Diuretics in Chronic Heart Failure

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Diuretics in Chronic Heart Failure

Diuretics are used to achieve and maintain euvolaemia (the patient’s ‘dry weight’) with the lowest possible dose. This means that the dose must be adjusted, particularly after restoration of the dry body weight, to avoid the risk of dehydration, which leads to hypotension and renal dysfunction.10 It is important that treatment with diuretics is always coupled with neuro-hormonal system blocking, in order to slow down the progress of the disease.

In general, due to their greater effectiveness, loop diuretics, such as furosemide, are the mainstay of diuretic therapy in HF. Indeed loop diuretics produce more intense and shorter diuresis than thiazides, which results in more gentle and prolonged diuresis. They are, however, less effective in patients with reduced kidney function.10 As a general rule, doses of loop diuretics should be as low as possible, in order to maintain a euvolaemic state. Restricting the amount of sodium and water, daily weight monitoring and avoidance of NSAIDs are critical in preventing salt and water retention.

The commonly used loop diuretics only act for a short time, so common therapy schemes require twice-daily administration, in order to avoid post-diuretic rebound sodium retention.

Furosemide is by far the most common oral loop diuretic, but patients with resistance to oral furosemide therapy may benefit from trials with second-generation oral loop diuretics (bumetanide and torasemide). These may be more efficacious, due to their increased oral bioavailability and potency. The longer half-life of torasemide may limit the previously described rebound phenomenon.11 In the prospective TORasemide In Chronic heart failure (TORIC) study, the use of torasemide was associated with lower mortality than furosemide in patients with HF. Furthermore, torasemide has been reported to attenuate LV remodelling in patients with congestive HF (CHF) to a greater extent than furosemide.12 Torasemide has also been reported to attenuate LV remodelling in patients with HF to a greater extent than furosemide.13 Although international guidelines do not define which diuretic should be preferred, there is not enough strong evidence to recommend torasemide and bumetanide over furosemide in HF.

Careful monitoring and supplementation of electrolytes, particularly potassium and magnesium, are a crucial aspect of loop diuretic therapy.

Randomised clinical trials have shown that potassium-sparing diuretics are able to reduce both hospitalisations and mortality in patients with chronic HF, although they are less useful than loop diuretics in cases of acute decompensate HF.14 Aldosterone levels are elevated in patients with acute decompensated heart failure (ADHF) despite the use of angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and beta-blockers. In this setting, aldosterone elevation may contribute to cardiorenal dysfunction, increasing the risk of death and ventricular arrhythmias.15,16

Studies have shown benefits using aldosterone antagonists in HF using non-diuretic doses of mineralcorticoid receptor antagonists. The objective was to completely inhibit the angiotensin–aldosteron axis. In the Emphasis-HF study, a double-blinded trial enrolling patients with chronic HF and low ejection fraction (EF), the aldosterone antagonist eplerenone compared with placebo showed a significant reduction in deaths from all causes, hospitalisation for HF and of the primary outcome (cardiovascular death or hospitalisation for HF).17

For these reasons, their use is strongly recommended in patients with HF. Their greater usefulness, as has already been mentioned, is not their diuretic properties, but their ability to antagonise the many harmful effects of hyperaldosteronism on the cardiovascular system. There are few studies in the literature describing the usefulness of high diuretic doses of aldosterone antagonists in ADHF in order to overcome congestion. In a exploratory study in ADHF patients, high doses of mineralcorticoid receptor antagonists (in more detail, about 100 mg spironolactone) were safe and were also associated with an earlier resolution of the congestive signs and with a more pronounced N-terminal of the prohormone brain natriuretic peptide (NT-proBNP) reduction.18

Potassium-sparing diuretics have the disadvantage that their use results in a greater incidence of hyperkalaemia. However, when combined with loop diuretics, as happens frequently in clinical practice, this side effect is greatly reduced.

After overcoming the acute phase of HF, in selected subgroups it will be possible to make an attempt to withdraw diuretics. A history of hypertension, baseline furosemide dose of >40 mg/day, and a low LVEF (<27 %) were independent predictors of diuretic restarting.19

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