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with AF, the percentage of effective biventricular pacing (without fusion or pseudofusion) is an important focus. Further details on CRT follow-up and optimization are outlined in an HFA position paper.435

6.2.5 Other cardiac implantable electronic devices

In a small unblinded RCT, cardiac contractility modulation marginally improved peak oxygen uptake and QoL in patients with advanced HFrEF and a QRS <130 ms.438 In a small pilot study, cardiac contractility modulation improved the Kansas City Cardiomyopathy Questionnaire (KCCQ) score by 18 points in patients with HFpEF.439 No clinical outcome studies have emerged. Similarly, baroreceptor activation therapy led to improvements in 6-min walk distance and QoL in an unblinded RCT, but long-term clinical outcome data were neutral.440,441 Current evidence for these CIEDs is insufficient to support guideline recommendations. Although promising, these findings require confirmation in large, well-designed trials.439

6.2.6 Other implantable devices

It has been hypothesized that an interatrial shunt could improve HF symptoms and outcomes by decompressing the left atrium. In the RELIEVE-HF study, 508 patients with HF and predominantly NYHA class III symptoms and any LVEF were randomized to transcatheter shunt implantation vs a sham procedure.442 After 2 years, no difference emerged in the primary effectiveness outcome [hierarchical composite ranking of all-cause death, cardiac transplantation or LV assist device (LVAD) implantation, HFH, outpatient WHF events, and change in QoL]. Importantly, patients with reduced LVEF had fewer adverse CV events with shunt treatment, whereas patients with HFpEF had more CV events. In the REDUCE LAP-HF II study in patients with LVEF ≥40%, the atrial shunt device was no better than the sham procedure in terms of the hierarchical composite of CV death or nonfatal ischaemic stroke at 12 months, rate of total HF events up to 24 months, and change in QoL at 12 months.443

7 Decompensated heart failure

7.1 Definition and epidemiology

Decompensated HF is defined as acute or gradual onset of symptoms and/or signs of HF, severe enough to require urgent medical attention and treatment initiation or intensification. DHF can lead to an unplanned hospital admission, an emergency department visit, or an unplanned ambulatory visit requiring treatment for HF. DHF may present as either worsening of preexisting HF or as the initial manifestation of the disease (de novo HF). In the setting of patients with pre-existing HF, WHF is characterized by a deterioration in the symptoms and/or signs of HF and represents an event in HF progression, whereas DHF is specifically characterized by the requirement for treatment modification.444 Decompensated HF is associated with a high risk of death: 3%–10% during HF admission; 20%–30% at 1 year, >50% after 5 years.445–450 Compared to DHF occurring in patients with preexisting HF, de novo DHF may be associated with higher inhospital death, but lower post-discharge death and rehospitalization rates.451–453 Following a hospitalization for DHF, 1-year rehospitalization rates range between 35% and 44%.447,448,453–455 In addition, up to 50% of patients with HF require intensification of treatment in the emergency service or in outpatient settings.456–462

7.2 Diagnosis

Decompensated HF requires prompt diagnosis to ensure early treatment.463 If DHF is suspected, assessment of signs and symptoms of congestion and hypoperfusion must be done at the first medical contact. Non-invasive blood pressure, respiratory rate, pulse oximetry monitoring, body temperature measurement, and ECG should be performed early.464 In haemodynamically unstable patients with suspected hypoperfusion, assessment of serum lactate levels should be performed promptly.465 The currently recommended, non-age-adjusted, natriuretic peptide ‘rule-out’ thresholds for DHF are: NT-proBNP <300 pg/mL, or BNP <100 ng/mL, or MR-proANP <120 pg/mL.157,466–469 However, if clinical suspicion of HF remains despite values below ‘rule-out’ thresholds, specialist assessment and echocardiogram should be sought. Age-related thresholds for NT-proBNP, above which DHF is considered ‘likely’, are given in the footnote of Figure 11. In the older population, using the age-related NT-proBNP threshold may aid appropriate triage and help reduce unnecessary exams. NT-pro-BNP >5000 pg/mL indicates very high risk, and admission is generally recommended. For other laboratory tests and investigations for patients with suspected DHF, see Supplementary data online, Table S11. Initial investigations are carried out to diagnose DHF and rapidly detect any possible triggers. Transthoracic echocardiography should be performed in patients with high levels of NT-proBNP and in those for whom there is a high clinical suspicion of DHF. Where trained personnel are available, lung ultrasound identifies patients with pulmonary congestion and has utility in serial assessments.470–473

7.3 Clinical presentation

Congestion and hypoperfusion are two major clinical manifestations of DHF.447,453 Congestion may stem from fluid overload, fluid redistribution, increased vascular permeability, and increased intracardiac pressures. Different clinical, laboratory, and imaging utilities should be used to assess congestion and its dynamic changes (see Supplementary data online, Table S12). Hypoperfusion is not a synonym for hypotension,474,475 although patients with DHF and hypotension also experience inadequate perfusion. An objective marker, serum lactate, may help identify patients with peripheral hypoperfusion and monitor therapy.465 Signs and symptoms associated with congestion and hypoperfusion are reported in Table 12. Four categories of DHF can be recognized based on clinical presentation: decompensated left-sided HF, decompensated right-sided HF, acute pulmonary oedema (APO), and cardiogenic shock (CS). Pathophysiology, timing of onset, and speed of deterioration differ between the four categories, but possible overlaps exist.

7.3.1 Decompensated left-sided heart failure

Decompensated left-sided HF, in its classical clinical presentation, is characterized by a gradual onset of signs and symptoms with accumulating congestion as the primary pathophysiological process.476 It may occur in patients across the spectrum of LVEF and, in advanced stages, can lead to RV dysfunction and Downloaded from academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehag100/8766302 by guest on 31 August 2026