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Congestive heart failure

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired (1)

  • caused by structural or functional abnormalities of the heart
  • around 920,000 people in the UK today have been diagnosed with heart failure
  • the incidence and prevalence of heart failure increase steeply with age, and the average age at diagnosis is 77
  • overall prevalence of heart failure is rising because of population ageing and increasing rates of obesity

Heart failure (HF) is a syndrome and not a single pathological process in which there is impairment of the heart as a pump supporting physiological circulation (1,2). Patients with heart failure will have the following features:

  • symptoms typical of heart failure e.g. - breathlessness and exhaustion at rest or with less than the normal degree of exertion, fatigue and
  • signs of fluid retention e.g. - pleural effusion, increased JVP, peripheral oedema and
  • objective evidence of an abnormality of the structure or function of the heart at rest e.g. - cardiac murmurs, third heart sound (3)

The functional reserve of the heart is grossly reduced and there are associated changes in many organ systems.

Heart failure may be described as acute or chronic:

  • acute heart failure - a rapid onset or change in the following signs and symptoms:
    • dyspnoea
    • oedema, either pulmonary or peripheral
    • organ underperfusion
    • tachycardia
  • chronic heart failure may be more insidious:
    • chronic exercise limitation

Due to the confusion in the rate of onset and duration of symptoms in acute and chronic HF, the European Society of Cardiology suggested that HF could more accurately be described as new onset, transient, or chronic (2).

A syndrome which may present similarly to heart failure is seen in patients with normal hearts who have extreme pressure or volume stresses.

Following the evidence of benefit for ARNIs (angiotensin receptor-neprilysin inhibitor) and sodium glucose transporter 2 inhibitor (SGLT2i) in heart failure with reduced ejection fraction (HFrEF) McMurray et al proposed:

an algorithm for chronic heart failure in HFrEF (heart failure with reduced ejection fraction) in patients whom diuretic therapy has achieved euvolemia (4):

  • Step 1: Simultaneous initiation of a beta-blocker and an sodium glucose transporter 2 inhibitor (SGLT2i)

  • Step 2: Addition of sacubitril/valsartan, within 1-2 weeks of Step 1. If SBP <100 mmHG, it may be prudent to first evaluate tolerance with an ARB before switching to ARNI (angiotensin receptor-neprilysin inhibitor)

  • Step 3: Addition of an mineraolocorticoid receptor antagonist (MRA), within 1-2 weeks of Step 2, if renal function is not severely impaired and serum potassium levels are normal. MRAs may also be initiated in Step 2 in patients with troublesome hypotension.

The algorithm can be individualized to specific circumstances and is most appropriate for outpatients.

Caution is required in hospitalized patients with decompensated HF.

This approach achieves treatment with beta-blocker, SGLT2i, ARNI and MRA within 4 weeks. Up-titration to target doses should be pursued after this period.

The algorithm is based on five principles:

1) magnitude of the treatment benefit of each individual drug class is independent of the treatment benefits of other drug classes

2) foundational drugs are effective in reducing morbidity and mortality at low starting doses

3) addition of a new drug class to the treatment yields greater benefit than up-titrating existing drug classes - target doses are often only modestly more effective in comparison with starting doses in reducing risk of CV death

4) safety and tolerability can be improved by proper sequencing of drug classes

5) much of the benefit of foundational treatments can be seen within 30 days

Therapy with all four drug classes should therefore be achieved within 4 weeks.

The conventional approach assumes that clinical trials tested the efficacy and safety of each drug class in presence of all background therapies at target doses - however the majority of patients in heart failure trials were actually receiving sub-evidence based doses of recommended treatment (4,5). Also, if considering trials such as DAPA-HF and EMPEROR-reduced, then substantial proportion of patients were not treated with an MRA or ARNI.

McMurray and Packer expect that this will prevent HF death and HF hospitalizations and will enhance the tolerability of concurrently or subsequently administered treatments.


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