p.73 抽出テキスト

.................................................................................................................................................................... severe, e.g. >124 mmol/L, and in the absence of symptoms. As the pathogenesis of hyponatraemia in HF is dilutional, e.g. caused by water retention induced by increased vasopressin secretion, treatment is based on water restriction or vasopressin antagonists. Fluid restrictions to less than 8001000 mL/day may be indicated to achieve a negative water balance and treat hyponatraemia. Water restriction was associated with improved QOL in a small, randomized study but with only slight increases in serum sodium in an observational registry.780,781 Tolvaptan, an orally active selective arginine vasopressin V2 receptor antagonist, can be considered to increase serum sodium and diuresis in patients with persistent hyponatraemia and congestion. However, no effects on outcomes have been shown in RCTs782785 (see Supplementary text 13.1). The infusion of hypertonic saline combined with loop diuretics was associated with an increase in serum sodium levels and greater diuretic efficacy in small trials and observational studies.786788

Hypochloraemia (<96 mmol/L) is a powerful independent predictor of mortality in patients with acute and chronic HF.439,789792 Serum chloride may have a direct role in the control of renin secretion and the response to loop or thiazide diuretics.439,793 The carbonic anhydrase inhibitor acetazolamide increases chloride reabsorption causing a greater bicarbonate and sodium excretion in the proximal tubule of the nephron. It can increase serum chloride levels and diuresis in patients with severe HF at risk of diuretic resistance.145,794 It is currently being tested in a multicentre randomized study in decompensated HF.469

13.8 Lung disease, sleep-disordered

breathing Overall, COPD affects about 20% of patients with HF and has a major impact on symptoms and outcomes.795797 Due to the overlap in symptoms and signs, the differentiation between HF and COPD may be difficult. Pulmonary function testing with spirometry is recommended as the first diagnostic tool and should be considered in patients with suspected COPD. For adequate interpretation, it should be performed in stable and euvolaemic patients to avoid congestion related to obstructive pulmonary function patterns. If there is uncertainty about the reversibility of airflow obstruction, pneumology referral for more sophisticated tests (bronchodilatatory test, bronchial provocation tests, diffusion capacity) is warranted.798,799 Treatment of HF is generally well tolerated in COPD.800 Betablockers can worsen pulmonary function in individual patients but are not contraindicated in either COPD or asthma, as stated in the Global initiative for chronic Obstructive Lung Disease (GOLD) and the Global INitiative for Asthma (GINA), respectively.801,802 GINA states that asthma should not be regarded as an absolute contraindication to the use of cardioselective beta-blockers (bisoprolol, metoprolol succinate, or nebivolol) with consideration of relative risks and benefits. In clinical practice, starting with low doses of cardioselective beta-blockers combined with close monitoring for signs of airway obstruction (wheezing, shortness of breath with lengthening of the expiration) should be encouraged. Although not tested in HF patients, inhaled corticosteroids and beta-adrenergic agonists do not seem to increase CV events, including HF, in patients at high risk.803,804 Moreover, optimal COPD management can improve cardiac function.805

Sleep-disordered breathing occurs in more than one third of patients with HF and is even more prevalent in patients with AHF. The most common types are: central sleep apnoea (CSA, similar to Cheyne-Stokes respiration), OSA, and a mixed pattern of the two. CSA and OSA have been shown to be associated with a worse prognosis in HF. OSA is associated with an increased risk of incident HF in men. CSA is the most common form of sleep-disordered breathing in HFrEF and HFmrEF is the most common cause of CSA.806,807 Patients with HF can be investigated for sleep-disordered breathing. History taking should involve partners. Questionnaires are instrumental in identifying patients at risk. Home monitoring can usually identify and distinguish the type of sleep apnoea. However, overnight polysomnography remains the definitive investigation.807 The use of adaptive servo-ventilation in patients with HFrEF and predominantly CSA is not recommended, based on the results of SERVE-HF, which was neutral regarding the composite primary endpoint of death from any cause or lifesaving CV intervention, but showed an increase in both all-cause mortality and CV mortality with adaptive servo-ventilation.808 Transvenous phrenic nerve stimulation was tested in a prospective, multicentre, randomized trial involving 151 patients with CSA.809 The primary efficacy endpoint was the reduction of the apnoea-hypopnoea index from baseline to 6 months and was achieved by a larger percentage of patients with the active treatment. Other measurements of sleep quality and QOL were improved and no difference in any safety endpoint was found between active treatment and control.809 Similar results were observed in the 96 patients with HF.810 Patients with HFrEF being considered for a sleep-disordered breathing treatment with positive pressure airway mask must undergo formal sleep study to document the predominant type of sleep apnoea (central vs. obstructive). When sleep-disordered breathing is caused by OSA, nocturnal hypoxaemia can be treated with nocturnal oxygen supplementation, continuous positive airway pressure, bi-level positive airway pressure, and adaptive servoventilation. However, none of these interventions has been shown to have beneficial effects on outcomes in HF.807 When sleepdisordered breathing is caused by CSA, positive pressure airway masks are contraindicated in HFrEF patients.808 In these patients, implantable phrenic nerve stimulation can be considered for symptomatic relief.

13.9 Hyperlipidaemia and lipid-modifying

therapy Two large RCTs, including mainly patients with HFrEF, as well as a meta-analysis of 24 RCTs, showed no benefit of statin treatment on CV mortality or stroke in patients with HFrEF.811,812 A reduction in HF hospitalizations as well as a small reduction in MI was observed in a meta-analysis of the CORONA and GISSI-HF trials.813815 Based on current evidence, routine administration of statins in patients with HF without other indications for their use (e.g. CAD) is not Downloaded from academic.oup.com/eurheartj/article/42/36/3599/6358045 by guest on 07 October 2026