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