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Diagnosing on clinical grounds alone is not recommended because the symptoms of heart failure (breathlessness, exercise intolerance, fatigue, and fluid retention) are often non-specific, while some people with left ventricular dysfunction may be asymptomatic.[1,2]
Echocardiograms measure ventricular function and help make the distinction between abnormalities associated with ventricular contraction (systolic heart failure; left ventricular ejection fraction < 40%) and ventricular filling (diastolic heart failure).[1]
Echocardiograms can also identify surgically correctable causes of symptoms like aortic stenosis.
Other possible causes of heart failure-like symptoms:
Treat underlying conditions which contribute to heart failure, including coronary heart disease, hypertension, diabetes, obesity, obstructive sleep apnoea, smoking, and inactivity.
Drugs known to exacerbate heart failure include nonsteroidal antiinflammatory drugs (including COX-2 selective NSAIDs), calcium-channel blockers (verapamil, diltiazem), thiazolidinediones (pioglitazone, rosiglitazone), tricyclic antidepressants and some antipsychotics (thioridazine).[2–4]
ACE inhibitors relieve symptoms, reduce hospitalisations and improve survival in patients with systolic heart failure and should be used regardless of the severity of heart failure.[5,6]
A meta-analysis found that treating 100 patients with heart failure with an ACE inhibitor for two-and-a-half years prevents seven major events (defined as death, hospitalisation for heart failure or re-infarction).[5]
The benefits of treatment occur in all functional (New York Heart Association) classes of heart failure but are greatest in patients with more severe impairment.
Despite a wealth of evidence demonstrating benefits, ACE inhibitors continue to be under-prescribed in heart failure: ACE inhibitors were prescribed by GPs in 58% of patients over 60 years with heart failure in 19987; more recent general practice data from 2002 revealed prescribing at 32%.8 Concerns about adverse effects, particularly hypotension and renal function, have been cited as barriers to prescribing ACE inhibitors.[9]
Starting an ACE inhibitor at low doses reduces the risk of first-dose hypotension. If lower doses are well tolerated, increase the dose at not less than two-weekly intervals.[2]
While studies with valsartan10 (Diovan), candesartan11 (Atacand) or losartan12 (Cozaar) have shown angiotensin II receptor antagonists† are effective in heart failure, they should only be used in patients who are unable to tolerate ACE inhibitors.[1,2,13]
Angiotensin II receptor antagonists are contra-indicated in patients who have experienced angioedema with an ACE inhibitor.3,13
† No angiotensin II receptor antagonists currently available in Australia are approved for use in heart failure at the time of writing.
Life-threatening hyperkalaemia can occur when ACE inhibitors are used with spironolactone, particularly in the elderly or patients with renal impairment.[15,16] Careful monitoring of potassium is essential.
Contrary to practice some years ago, beta-blockers are now recommended for patients with heart failure as an adjunct to ACE inhibitor therapy at appropriate doses (with or without a diuretic, depending on the presence of fluid overload).[1]
Beta-blockers improve survival in addition to the benefits gained through using ACE inhibitors
Beta-blockers improve survival and decrease hospitalisations.[17–22] Overall, 22 patients need to be treated with a beta-blocker for one year to prevent one death.[23]
Three beta-blockers are approved to treat heart failure: bisoprolol (Bicor), carvedilol (Dilatrend, Kredex) and metoprolol controlled-release (Toprol-XL).
As with ACE inhibitor initiation and dose titration, ‘start low and go slow’ is recommended with beta-blockers. This reduces the risk of hypotension, bradycardia and initial worsening of heart failure symptoms. Increase doses at 2–4 week intervals if the patient has tolerated the lower dose.[2,13] See NPS News 36 for a table of starting doses and target doses for beta-blockers.
A systematic review of disease management programs observed that specialised follow-up and post-discharge support by a multidisciplinary team reduced hospitalisations by 23%.[24] The effect on mortality is less conclusive but an Australian study found a 20% reduction in mortality following multidisciplinary intervention.[25]
Metropolitan and regional hospitals may have specialist heart failure clinics or services. These programs generally have structured educational and counselling components and may also include supervised exercise programs.[1,13]
Patients with heart failure may be suitable candidates for Enhanced Primary Care (EPC) multidisciplinary care planning (items 720–730 of the Medicare Benefits Schedule) and home medicines review.
Regular medical review, coupled with an active role for patients and carers, is essential in promoting adherence to lifestyle measures
Informed, motivated patients who are supported in managing their condition themselves are critical to good care in chronic illnesses.[26] Patients can contribute to managing their heart failure in parallel with medical support—see recommendations below. High-quality information is available for patients (see enclosed insert).
1. National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand. Guidelines on the contemporary management of the patient with chronic heart failure in Australia; 2002.new.heartfoundation.com.au/downloads/cont.management.pdf. Accessed August 2004.
2. The National Collaborating Centre for Chronic Conditions. NICE Guideline No.5, Chronic Heart Failure: National clinical guideline for diagnosis and management in primary and secondary care; 2003.
3. Australian Medicines Handbook 2004.
4. Amabile CM, Spencer AP. Arch Int Med 2004;164:709–20.
5. Flather MD, et al. Lancet 2000;355:1575–81.
6. Garg R, Yusuf S. JAMA 1995;273:1450–6.
7. Krum H, et al. Med J Aust 2001;174:439–44.
8. AIHW GPSCU. SAND abstract No. 38 from the BEACH program 2002–03: Prevalence of chronic heart failure, management and control. Sydney: GPSCU and AIHW; 2003.
9. Phillips SM, et al. Med J Aust 2004;181:78–81.
10. Cohn JN, et al. N Engl J Med 2001;345:1667–75.
11. Granger CB, et al. Lancet 2003;362:772–6.
12. Pitt B, et al. Lancet 2000;355:1582–7.
13. Therapeutic Guidelines: Cardiovascular, Version 4, 2003. North Melbourne: Therapeutic Guidelines Ltd; 2003.
14. American College of Cardiology/American Heart Association. Guidelines for the evaluation and management of chronic heart failure in the adult; 2001.
15. Wrenger E, et al. BMJ 2003;327:147–9.
16. Juurlink DN, et al. N Engl J Med 2004;351:543–51.
17. Packer M, et al. Circulation 2002;106:2194–9.
18. CIBIS investigators. Lancet 1999;353:9–13.
19. Packer M, et al. N Engl J Med 1996;334:1349–55.
20. Australia/New Zealand Heart Failure Research Collaborative Group. Lancet 1997;349:375–80.
21. Hjalmarson A, et al. JAMA 2000;283:1295–302.
22. Poole-Wilson PA, et al. Lancet 2003;362:7–13.
23. National Heart Foundation of New Zealand. A guideline for the management of heart failure: health professionals guide. Auckland: National Heart Foundation of New Zealand; 2001. www.nzgg.org.nz/guidelines/0026/CHF_Guide.pdf. Accessed August 2004.
24. McAlister FA, et al. Am J Med 2001;110:378–84.
25. Stewart S, et al. Arch Int Med 1999;159:257–61.
26. Phillips SM, et al. Med J Aust 2004;181:297–9.
Date published: 2004-11-09 00:00:00
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