Chronic Heart Failure

128px-Broken_Love_Heart_bandaged_2_nevit.svgI was scheduled to give a tutorial to our clinic’s registrars recently and was requested to talk about chronic heart failure. Uh-oh… didn’t they realise that internal medicine is NOT my forte?? Unfortunately I couldn’t talk them into a gynaecology topic, so CHF it was. But the beauty of teaching is that you always learn something yourself and I’ve certainly picked up a few pearls from preparing this topic. Here’s my summary of the topic, which hopefully will be useful for other self-confessed “hopeless cardiologists”.

So back to basics. What actually IS chronic heart failure?

CHF is essentially an impairment of the ability of the left ventricle to fill with or eject blood. It’s divided into two main types:

  • Systolic heart failure – where LV ejection fraction is <40%, and
  • Heart failure with preserved systolic function (HFPSF) – aka diastolic heart failure, where LVEF is >40% but there is evidence of impaired relaxation and/or raised filling pressure.

What causes it?

The most common cause is heart muscle damage from coronary heart disease. Other common causes include conditions that cause pressure overload (eg aortic stenosis or chronic hypertension) and idiopathic dilated cardiomyopathy. It is less commonly caused by volume overload disorders (eg mitral regurgitation), atrial fibrillation, thyroid disorders and other cardiomyopathies..

What symptoms might my patients present with?

Symptoms include:

  • Dyspnoea
  • Orthopnoea
  • Paroxysmal noctural dyspnoea or nocturnal cough
  • Fatigue
  • Weight gain or loss
  • Peripheral oedema
  • Palpitations / syncope / dizziness

However, it’s important to realise that patients with early heart failure may have no symptoms at all, or might present with vague non-specific symptoms like “I just don’t feel right”. It’s important to consider CHF as a diagnosis in any patient who has risk factors or unexplained vague symptoms, particularly in the older patients (>65 years). Risk factors include: history of cardiovascular disease, hypertension, diabetes, valve disease, cardiomyopathy, excessive ETOH, smoking.

What examination findings support the diagnosis of CHF?

The purpose of the examination is to look for signs of CHF and it’s underlying causes.

Predominantly left sided signs:

  • Pulse (eg compensatory tachycardia, underlying arrhythmias or low volume pulse)
  • BP (chronic hypertension)
  • Tachypnoea or increased work of breathing
  • Displaced apex beat
  • Lung creps (basal, bilateral) & dull basal percussion note
  • Murmurs & s3 gallop

Predominantly right sided signs:

  • Elevated JVP
  • Right ventricular heave
  • Hepatomegaly
  • Peripheral oedema
  • Ascites

Again, note that in early CHF, physical examination may be completely normal.

But, if the symptoms are mild or absent, or the examination is normal, do we really need to bother with investigations? 

Chronic heart failure is common, affecting 1.5-2% of Australians, and becoming even more common with our ageing population. It’s also disabling, progressive and ultimately life threatening. It seems that we are not always that great at diagnosing and treating early CHF and so we’re potentially missing opportunities to instigate disease-modifying treatments in the early stages.

So, yes, if there is any suggestion that the patient may have CHF, it is important to investigate, even in the absence of clinical signs.

So what are the investigations?

The gold standard investigation is echocardiogram, which should be done in every patient with suspected CHF even if all other investigations are normal. It can assess systolic and diastolic function and severity of disease as well as identifying causes such as valve disease and other structural abnormalities.

Other investigations may include:

  • ECG (looking for evidence of ischaemia, conduction defects, arrhythmias and LV hypertrophy)
  • CXR (cardiomegaly, upper lobe vascular diversion, peri-hilar alveolar oedema, Kerley B lines / interstitial oedema and pleural effusions)
  • FBC (? anaemia)
  • UEC (important for monitoring, particularly after commencing therapy)
  • LFTs (may be raised in congestive hepatomegaly)
  • TFTs (particularly in AF)
  • BNP (B type natriuretic peptide) – a useful marker to rule out CHF if it’s negative (<100 ng/L), but not useful as a diagnostic test as it is not very specific. May be helpful as a marker of prognosis and progression.
  • Spirometry
  • Exercise stress test, coronary angiography etc to assess ischaemia

Ok, I’ve made the diagnosis. Now what?

Step one is to classify the severity of the disease, as this influences treatment. Classification is based on the New York Heart Association system, categorised based on functional limitation:

Class I No limitations, ordinary physical activity does not cause undue fatigue, dyspnoea or palpitations (asymptomatic LV dysfunction). 5% 1 year mortality.

Class II Slight limitation of physical activity, ordinary physical activity results in fatigue, palpitation, dyspnoea, or angina (Mild CHF). 10% 1 year mortality.

Class III Marked limitation of physical activity. Less than ordinary physical activity causes symptoms (moderate CHF). 20% 1 year mortality.

Class IV Unable to carry on any physical activity without discomfort. Symptoms of CHF present at rest (severe CHF). 50% 1 year mortality.

What is the best way to improve symptoms? 

The mainstay of symptomatic treatment is loop diuresis. Fortunately, a Cochrane review concluded that, in addition to helping patients feel better, diuretics may also help improve mortality.

  • Commence frusemide
    • Aim for diuresis of 0.5 – 1kg / day
    • Don’t “set and forget”!
    • When euvolaemia is acheived, cease or titrate back to lowest required dose
    • Monitor UEC

Let’s not forget non-pharmacological management. Dietary advice traditionally includes limiting sodium (<2g/day) and fluid restricting to <2L/day to maintain euvolaemia. However – apply this advice with extreme caution, particularly in hot and humid parts of the world where harm from dehydration is a significant risk. Perhaps reserve fluid restriction for severe or resistant cases, taking into account co-morbidities such as renal disease. Caffeine, alcohol and smoking should ideally be minimised or ceased.  Patients can be counselled regarding monitoring their own weight and to seek medical review if they are +/- 2kg from their euvolaemic weight.

This is a pretty deadly disease. How can we save some lives? 

The management recommendations for CHF are primarily referring to systolic heart failure. The drug classes which have been shown improve mortality and slow progression of disease are ACE-inhibitors & angiotensin receptor blockers, B-blockers and aldosterone antagonists. All seem to have roughly similar efficacy with an absolute risk reduction of death and significant morbidity of around 7%, and relative risk reduction for mortality in the ball park of 23-29%.

A suggested approach for all patients with CHF

  • Commence ACE-inhibitor*
    • Eg ramipril, enalapril, quinapril
    • A Meta-analysis of 5 RCTs of ACE-I vs placebo and followed up for an average of 35 months showed mortality rates of 23% vs 26.8%  respectively. NNT = 26
    • Start low and titrate up slowly over weeks-months
    • Change to ARB if intolerant (eg cough)
    • Monitor UEC / potassium
  • Add in beta-blocker*
    • Eg metoprolol, carvedilol, bisoprolol
    • A Meta-analysis of 22 trials of B-blocker vs placebo estimated an absolute risk reduction of around 4% after 12 months. NNT = 25
    • Again, start low and titrate slow, but not until the patient is clinically stable,  ie if requires diuresis, wait for a week or so after euvolaemia is acheived before commencing the B-blocker
  • Consider adding in aldosterone antagonist**
    • RALES trial: Spironolactone vs placebo in class III and IV patients (in addition to ACE-I and diuretics) at 24 months – mortality rates of 35% and 46% respectively. NNT = 10
    • EMPHASIS-HF trial: Eplerenone vs placebo in class II, III and IV patients (in addition to ACE-I and B-blockers) at 21 months – mortality rates of 13% vs 16% respectively. NNT = 34
    • Not recommended if GFR <30mL/min
    • Monitor potassium

*It probably doesn’t matter which drug you pick within the drug class, so just pick your favourite. The guidelines all recommend titrating up to the maximal doses of ACE-I and B-blockers but the evidence for such aggressive dosing is pretty sketchy. Small additional benefits in mortality are balanced by significant increase in harms, and many patients simply won’t be able to tolerate maximal dosing.

**Aldosterone antagonists are prescribed far less frequently than ACE-I and B-blockers but have similar mortality benefits and respresent a great potential for improving heart failure survival. There are no head to head trials of epleronone vs spironolactone, but spironolactone is significantly cheaper so consider using it first, then changing to eplerenone if breast symptoms develop. I highly recommend this great “Tools for Practice” summary on the role of aldosterone antagonists in chronic heart failure, from the Alberta College of Family Physicians.

Digoxin has some improvement in hospitalisations but no great evidence of mortality benefit, with the downside of the associated risks of dig toxicity. However, it may be useful in patients with AF and CHF as a rate controller with some inotropic activity. Isosorbide mononitrate has limited data of benefit when used in combination with hydralazine in patients with ischaemic heart disease, so it’s place in the treatment of chronic heart failure is somewhat unclear. It may be considered if first and second line agents are contraindicated or not tolerated.

Are there any new therapies on the horizon?

Hot off the press are the results from the PARADIGM-HF trial, published in the NEJM last month, comparing and ACE-I (enalapril) against a LCZ696 – a combination ARB (valsartan) & a neprilysin inhibitor (sacubitryl) – in patients with class II, III or IV CHF. The overall mortality was 19.8% in the enalapril group and 17% in the LCZ696 group; a statsitically significant relative risk reduction of ~14%, and absolute risk reduction of 2.8%. However, there is significant debate over the quality of the study design, with concerns raised about the relative under-dosing of enalapril, and the decision to use a run-in study design. Further trials may be needed before LCZ696 can be confidently added to the CHF treatment algorithm.

How do we keep our patients stable?

Aggressively managing precipitating factors is important. For example:

  • Optimise management of CHD and diabetes
  • Aggressively control HTN by adding in a dihydropyridine CCB if required, eg amlodipine or felodipine
  • Control arrythmias – digoxin could be considered first line in patients with AF, and other agents may also need to be added such as amiodarone.
  • Aim for euthyroid
  • Diagnose and treat sleep apnoea
  • Watch and treat for infections (pneumonia, UTI, endocarditis)
  • Correct anaemia
  • Vaccinate for influenza and pneumococcal
  • Consider the need for anticoagulation, particularly in patients with co-existing AF in accordance with CHADS-2 score

And also minimise or avoid prescribing medications which can worsen heart failure:

  • Anti-arrhythmics (other than beta blocker and amiodarone)
  • Non-dihydropyridine calcium channel blockers (verapamil/diltiazem)
  •  TCAs
  • Macrolide ABs
  • NSAIDs, COX-2 inhibitors
  • Clozapine
  • Rosiglitazone/pioglitazone
  • Corticosteroids
  • Moxonidine, TNF antagonists, tyrosine kinase inhibitors, trastuzumab, dronedarone

Is there anything we can specifically do for the HFPSF / diastolic heart failure patients?

This is tricky as there’s not much information to guide specific treatment. Poor diastolic filling may be improved by B-Blockers or verapamil / diltiazem. The main priority is treating underlying causes and managing exacerbating factors.

As opposed to systolic heart failure, use diuretics, venodilators and arterial vasodilators with extreme caution. Also, avoid digoxin and other drugs with inotropic activity.

Who else can help us care for these patients?

Multidisciplinary care is essential. Consider referral to an exercise physiologist to design an appropriate physical activity program. Psychological support is also really important. A GP management plan and Team Care Arrangement may be used to facilitate the allied health team input.

It might be worth getting our cardiology friends involved if there is diagnostic uncertainty, complex co-morbidities or acute decompensations. Referral is also warranted if there is the possibility of structural intervention, eg in valvular disease, when there’s an indication for implantable devices or where there is a potential for transplant in young patients <65.

When are implants or devices indicated?

The main device based therapies are:

  • Implantable cardiac defibrillators
    • Indicated for patients who have been resuscitated from VF / VT
    • Should also be considered in those at high risk of sudden arrhythmias eg patients with LVEF <30% with previous MI, or symptomatic patients with LVEF <35% from any cause
  • Biventricular pacing
    • Shown to improve mortality in patients with class III-IV symptomatic disease, sinus rhythm and with evidence of “ventricular dyssynchrony”

What can we do for patient approaching end-stage disease? 

The average life expectancy after diagnosis of CHF is 3-4 years, so end-of-life management is important, including discussions around advanced care planning. As disease progresses, patients may need interventions such as inotropes, CPAP or BiPAP. Involve palliative care as appropriate.

 My top learning points

  • CHF can be asymptomatic or present with vague, non-specific symptoms and examination may be completely normal. We need to have a low threshold of suspicion and investigate accordingly.
  • Echocardiogram is the gold standard investigation and should be performed even if other investigations are negative.
  • BNP is useful to rule out CHF if it’s negative.
  • Loop diuretics are the mainstay of symptomatic management.
  • ACE-inhibitors and B-blockers (when clinically stable) are recommended for all CHF patients.
  • It probably doesn’t matter drug you pick, but start low, titrate slowly and adjust maximal target dose according to patient side effects.
  • Aldosterone antagonists are perhaps underused and have a great potential to help further improve mortality.

Resources and References

Australian Heart Foundation – 2011 Guidelines for the prevention, detection and management of chronic heart failure in Australia – Full version and Quick Reference Guide

American Heart Association – 2013 ACCF/AHA Guideline for the Management of Heart Failure

Medical Journal of Australia – Management of Heart Failure – 2013

Medical Journal of Australia – Digoxin in Heart Failure and Cardiac Arrhythmias – 2003

Best Science in Medicine Podcast – A Passing Podcast for the Failing Heart, part 1 and part 2 – NB this requires a premium membership but it is well worth the subscription fee for a comprehensive run down of all the evidence

Alberta College of Family Physicians – Tools for Practice: Aldosterone Antagonists in Heart Failure

As always – comments, criticisms and corrections more than welcome.

Many thanks to Casey Parker and Minh Le Cong for pre-publication review and suggestions!  


4 thoughts on “Chronic Heart Failure

  1. Great summary. I hope you feel more confident now Penny. May I ask would you add an echo to the list of tests for someone who comes in saying “I’m tired all the time”? Or maybe a proBNP? I know there is no medicare rebate for the latter.

    • Hi Mark, thanks for reading. I definitely feel a LOT more confident now. The question of adding an echo to the standard investigations for “tired all the time” would probably depend on risk factors and whether there is another obvious cause. In a 30-something mum with a stressful job and 3 young kids who’s got mood symptoms, probably not. But in a 70 year old with CVS risk factors then most likely yes. BNP would be useful it it’s negative but you’re right, the lack of medicare rebate would come in to play for some people.

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