|
Henry Krum, Andrew M Tonkin, Robert Currie, Robert Djundjek and Colin
I Johnston
MJA 2001; 174: 439-444
For editorial comment, see Horowitz & Stewart; see also Krum
Abstract -
Methods -
Results -
Discussion -
Acknowledgements -
Reference -
Authors' details
-
-
More articles on Cardiology and cardiac surgery
Abstract |
Objectives: To investigate the frequency and
general practitioner awareness of patients with chronic heart
failure (CHF), and to evaluate a cardiac algorithm and document
cardiac investigations performed in establishing this
diagnosis.
Design and setting: Between March and August 1998,
consecutive patients aged 60 years and older presenting to their GP
were assessed. In patients previously diagnosed with CHF, aetiology
and diagnostic assessments were documented. In patients with
suspected CHF (by a standardised algorithm, based on World Health
Organization guidelines), further investigations and GP diagnosis
were recorded.
Patients: 80 consecutive patients were assessed by each
of 341 GPs throughout Australia, reflecting the Australian
metropolitan/rural population mix of 1996. This provided a total of
22 060 evaluable patients.
Main outcome measures: Estimated numbers of patients
with CHF in general practice (previously and newly diagnosed); major
aetiological factors; use of ancillary diagnostic tests; drugs
prescribed.
Results: CHF was diagnosed in 2905 of 22 060 patients
(13.2%) (2485 previously diagnosed and 420 newly diagnosed). Major
aetiological factors were ischaemic heart disease and
hypertension. Echocardiography had been performed in 64% of
previously diagnosed patients, but was performed in only 22% of
possible CHF patients. Angiotensin-converting enzyme (ACE)
inhibitors were prescribed in 58.1% of patients with CHF. Patients
with evidence of left ventricular dysfunction were more likely to
have received ACE inhibitors.
Conclusions: CHF appears to be very common in the elderly,
based on GP diagnosis of the condition. Of 100 patients aged 60 years
and over presenting to their GP, two new cases of CHF will be detected
using a simple clinical algorithm in conjunction with appropriate
diagnostic tests. ACE inhibitors appear to be underutilised.
|
| |
Chronic heart failure (CHF) is a debilitating condition with high
morbidity and mortality, and is a major public health burden. Its
prevalence is increasing,1 despite a reduction in
age-standardised mortality associated with cardiovascular
diseases such as myocardial infarction and stroke.2 Factors
implicated in this increased prevalence include the ageing of the
population, decreased mortality rates following myocardial
infarction, and more frequent diagnosis of CHF after investigations
such as echocardiography.3 The epidemiology of CHF in Australia has been assumed to be similar to
that in the United States,4-6 the United
Kingdom7-10 and Europe.11,12 However,
substantive data have been lacking, and the approach taken to
diagnosis of patients with suspected CHF in general practice in
Australia is also unknown.
Similarly, although international studies have suggested marked
underutilisation of angiotensin-converting enzyme (ACE)
inhibitors and β-blockers,4-11,13-17 no evaluation of
use of drug therapies for CHF in Australia has been reported.
Accordingly, the aims of the Cardiac Awareness Survey and Evaluation
(CASE) Study were:
- to investigate the frequency,
awareness, and aetiology of heart failure in general practice in
Australia;
- to document cardiac investigations used by general practitioners
in establishing the diagnosis of CHF; and
- to determine prescribing patterns in the treatment of CHF by
Australian GPs.
As the prevalence of heart failure increases steeply with age, the
study focused on people aged 60 years and older.
|
| |
|
Recruitment into the CASE study | |
GPs were recruited solely on the basis of interest in participating in
the study. Interest was first ascertained by the local
pharmaceutical representative of the study sponsor (see
Acknowledgements). The CASE steering committee then sent
interested GPs a formal letter of invitation to participate in the
study. GPs agreeing to participate attended a local education and
information session. These sessions were spread across all
Australian States and Territories with a mix of metropolitan, rural
and remote regions in an effort to recruit a sample of GPs (and thus
patients) representative of their distribution.
Each GP was asked to assess 80 consecutive patients aged 60 years or
older for the possibility of heart failure.
GPs were recruited from March 1998, data were collected
prospectively and the study was completed in August 1998.
|
Assessment for CHF | |
New patients: Patients not previously diagnosed as having CHF were
assessed for that possibility using modified World Health
Organization criteria (Box 1).18 Alternative conditions
that may have contributed to these symptoms and signs were recorded.
In patients suspected of having CHF based on the above criteria,
further investigations (chest x-ray [CXR], electrocardiogram
[ECG], and echocardiogram) were suggested (but not mandated). GPs
were also asked to note any investigations that had been performed in
the previous 12 months. For patients who had an echocardiogram, the GP
was asked to indicate whether there was evidence of systolic or
diastolic ventricular dysfunction (or both) from the
echocardiogram report.
At the conclusion of this process, the GPs assessed whether they
thought the patient had CHF.
Previously diagnosed patients: For patients who had previously been
diagnosed as having CHF by their GP, records were retrospectively
analysed for clinical and diagnostic criteria that contributed to
that diagnosis. These included use of ECG, CXR and echocardiography,
hospital admission for heart failure, and specialist referral for
CHF.
|
Pharmacotherapy |
For patients with previously diagnosed CHF, GPs were asked to
document current drug therapy specifically prescribed for this
condition (name of drug, daily dose, and frequency of
administration). For patients with newly diagnosed CHF, GPs were
asked whether they instituted pharmacotherapy immediately and what
that pharmacotherapy comprised.
A dosage equivalence table of commonly prescribed ACE inhibitors was
compiled, and prescribing was divided into low, medium and high
doses. To determine prescribing according to decade of life,
prescribing was assessed in patients aged 60-69 years (n =
569), 70-79 years (n = 1360), and 80 years and older (n =
976). GP prescribing in patients with echocardiographic evidence of
systolic or diastolic left ventricular dysfunction was
specifically determined.
Initial pharmacotherapy prescribed for patients diagnosed with CHF
as part of the CASE study was evaluated. Because of the
cross-sectional nature of the assessment in CASE, most of these
patients did not have the opportunity to be up-titrated to target
doses of drugs. For this reason, newly diagnosed patients were not
included in the analysis of dose of ACE inhibitor prescribed.
|
| | |
Of 523 GPs who originally expressed interest in participating, 341
completed the study. Their geographical distribution (78%
metropolitan, 22% rural or remote) was similar to that observed for
all Australian GPs (77% metropolitan, 23% rural or remote).
In all, 23 845 patients were entered into the study. Of these, 1785 were
excluded from analysis because of patient refusal or missing data,
leaving 22 060 who made up the baseline population.
|
Baseline demographics | |
The distribution of the CASE patient population by area (capital
city, 58.7%; metropolitan, 10.7%; rural, 21.4%; remote, 1.2%; 8%
unclassified) was similar to the 1996 Australian population aged 60
years or older.19 However, there were fewer
rural patients among the CASE cohort than in the census population.
The total CASE study population comprised 45% men and 55% women; 8612
(39%) were aged 60-69 years (48% men), 9371 (42.5%) were aged 70-79
years (45% men) and 4077 (18.5%) were aged 80 years or older (39% men).
|
Patients not previously diagnosed with CHF | |
Box 2 shows the assessment process and results for the 22 060 patients.
In the 4807 patients assessed as having possible CHF, at least one
further investigation was performed in 2903 (60.4%). To determine
whether the CASE audit itself may have prompted further
investigation of these patients, the tests were divided into those
ordered within the previous 12 months and those ordered subsequent to
the CASE audit. Investigations ordered within the 12 months before
the CASE audit were ECG in 1953 (40.6%), CXR in 1894 (39.4%), and
echocardiogram in 366 patients (7.6%). Investigations subsequent
to the CASE clinical assessment were performed in 488 patients who had
ECGs (10.2%), 493 who had CXR (10.2%), and 466 who had echocardiograms
(9.7%).
The diagnosis of CHF was based on symptoms in 73%, signs in 66%,
causative factors in 61%, and investigations in 49% (not mutually
exclusive). Presence of at least one symptom and one causative factor
had the highest sensitivity for detection of new heart failure (323 of
the 420 [76.9%] new cases of heart failure). The sensitivity of the
other diagnostic groupings for possible heart failure were > 2
symptoms, 68.6%; > 2 signs, 47.3%; > 1 symptom and > 1
sign, 68.6%; > 1 sign and > 1 causative factor, 66.9%.
Possible false negative diagnoses: Of the 4807 patients who met
diagnostic criteria for suspected CHF, 466 underwent
echocardiography after the CASE audit (when systolic, diastolic or
no dysfunction was specifically noted). Of these 466 patients, 108
had an echocardiographic report of left ventricular systolic or
diastolic dysfunction. However, despite this objective evidence of
ventricular dysfunction, GPs diagnosed CHF for only 77 of these 108
patients.
Possible false positive diagnoses: Of the 420 patients newly
diagnosed as having CHF, 162 underwent echocardiography. Nineteen
of these 162 patients (11.7%) had no evidence of left ventricular
systolic or diastolic dysfunction on this test, yet were still
classified as having CHF by their GP.
|
Patients previously diagnosed as having CHF | |
CHF had been previously diagnosed in 2485 of the baseline population
of 22 060 (11.3%). Both electrocardiograms and CXRs had been
performed in 96% of the patients previously diagnosed as having heart
failure, and 64% had had echocardiography performed. For these
patients, in the previous 12 months:
- 1640 patients (66%) had been
referred to a specialist;
- 1744 patients (70%) had either not been admitted to hospital with CHF
or their hospitalisation status was unknown; and
- of the 741 patients admitted for CHF, 459 (62%) had one admission, 165
(22%) had two admissions, and 58 (8%) had three admissions. Six
patients (1%) had been admitted 10 or more times for CHF.
|
CHF patients in the CASE study | |
At the end of the study, 2905 of the 22 060 baseline population (13.2%)
were considered to have CHF: 2485 (11.2%) with a previous diagnosis,
and 420 (1.9%) with a new diagnosis. The prevalence of CHF in these
patients was closely related to age group (Box 3).
The cardiovascular diagnoses that may be contributing to CHF in these
patients are summarised in Box 4. Hypertension and ischaemic heart
disease were major comorbidities and potential aetiological
factors in both the new and previously diagnosed cohorts.
|
Pharmacotherapy |
Specific CHF pharmacotherapy for the 2905 patients with CHF is
summarised in Box 5. Most patients were receiving diuretics and ACE
inhibitors. Alternatives to ACE inhibitors in patients who can not
tolerate this medication include nitrates and hydralazine
(prescribed for 0.6%) and/or angiotensin II receptor antagonists
(prescribed for 4.3%).
β-Blockers were prescribed for 12% of patients. Less than 50% of
β-blocker prescribing was of the non-selective, vasodilating
β-blocker carvedilol, approved for CHF in Australia.
The dose of ACE inhibitor was determined in patients previously
diagnosed as having CHF (Box 6). Based on our dosage equivalence
table, prescribed doses were low in 60%, medium in 31%, and high in 9% of
patients.
Prescribing according to echocardiographic findings:
Pharmacotherapy prescribed for CHF according to left
ventricular (LV) systolic (found in 932 patients) or diastolic
(found in 376 patients) dysfunction is summarised in Box 5. The
presence of LV dysfunction on echocardiography resulted in higher
prescribing of ACE inhibitors than in the overall patient cohort.
However, the frequency of ACE inhibitor prescribing was not
different between the systolic and diastolic LV dysfunction groups.
Furthermore, there were very few differences among other agents in
these groups according to systolic or diastolic LV dysfunction.
Prescribing according to decade of life: Prescribing of drug therapy
specifically for CHF according to decade of life is summarised in Box
5. ACE inhibitor prescribing was unaltered in the very elderly (≥
80 years). Prescribing of β-blocker demonstrated an age-dependent
decrease, whereas prescribing of digoxin and diuretics (thiazide
and loop) demonstrated an age-dependent increase.
Prescribing in patients with newly diagnosed CHF: Use of
pharmacotherapy among newly diagnosed CHF patients was less than
that observed in patients with previously diagnosed CHF. In
particular, only 51% of newly diagnosed patients were prescribed ACE
inhibitors, 37% diuretics, 17% received calcium-channel blockers,
10% digoxin and 8% β-blockers.
|
| |
We undertook a clinical algorithm approach to the possible diagnosis
of CHF. By identifying possible CHF based on the grouping of symptoms,
signs and causative factors, we demonstrated an 8.7% rate of
identification of CHF (420 of 4807 patients). Although this approach
resulted in a relatively low rate of successful diagnosis of CHF, the
algorithm used was entirely clinical with a very simple screening
process. Our results suggest that, of 100 patients aged 60 years or
older presenting to a GP, two will have previously undetected CHF that
can be simply diagnosed by attention to clinical symptoms and signs in
conjunction with appropriate diagnostic tests.
|
Prevalence of CHF | |
We found somewhat higher rates of CHF patients (13.2%) than in earlier
general practice based studies.4,7-9 Specifically,
reported prevalence of CHF among patients aged 65 years or older in UK
general practice ranged from 2.8%9 to 8.0%.7 The higher rate
in the CASE study may reflect the differing methods by which the
diagnosis of CHF was made (eg, patient file review,4,9 morbidity
registry8), greater use of objective
testing (ie, echocardiography in our patient cohort), or our study
being a more representative sample of the true CHF population than
previous geographically restricted studies performed in the US or
UK.
In contrast to the above assessments of CHF frequency, population
studies where echocardiographic ventricular dysfunction was the
main criterion for diagnosis detected fewer CHF patients within
these age groups than in the CASE study.10,12
Numbers of CHF patients in the CASE Study increased dramatically with
each decade of life — more than 20% of patients aged 80 years or older
were diagnosed with CHF. Given the ageing of the population, these
findings have important implications for resource allocation.
|
Aetiology |
The aetiology of CHF was as expected, with a major contribution from
ischaemic heart disease and previous myocardial infarction, as well
as hypertension. Hypertension was a major contributor to CHF in the
Framingham study,20,21 but less so in analysis
of the Studies of Left Ventricular Dysfunction (SOLVD)22 and other,
more recent data.23 The major contribution of
hypertension in the CASE cohort may reflect the advanced age of the
population studied, in which hypertension is a frequent
comorbidity.
|
Investigations |
Use of ECG and CXR was high, and echocardiography was used in more than
half the patients. The lower use of echocardiography (despite
recommendations by major organisations such as WHO)18 may reflect
lack of full knowledge of the sensitivity and specificity of this
diagnostic test, concerns regarding expense, and difficulty with
access.
|
Pharmacotherapy |
Use of ACE inhibitors: ACE inhibitor prescribing by Australian GPs
ranges from 51%-71% of CHF patients, depending on the specific
population studied. Prescribing of ACE inhibitor was more likely in
patients in whom ventricular dysfunction had been objectively
documented. These findings are consistent with international
studies, in which prescribing of ACE inhibitors ranges from 10% to
60%.5,6,8-10,14-17 ACE inhibitors reduce morbidity and mortality across the entire
spectrum of CHF severity, including in patients with asymptomatic
systolic left ventricular dysfunction.24-26 Therefore, all
patients with systolic left ventricular dysfunction should be
receiving ACE inhibitors unless contraindicated or intolerant.
Lack of compliance with these prescribing recommendations may
relate to contraindications to ACE inhibitor therapy (ie, bilateral
renal artery stenosis) or observed side effects such as
hyperkalaemia or cough. Furthermore, ACE inhibitors are not of
proven benefit in patients with diastolic CHF. Definitive diastolic
dysfunction on echocardiography comprised only a small percentage
in the CASE study, although the true percentage is undoubtedly
considerably higher. Potential alternatives to ACE inhibitors in
patients who are ACE intolerant or have contraindications include
angiotensin II receptor antagonists and hydralazine (the latter as
part of the hydralazine/nitrate combination). However, only 4.3% of
patients were taking angiotensin II receptor antagonists and 0.6%
were taking hydralazine. Our findings suggest that, despite the
definitive data supporting the use of ACE inhibitors in CHF, these
agents are still being underutilised.
Dose of ACE inhibitors: Submaximal doses of ACE inhibitors were
prescribed for those patients who are taking these drugs. The major
clinical trials conducted in patients with CHF (SOLVD,24
CONSENSUS25) and LV dysfunction
post-MI (SAVE27) used much higher doses
(150 mg of captopril or 20-40 mg of enalapril) than the median and mean
doses prescribed in this study. Doses prescribed by Australian GPs
were generally lower than both the target and achieved ACE inhibitor
doses used in these major trials.
There are a number of reasons why the recommended target doses may not
be achieved in general practice. First, patients may not tolerate the
highest dosage because of hypotension, particularly if
up-titration is rapid. Second, because these agents improve
symptomatology, patients may become asymptomatic at lower doses of
drug and the need to go to higher doses not be entertained in an
asymptomatic patient. Finally, until recently, there has been no
clear evidence that higher doses offer substantial clinical
benefits over and above the use of ACE inhibitors at lower doses. The
ATLAS study28
demonstrated a reduction in the combined
endpoint of death/heart failure related hospitalisation with
lisinopril 32.5-35 mg daily compared with lisinopril 2.5-5 mg daily.
Mortality alone was reduced by 8% in the high-dose lisinopril
subgroup. Although this reduction is modest, it does suggest that an
attempt should be made to maximise ACE inhibitor dosage in every
patient.
β-Blockers: Prescribing of β-blockers was low, despite
overwhelming evidence supporting the benefits of these agents in
patients with New York Heart Association (NYHA) Class II-III
symptoms.29-31 However, much of this
evidence has only been published subsequent to the completion of the
CASE study.30,31 Prescribing of the β-blocker vasodilator carvedilol occurred in
fewer than half the patients receiving β-blockers. As carvedilol is
the only β-blocker approved in Australia for CHF, this suggests that
much of the prescribing of β-blockers for the CASE cohort was for
indications other than CHF (eg, ischaemic heart disease and
hypertension). As GPs in Australia are not permitted to prescribe
carvedilol, our observed rate of use of β-blockers reflects
specialist prescribing.
Factors affecting prescribing: In patients with a definitive
diagnosis of ventricular dysfunction by echocardiography,
prescribing of ACE inhibitor therapy was higher than for the overall
CASE CHF cohort. This may reflect more confidence with the cause of
patient symptomatology as being related to CHF. Alternatively, it
may be that a GP who is more likely to perform echocardiography to
diagnose CHF is also more likely to prescribe best-practice
pharmacotherapy.
It was also noteworthy that the difference in overall prescribing for
systolic versus diastolic dysfunction in these patients appeared
similar, although many of the agents (eg, ACE inhibitors) are not of
proven benefit in diastolic CHF. Furthermore, some drugs, such as
non-dihydropyridine calcium-channel blockers, are relatively
contraindicated in patients with systolic heart failure, yet
prescribing rates were similar for the entire patient cohort.
Conversely, these agents may be of particular benefit in diastolic
heart failure, but again prescribing rates appeared similar to the
entire patient cohort.
There was no reduction in prescribing of ACE inhibitor with each
decade of life, suggesting that GPs supported the use of these agents
in CHF management in the very elderly (≥ 80 years). Very few data
exist to support the use of ACE inhibitors in this group of patients,
although studies are currently being conducted. In contrast,
β-blocker use declined with each decade of life, suggesting less
comfort in prescribing these agents for older patients. Increased
digoxin and diuretic use with advanced age may reflect the need to
increasingly prescribe these agents for comorbidities such as
atrial fibrillation and oedema of other causes.
|
Study limitations | |
The CASE study had a number of potentially significant limitations.
- Selection of GPs was not random, but was based on interest in
undertaking the study. This could introduce significant bias, and
therefore we have not classified our evaluation as a prevalence or
incidence study. Nevertheless, every effort was undertaken to
ensure a representative distribution of general practices
according to State, regional area and metropolitan versus rural
practice.
- The study has also demonstrated the difficulty in making a clinical
diagnosis of CHF. Diagnosis of CHF was left to the clinical judgement
and decision of the GP. We noted a significant false positive and
negative rate using documented left ventricular dysfunction on
echocardiogram as the "gold standard" of CHF in conjunction with
relevant signs, symptoms and causative factors. This is a limitation
of many surveys of this type, in which the diagnosis is made based on
subjective clinical criteria.4,9
- A further limitation may have been the algorithm used to assist the GP
in making the diagnosis. This clinical algorithm approach has not
been used previously in the diagnosis of CHF. Therefore, the
possibility exists of patients being wrongly assigned as having CHF
using this approach. This is particularly true as echocardiography
was not mandated for all patients. Nevertheless, this algorithm did
yield an extra two new CHF patients for every 100 patients aged 60 years
and older studied in this way.
|
| |
The CASE study was supported by the National Heart Foundation of
Australia and the Royal Australasian College of General
Practitioners.
The CASE Management Committee wish to thank all 341 GPs who
participated in the CASE study and Servier Laboratories, Australia,
who provided input into the study design as well as financial and
logistical assistance in the conduct of the study. Servier
Laboratories were not involved in the analysis of data. In addition,
the Committee acknowledges the expert statistical assistance
provided by Dr Chris Reid and Mr Stephen Lim (Baker Medical Research
Institute, Prahran, VIC).
|
| |
|
- Bonneaux L, Barendregt J, Meeter K, et al. Estimating clinical
morbidity due to ischemic heart disease and congestive heart
failure: the future risk of heart failure. Am J Public Health
1994; 84: 20-28.
-
Waters A-M, Bennett S. Mortality from cardiovascular disease in
Australia. Cardiovascular Disease Series No. 3. Canberra:
Australian Institute of Health and Welfare, 1995.
-
McGovern PG, Pankow JS, Shahar E, et al. Recent trends in acute
coronary heart disease. Mortality, morbidity, medical care and risk
factors. N Engl J Med 1996; 334: 884-890.
-
Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart
failure: the Framingham Study. J Am Coll Cardiol 1993; 22:
6A-13A.
-
Gardin JM, Siscovick D, AntonCulver H, et al. Sex, age and disease
affect echocardiographic left ventricular mass and systolic
function in the free-living elderly: the Cardiovascular Health
Study. Circulation 1995; 91: 1739-1748.
-
Lauer MS, Evans JC, Levy D. Prognostic implications of subclinical
left ventricular dilatation and systolic dysfunction in men free of
overt cardiovascular disease (the Framingham Heart Study). Am J
Cardiol 1992; 70: 1180-1184.
-
Mair FS, Crowley TS, Bundred P. Prevalence, aetiology and
management of heart failure in general practice. Br J Gen Pract
1996; 46: 77-79.
-
Morbidity statistics from general practice. 4th National Survey,
1991-92. Royal College of General Practitioners, Office of
Population Census and Survey and Department of Health and Social
Security. London: HMSO, 1995.
-
Parameshwar J, Shackell MM, Richardson A, et al. Prevalence of
heart failure in three general practices in west London. Br J Gen
Pract 1992; 42: 287-289.
-
McDonagh TA, Morrison CE, Lawrence A, et al. Symptomatic and
asymptomatic left-ventricular systolic dysfunction in an urban
population. Lancet 1997; 350: 829-833.
-
Ambrosio GB, Riva LM, Casiglia E. Prevalence, clinical features
and prognosis of congestive heart failure (CHF) in the elderly. A
survey from a population in Veneto region. Acta Cardiologica
1994; 49: 324-325.
-
Mosterd A, Bruijne de MC, Hoes AW, et al. Usefulness of
echocardiography in detecting left ventricular systolic
dysfunction in population based studies (The Rotterdam Study).
Am J Cardiol 1997; 79: 103-104.
-
Hillis GS, Trent RJ, Winton P, et al. Angiotensin-converting
enzyme inhibitors in the management of congestive heart failure: are
we ignoring the evidence? Q J M 1995; 89: 145-150.
-
Mosterd A, Hoes AW, de Bruijne MC, et al. Prevalence of heart
failure and (a) symptomatic left ventricular dysfunction in the
general population. The Rotterdam Study. Eur Heart J 2001; in
press.
-
Bart BA, Gattis WA, Diem SJ, O'Connor CM. Reasons for underuse of
angiotensin-converting enzyme inhibitors in patients with heart
failure and left ventricular dysfunction. Am J Cardiol 1997;
79: 1118-1120.
-
Newman J, Ahmed O, Hyngstrom T, et al. Heart failure treatment with
angiotensin converting enzyme inhibitors in hospitalized Medicare
patients in 10 large states. Arch Int Med 1997; 157:
1103-1108.
-
Stafford RS, Saglam D, Blumenthal D. National patterns of
angiotensin converting enzyme inhibitor use in congestive heart
failure. Arch Intern Med 1997; 157: 2460-2464.
-
World Health Organization/Council on Geriatric Cardiology Task
Force on Heart Failure Education. Concise guide to the management of
heart failure. Geneva: WHO/CGC, 1997; 6-9. Available at
<http://www.who.int/ncd/cvd/concguid.pdf>.
-
Rural, remote and metropolitan areas classification. 1991
Census Edition. Canberra: AGPS, 1994.
-
McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history
of congestive heart failure: the Framingham Study. N Engl J Med
1971; 285: 1441-1446.
-
Kannel WB, Belanger JA. Epidemiology of heart failure. Am
Heart J 1991; 121: 951-956.
-
Bangdiwala SI, Weiner DH, Bourassa MG, et al. Studies of Left
Ventricular Dysfunction (SOLVD) Registry: rationale, design,
methods and description of baseline characteristics. Am J
Cardiol 1992; 70: 347-353.
-
Teerlink JR, Goldhaber SZ, Pfeffer MA. An overview of
contemporary etiologies of congestive heart failure. Am Heart J
1991; 121: 1852-1853.
-
The SOLVD Investigators. Effect of Enalapril on survival in
patients with reduced left ventricular ejection fraction and
congestive heart failure. N Engl J Med 1991; 325: 293-302.
-
The CONSENSUS Trial Study Group. Effects of enalapril on
mortality in severe congestive heart failure. Results of the
Cooperative North Scandinavian Enalapril Survival Study
(CONSENSUS). N Engl J Med 1987; 3161: 1429-1435.
-
Nicklas JM, Pitt B, Timmis G, et al. Effect of enalapril on
mortality and the development of heart failure in asymptomatic
patients with reduced left ventricular ejection fractions. N
Engl J Med 1992; 327: 685-691.
-
Pfeffer MA, Braunwald E, Moye LA, et al. Effect of captopril on
mortality and morbidity in patients with left ventricular
dysfunction after myocardial infarction. Results of the Survival
and Ventricular Enlargement Trial. N Engl J Med 1992; 327:
821-828.
-
Packer M, Poole-Wilson PA, Armstrong PW, et al. Comparative
effects of low and high doses of the angiotensin-converting enzyme
inhibitor, lisinopril, on morbidity and mortality in chronic heart
failure. ATLAS Study Group. Circulation 1999; 100:
2312-2318.
-
Packer M, Bristow MR, Cohn JN, et al. The effect of carvedilol on
morbidity and mortality in patients with chronic heart failure. N
Engl J Med 1996; 334: 1349-1355.
-
CIBIS II investigators and committees. The cardiac
insufficiency bisoprolol study II (CIBIS II): a randomised trial.
Lancet 1999; 353: 9-13.
-
Effect of metoprolol CR/XL in chronic heart failure: Metoprolol
CR/XL Randomised Intervention Trial in Congestive Heart Failure
(MERIT-HF). Lancet 1999; 353: 2001-2007.
(Received 24 Dec 1999, accepted 28 Oct 2000)
|
| |
Alfred Hospital, Melbourne, VIC.
Henry Krum, PhD, FRACP, Associate Professor, Clinical
Pharmacology Unit, Department of Epidemiology and Preventive
Medicine, and Department of Medicine, Monash University.
National Heart Foundation of Australia, Melbourne, VIC.
Andrew M Tonkin, MD, FRACP, Director, Health, Medical and
Scientific Affairs.
North East Valley Division of General Practice, Melbourne, VIC.
Robert Currie, MB BS, FRACGP, Director.
Servier Laboratories, Melbourne, VIC.
Robert Djundjek, BSc, Manager, Scientific Projects.
Austin and Repatriation Medical Centre, Melbourne, VIC.
Colin I Johnston, MD, FRACP, Professor and Head, Department
of Medicine, University of Melbourne.
Reprints will not be available from the authors.
Correspondence:
Professor C I Johnston, Baker Medical Research Institute, Prahran,
VIC 3181.
Make a
comment
| | |
| | | |
|
1: Modified World Health Organization18 criteria for
assessment of possible chronic heart failure
Symptoms:
Dyspnoea, chronic fatigue, oedema, and exercise intolerance. Signs: Third
or fourth heart sounds, heart murmur, cardiomegaly, pulmonary crackles,
raised jugular venous pressure, and dependent oedema. Causative factors:
Angina, previous myocardial infarction, hypertension, valvular heart disease/rheumatic
fever, and cardiomyopathy. Patients were considered to have possible CHF
if they had:
|
| |
> 2 symptoms,
> 2 signs,
> 1 symptom and > 1 sign, or
> 1 symptom and > 1 causative factor. |
|
|
| | Back to text | | | | | | Back to text | | | | | | Back to text | | | | | | Back to text | | | |
| 5: Percentage (95% CI) of patients with
chronic heart failure prescribed each class of drug, by evidence of left
ventricular dysfunction, and by age group |
| |
|
|
|
| |
|
Left ventricular dysfunction* |
| |
All patients |
|
| |
(n = 2905) |
Systolic (n = 932) |
Diastolic (n = 376) |
|
| Diuretics (thiazide, loop) |
63.3 (62.4-64.2) |
60.3 (58.7-61.9) |
62.2 (59.7-64.7) |
| ACE inhibitor |
58.1 (57.2-59.0) |
70.7 (69.2-72.2) |
70.5 (68.1-72.9) |
| Digoxin |
31.3 (30.4-32.2) |
35.0 (33.4-36.6) |
33.2 (30.8-35.6) |
| beta-Blocker |
11.8 (11.2-12.4) |
13.9 (12.8-15.0) |
17.8 (15.8-19.8) |
| CCB-DHP |
10.1 (9.5-10.7) |
11.1 (10.1-12.1) |
12.0 (10.3-13.7) |
| CCB-NDHP |
10.0 (9.4-10.6) |
10.3 (9.3-11.3) |
11.2 (9.6-12.8) |
| Aspirin |
10.3 (9.7-10.8) |
9.3 (8.3-10.3) |
9.6 (8.1-11.1) |
| Warfarin |
7.7 (7.2-8.2) |
8.2 (7.3-9.1) |
8.8 (7.3-10.3) |
| Spironolactone |
8.1 (7.6-8.6) |
6.9 (6.1-7.7) |
1.0 (0.5-1.5) |
| Hydralazine |
0.6 (0.5-0.7) |
0.2 (0.1-0.3) |
0.0 (0.0-0.0) |
| AIIA |
4.3 (3.9-4.7) |
6.4 (5.6-7.2) |
7.7 (6.3-9.1) |
|
|
|
|
|
Age group (years) |
|
|
|
60-69 (n = 569) |
70-79 (n = 1360) |
≥80 (n = 976) |
|
| Diuretics (thiazide, loop) |
57.1 (55.0-59.2) |
62.1 (60.8-63.4) |
68.4 (66.9-69.9) |
| ACE inhibitor |
58.7 (56.6-60.8) |
58.0 (56.7-59.3) |
58.1 (56.5-59.7) |
| Digoxin |
24.8 (23.0-26.6) |
29.9 (28.7-31.1) |
37.2 (35.7-38.7) |
| beta-Blocker |
14.1 (12.6-15.6) |
13.2 (12.3-14.1) |
8.4 (7.5-9.3) |
| CCB-DHP |
9.5 (8.3-10.7) |
11.0 (10.2-11.8) |
9.0 (8.1-9.9) |
| CCB-NDHP |
10.2 (8.9-11.5) |
11.0 (10.2-11.8) |
11.2 (10.2-12.2) |
| Aspirin |
10.0 (8.7-11.3) |
11.4 (10.5-12.3) |
8.9 (8.0-9.8) |
| Warfarin |
9.5 (8.3-10.7) |
8.8 (8.0-9.6) |
5.0 (4.3-5.7) |
| Spironolactone |
6.7 (5.7-7.7) |
8.8 (8.0-9.6) |
8.0 (7.1-8.9) |
| Hydralazine |
1.1 (0.7-1.5) |
0.6 (0.4-0.8) |
0.3 (0.1-0.5) |
| AIIA |
3.5 (2.7-4.3) |
5.4 (4.8-6.0) |
3.4 (2.8-4.0) |
|
| * According to echocardiography. ACE = angiotensin-converting
enzyme. CCB-DHP = calcium-channel blocker - dihydropyridine. CCB-NDHP =
calcium-channel blocker - non-dihydropyridine. AIIA = angiotensin II receptor
antagonist. |
|
| | Back to text | | | | | | Back to text |
|
