinical status, whether transient or permanent,
were then assessed at a remote time point.6-8
However, given the magnitude of the problem, knowledge of the immediate precipitants
of CHF exacerbation, particularly if avoidable, provides useful insight for
clinicians in preventing the deterioration. Therefore, the purpose of this
study was to prospectively and systematically explore the immediate precipitants
associated with exacerbation of CHF in patients enrolled in a 43-week multicenter
clinical trial.
PATIENTS AND METHODS
The precipitants of CHF exacerbations were determined within the context
of the Randomized Evaluation of Strategies for Left Ventricular Dysfunction
Pilot Study. The purpose, methods, and main results of this double-blind,
randomized, 2-stage, multicenter trial in 768 patients with symptomatic CHF
(New York Heart Association functional class [NYHA-FC] II-IV), an ejection
fraction of less than 40%, and a 6-minute walk distance of less than 500 m
have been described previously.9-11
In stage I, patients were randomized to receive the angiotensin II receptor
blocker candesartan cilexetil alone (4, 8, or 16 mg daily), candesartan cilexetil
plus enalapril maleate (4 or 8 mg of candesartan cilexetil daily plus 10 mg
of enalapril twice daily), or enalapril alone (10 mg twice daily). Patients
were followed up for 17 weeks, at which time they were considered for a second
randomization to receive controlled-release metoprolol succinate (200 mg daily)
or placebo (stage II). Doses of all medications were titrated upwards to the
target doses in 6 to 8 weeks. Patients were followed up in stage II for 26
weeks, for a total study duration of 43 weeks. Patients not randomized in
stage II (usually because of  -adrenergic blocking agent contraindications
or patient refusal) continued to receive candesartan, enalapril, or both and
were also followed up for another 26 weeks. Study end points were 6-minute
walk distance (primary end point), neurohormone levels, ejection fraction,
cardiac volumes, symptoms, quality of life, and safety. All end points were
measured at baseline and at the end of stage I and stage II. Written informed
consent was obtained from all study participants, and all study centers received
local research ethics committee approval.
As part of the clinical event reporting for the study, investigators
completed a CHF Event Form for all patients experiencing any worsening of
CHF. This form was completed regardless of whether the patient required hospitalization.
Data collected on the form included symptoms and physical signs present at
the time of diagnosis of the CHF exacerbation, treatments used, and factors
considered by the investigator to have contributed to the episode. Investigators
also indicated the single most responsible factor for the patient's deterioration.
For the purposes of the present analysis, each episode of worsening CHF was
treated as an independent event.
RESULTS
The demographic and clinical characteristics of patients in the Randomized
Evaluation of Strategies for Left Ventricular Dysfunction Pilot Study who
had 1 or more CHF events (episodes of worsening of CHF) compared with those
who did not are shown in Table 1.
A total of 180 patients experienced a total of 323 CHF events during the 43-week
trial. Patients who experienced CHF events were of similar sex distribution
(approximately 83% were men) and age (approximately 63 years) as those who
did not. Patients in both groups also had a similar duration (approximately
80% had a duration of >12 months) and cause (approximately 70% ischemic) of
CHF. More patients with a CHF event were in NYHA-FC III or IV at baseline
(51%) compared with those without an event (29%).
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Table 1. Demographic and Clinical Characteristics of 768 Patients With
and Without CHF Events in the RESOLVD Pilot Study*
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There were no striking differences in clinical examination findings
at baseline in patients with vs without a CHF event, with the exception of
more peripheral edema and jugular venous distention in patients with a subsequent
CHF event (Table 2).
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Table 2. Clinical Examination Findings at Baseline in Patients With
and Without CHF Events in RESOLVD*
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Nonstudy medications taken by patients in the 48 hours before the CHF
exacerbation are shown in Table 3.
Loop diuretics were received by 92% of patients, digoxin by 76%, acetylsalicylic
acid by 52%, nitrates by 47%, and open-label -adrenergic blocking agents
by 14%.
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Table 3. Nonstudy Medications Taken Just Before the Congestive Heart
Failure Exacerbation*
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Of the 323 CHF events, 143 events required that the patient be hospitalized,
and 180 cases were managed on an ambulatory basis (Table 4). Five patients died in the hospital. Patients gained an
average weight of 1.16 kg compared with baseline. Physical examination revealed
lung crackles in 66% of cases, peripheral edema in 52%, elevation of jugular
venous pressure in 55%, and a third heart sound in 36%. Hospitalized cases
had more crackles (76% vs 56%) and were more likely to have a chest radiograph
performed compared with those not hospitalized (76% vs 21%). Treatments administered
for the exacerbation of CHF included oral diuretics in 56% of cases, intravenous
diuretics in 48%, and addition of a new diuretic in 19%. Intravenous inotropes
were administered in 16% of cases and intravenous digoxin in 10%. Nitrates
were started or increased in 9% of cases. Mechanical ventilation and intra-aortic
balloon pump were used rarely. As expected, hospitalized patients received
intravenous therapy such as diuretics, inotropes, digoxin, and vasodilators
more frequently, although 22% of ambulatory patients also received intravenous
diuretics.
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Table 4. Clinical Presentation and Treatment of 180 Patients With 323
CHF Events*
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Factors that the investigators believed to be associated with exacerbation
of CHF are shown in the "Total" column of Table 5 (items are not mutually exclusive). The most commonly identified
causes of CHF exacerbation were excessive salt intake (22%), other noncardiac
disorders in 20%, study medications (chiefly metoprolol, as indicated by the
investigators) in 15%, use of antiarrhythmic agents in the past 48 hours in
15%, development of arrhythmias in 13%, calcium channel blockers in 13%, and
inappropriate reductions in CHF therapy in 10%. Other precipitants were identified
in 46% of cases and included a variety of potential causes. A review of the
investigators' free-text comments in the latter and "other noncardiac" categories
indicated that upper respiratory tract infections, especially pneumonia, accounted
for 37 events (11% overall). Noncompliance with medications, uncontrolled
hypertension, and coronary ischemia were implicated in only 7%, 2%, and 2%,
respectively. There were no major differences observed in the factors associated
with CHF exacerbation between patients who were hospitalized vs not hospitalized.
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Table 5. Precipitants of CHF Exacerbations*
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The most common primary causes of CHF exacerbations identified by the
investigators were excessive salt intake in 15%, other noncardiac disorders
in 15%, and inappropriate reductions in CHF therapy in 9% (Table 5). The primary precipitant was indicated as "other noncardiac"
or "other" in 15% and 38% of cases, respectively. A review of the free-text
summaries documented in these categories indicated respiratory tract infection
in 31 cases (10% overall), study metoprolol in 16 (5% overall), and excessive
fluid intake in 12 (4% overall). Noncompliance with medications, coronary
ischemia, uncontrolled hypertension, arrhythmias, and other medications were
not commonly indicated as primary causes of worsening CHF.
COMMENT
Congestive heart failure is one of the most common reasons for hospital
admission.12 Yet, for such a clinically and
economically important condition, there are only limited data describing the
precipitants of CHF exacerbation. Careful attention to these factors might
have an important impact in preventing clinical deterioration in these patients.
This study prospectively collected information on acute precipitants,
physical findings, and medications used immediately before and during treatment
for the episodes of acute exacerbation and showed that a variety of potentially
preventable factors led to the decompensation of patients with CHF. Except
for an excess of patients with NYHA-FC III and IV presenting with subsequent
exacerbations (as one might expect), baseline clinical characteristics and
physical findings did not show obvious differences between patients who subsequently
developed CHF events and those who did not. Thus, baseline variables are not
helpful in predicting subsequent events in this group of patients with characteristics
similar to that of the Studies of Left Ventricular Dysfunction Treatment Trial
in terms of sex distribution, age, proportion of patients with an ischemic
origin of CHF, and NYHA-FC.13
The medications taken by patients in the 48 hours before the exacerbation
were as expected for this type of patient, with diuretics, digoxin, acetylsalicylic
acid, and nitrates being used commonly. One major difference between the present
study population and unselected patients with CHF is that all study patients
were receiving an angiotensin-converting enzyme inhibitor or an angiotensin
II antagonist compared with only about half in unselected patients with CHF.14-15 In addition, most patients received
the study -adrenergic blocking agent, its placebo, or an open-label -adrenergic
blocking agent.
Patients presenting with worsening of CHF symptoms had the typical physical
signs of lung crackles, edema, and elevation of jugular venous pressure. At
least some weight gain was associated with most CHF exacerbations. The weight
gain observed was small (1.16 kg), which might be indicative of the fact that
many patients do not weigh themselves daily (and those who do, experience
less weight gain). This simple, important measurement should be used by patients
to help identify the onset of an impending exacerbation of their disease,
and they should seek medical attention before severe cardiovascular compromise
occurs.
As expected, in-hospital treatments administered for CHF exacerbation
required adjustment of therapies, including oral and intravenous diuretics;
initiation or adjustment of vasodilators; initiation of inotropic therapy;
and, for a few, mechanical ventilation and intra-aortic balloon pump. The
nonhospitalized group also had adjustments in diuretic and vasodilator therapies.
Twenty-two percent of nonhospitalized patients received intravenous diuretics,
which might be an important strategy to keep patients out of the hospital.
The most common factors contributing to CHF exacerbation include excessive
salt intake due to lack of knowledge of, or failure to comply with, salt restriction;
other miscellaneous noncardiac disorders; use of inappropriate medications
(antiarrhythmic agents, calcium channel blockers, or inappropriate reductions
in other CHF medications); and development of arrhythmias (primarily tachyarrhythmias).
It is notable that many of these precipitants are avoidable. Study medications,
particularly the -adrenergic blocking agent, or placebo were cited as
the causes of acute exacerbation in 15% of cases. Although long-term -blockade
has now been conclusively demonstrated to improve mortality and morbidity
rates in patients with CHF, it is not clear whether -adrenergic blocking
agents would account for this proportion of acute exacerbations if the patients
were not in a masked study (ie, half of the patients randomized in stage II
received a placebo -adrenergic blocking agent). Taken together, these
factors suggest that measures to prevent worsening of CHF should include patient
education regarding salt intake (preferably by a dietitian) and cautious use
or modification of medications that have negative inotropic properties. In
reviewing the free-text descriptions provided by the investigators, pulmonary
infectious processes were commonly implicated in CHF exacerbation. At least
some of these events would be potentially preventable with the use of pneumococcal
or influenza vaccine. A recent study has shown, however, that pneumococcal
vaccine is underused in this high-risk population.16
Our finding that medication noncompliance, myocardial ischemia, uncontrolled
hypertension, arrhythmia, and the effects of other medications were not common
causes of worsening CHF in this patient population differs somewhat from findings
from other studies. Chin and Goldman,6 in 1997,
reported on causal factors in 435 patients admitted to the hospital for CHF.
In this study, a single investigator retrospectively reviewed the medical
records of patients admitted to the hospital for CHF, looking for possible
precipitants of the event. The most commonly associated reasons for clinical
deterioration were acute anginal chest pain (33%), respiratory tract infection
(16%), uncontrolled hypertension (15%), and noncompliance with medications
(15%) (these categories are not mutually exclusive). The major limitation
of this study was the retrospective nature of the data collection, which depends
on the completeness of medical charting. Information on lifestyle factors
might not be systematically documented. As well, this type of retrospective
analysis cannot accurately determine the temporality or causality of the precipitants,
ie, whether the precipitant was a cause or an effect of CHF exacerbation (eg,
ischemia might cause worsening of CHF symptoms but might also be a result
of it). Ghali et al7 reported on precipitating
factors leading to decompensation of CHF in 101 patients admitted to Cook
County Hospital, Chicago, Ill. Patients were prospectively evaluated through
a systematic patient interview and medical chart review. The most common precipitating
factors identified were lack of compliance with diet, drugs, or both in 64.4%;
uncontrolled hypertension in 43.6%; and cardiac arrhythmias in 28.7% (these
categories are not mutually exclusive). The authors pointed out that their
study population included mostly individuals of low socioeconomic status and
that their results might not be applicable to other patient populations. Opasich
et al8 described patients who were referred
to the CHF service at an Italian hospital in 2 years. In their prospective
analysis of potential causative factors in 328 nonfatal decompensations in
161 patients, the presence of arrhythmias in 24%, infections in 23%, poor
compliance in 15%, and angina in 14% were identified (these categories are
not mutually exclusive). The investigators did not review cases of decompensation
in patients who died because of a stated lack of information surrounding the
event, which might somewhat limit the applicability of the results. It is
also possible that patients referred to their CHF service are not representative
of the general CHF population.
The present study may have underestimated the importance of poor compliance
with CHF medications for 2 reasons. First, the patients participating in this
study were enrolled in a clinical trial. Patients who volunteer to participate
in clinical trials may be more interested in their disease state, and therefore
may be more compliant with their medications. Second, it is known that patient
interview or clinician impression is notoriously insensitive to detect poor
compliance.17 Therefore, poor compliance may
well be an important and often unrecognized factor in CHF exacerbation, and
clinicians should consider the use of alternative data sources, such as pharmacy
records, in patients with poor control of symptoms.
The main strengths of the present study are that it was performed prospectively,
used a systematic approach to elucidate the precipitants of CHF, and was conducted
in 60 clinical centers using a well-defined cohort of patients. Documentation
of the precipitants of CHF in the present study was performed prospectively
using a standardized approach by the study physicians and research nurses
who had been following these patients closely rather than by a third party.
Presumably, study personnel might have had more insight into the patient's
condition antecedent to the exacerbation and thus provided a more accurate
assessment of causality. Another unique feature of the present study is that
it reports on all CHF exacerbations, including those requiring and not requiring
hospitalization. This might be important because knowledge of the acute precipitants
of CHF in all patients (not just those hospitalized) might help prevent hospitalization.
LIMITATIONS
As part of the study protocol, all patients received an angiotensin
II antagonist, an angiotensin-converting enzyme inhibitor, or both. Indeed,
more than 90% of patients reached their target dose. This might differ somewhat
from the real-world situation because many patients do not receive either
of these therapies14-15 or receive
suboptimal doses.18 The Studies of Left Ventricular
Dysfunction Treatment Trial3 showed a 26% relative
risk reduction in death or hospitalization for CHF with enalapril therapy
compared with use of placebo. Therefore, lack of angiotensin-converting enzyme
inhibitor use might be a significant (and preventable) cause of CHF exacerbation;
however, because of the design of the present study, the contribution of this
important variable could not be assessed.
Heart failure exacerbations were identified by the study investigators.
Although the study was regulated by trained research monitors, it is possible,
but unlikely, that some patients with worsening of symptoms (particularly
those not requiring hospitalization) were missed. The precipitants of CHF
exacerbation in the present study were identified within the context of a
clinical trial, which raises the issue of patient selection bias, particularly
for those most likely to be compliant with medical advice.
CONCLUSIONS
Deterioration of clinical status is a common occurrence in patients
with CHF. Such patients are clinically fragile, and a variety of preventable
factors can lead to deterioration, such as excessive salt intake and use of
negative inotropic medications. Ensuring that all patients with CHF receive
vaccination for influenza and pneumococcus might also reduce these causes
of CHF worsening. Health care providers involved in the care of these patients
should be aware of these factors and should take steps to incorporate this
information into the care and education of their patients.
AUTHOR INFORMATION
Accepted for publication March 13, 2001.
Corresponding author and reprints: Ross T. Tsuyuki, BSc(Pharm), PharmD,
MSc, Epidemiology Coordinating and Research (EPICORE) Centre, Division of
Cardiology, University of Alberta, 213 Heritage Medical Research Centre, Edmonton,
Alberta, Canada T6G 2S2 (e-mail: ross.tsuyuki{at}ualberta.ca).
From the Division of Cardiology, University of Alberta, Edmonton (Dr
Tsuyuki); the Division of Cardiology, McMaster University, Hamilton, Ontario
(Drs McKelvie, Kitching, Teo, and Yusuf); the Division of Cardiology, University
of Western Ontario, London (Dr Arnold); the Dante Pazzanese Cardiology Institute
(Drs Avezum and Piegas), the Heart Institute, University of São Paulo
Medical School Hospital (Dr Barretto), and the Paulista School of Medicine,
Federal University of São Paulo (Dr Carvalho), São Paulo, Brazil;
and the Division of Cardiology, University of Calgary, Calgary, Alberta (Dr
Isaac).
REFERENCES
| |
1. Packer M, Cohn JN. Consensus recommendations for the management of chronic heart failure. Am J Cardiol. 1999;83(2A):1A-38A.
2. Bourassa MG, Gurné O, Bangdiwala SI, et al. Natural history and patterns of current practice in heart failure. J Am Coll Cardiol. 1993;22(suppl A):14A-19A.
3. The SOLVD Investigators. Effect of enalapril on survival in patients with reduced left ventricular
ejection fractions and congestive heart failure. N Engl J Med. 1991;325:293-302.
ABSTRACT
4. The Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart
failure. N Engl J Med. 1997;336:525-533.
FREE FULL TEXT
5. McMurray J, Davie A. The pharmacoeconomics of ACE inhibitors in chronic heart failure. PharmacoEconomics. 1996;9:188-197.
ISI
| PUBMED
6. Chin MH, Goldman L. Factors contributing to the hospitalization of patients with congestive
heart failure. Am J Public Health. 1997;87:643-648.
FREE FULL TEXT
7. Ghali JK, Kadakia S, Cooper R, Ferlinz J. Precipitating factors leading to decompensation of heart failure: traits
among urban blacks. Arch Intern Med. 1988;148:2013-2016.
ABSTRACT
8. Opasich C, Febo O, Riccardi G, et al. Concomitant factors of decompensation in chronic heart failure. Am J Cardiol. 1996;78:354-357.
FULL TEXT
|
ISI
| PUBMED
9. Tsuyuki RT, Yusuf S, Rouleau JL, et al. Combination neurohormonal blockade with ACE inhibitors, angiotensin
II antagonists, and beta blockers in patients with congestive heart failure:
design of the Randomized Evaluation of Strategies for Left Ventricular Dysfunction
(RESOLVD) Pilot Study. Can J Cardiol. 1997;13:1166-1174.
ISI
| PUBMED
10. The RESOLVD Investigators. Comparison of candesartan, enalapril, and their combination in congestive
heart failure: the Randomized Evaluation of Strategies for Left Ventricular
Dysfunction (RESOLVD) Pilot Study. Circulation. 1999;100:1056-1064.
FREE FULL TEXT
11. The RESOLVD Investigators. Effects of metoprolol CR in patients with ischemic and dilated cardiomyopathy:
the Randomized Evaluation of Strategies for Left Ventricular Dysfunction Pilot
Study. Circulation. 2000;101:378-384.
FREE FULL TEXT
12. Graves EF. 1993 Summary: National Hospital Discharge Survey. Hyattsville, Md: National Center for Health Statistics; 1995. Advance
Data From the National Center for Health Statistics, No. 264.
13. Johnstone D, Limacher M, Rousseau M, et al. Clinical characteristics of patients in Studies of Left Ventricular
Dysfunction (SOLVD). Am J Cardiol. 1992;70:894-900.
FULL TEXT
|
ISI
| PUBMED
14. The Clinical Quality Improvement Network Investigators. Mortality risk and patterns of practice in 4606 acute care patients
with congestive heart failure: the relative importance of age, sex, and medical
therapy. Arch Intern Med. 1996;156:1669-1673.
ABSTRACT
15. The Large State Peer Review Organization Consortium. Heart failure treatment with angiotensin-converting enzyme inhibitors
in hospitalized Medicare patients in 10 large states. Arch Intern Med. 1997;157:1103-1108.
ABSTRACT
16. Ackman ML, Mason L, Gillespie A, Tsuyuki RT, Teo KK. Impact of type/severity of cardiac disease on vaccine utilization [abstract]. Can J Cardiol. 1998;14(suppl F):130F.
17. Sackett DL, Snow JC. The magnitude of compliance and noncompliance. In: Haynes RB, Taylor DW, Sackett DL, eds. Compliance
in Health Care. Baltimore, Md: Johns Hopkins University Press; 1979:11-22.
18. Chin ML, Wang JC, Zhang JX, Lang RM. Utilization and dosing of angiotensin-converting enzyme inhibitors
for heart failure. J Gen Intern Med. 1997;12:563-566.
FULL TEXT
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ISI
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