Management of heart failure requires a multimodal approach. It involves a combination of lifestyle modifications, medications, and possibly the use of devices or surgery. It may be noted that treatment can vary across continents and regions.
Lifestyle changes
People with heart failure, also known as congestive heart failure (CHF), are educated to undertake various non-pharmacological measures to improve symptoms and prognosis. Such measures include:Smith A, Aylward P, Campbell T, et al. Therapeutic Guidelines: Cardiovascular, 4th edition. North Melbourne: Therapeutic Guidelines; 2003. Moderate physical activity, when symptoms are mild or moderate; or bed rest when symptoms are severe. In individuals with heart failure, increasing physical activity offers significant prognostic benefits for the secondary prevention of the condition. If sleep apnea is identified, treat with CPAP, BiPAP, dental appliances or surgery. Sleep apnea is an under-recognized risk factor for heart failure. Uncontrolled sleep apnea may increase the risk of heart failure by up to 140%. Weight reduction – through physical activity and dietary modification, as obesity is a risk factor for heart failure and left ventricular hypertrophy. Effective weight management has been shown to significantly improve the heart's functional status and reduce the risk of all-cause mortality. Monitor weight – this is a parameter that can easily be measured at home. Rapid weight increase is generally due to fluid retention. Weight gain of more than 2 pounds is associated with admission to the hospital for heart failure. Sodium restriction – excessive sodium intake may precipitate or exacerbate heart failure, thus a "no added salt" diet (60–100 mmol total daily intake) is recommended for patients with CHF.
Fluid restriction According to a review in 2009, there is apparently no evidence of benefit of fluid restriction in patients with clinically stable heart failure otherwise receiving optimal pharmacological treatment. The same review suggested that clinicians still choosing to restrict fluid intake for patients with HF should consider an individualized fluid prescription, potentially based on patient body weight, sodium intake, and likelihood of adherence.
Generally water intake should be limited to 1.5 L daily or less in patients with hyponatremia, though fluid restriction may be beneficial regardless in symptomatic reduction.
Medication There is a significant evidence–practice gap in the treatment of CHF; particularly the underuse of ACE inhibitors and β-blockers and aldosterone antagonists which have been shown to provide mortality benefit. Treatment of CHF aims to relieve symptoms, to maintain a euvolemic state (normal fluid level in the circulatory system), and to improve prognosis by delaying progression of heart failure and reducing cardiovascular risk. Medications used include: diuretic agents, vasodilator agents, positive inotropes, ACE inhibitors, beta blockers, and aldosterone antagonists (e.g., spironolactone). SGLT2 inhibitors have also shown positive therapeutic outcomes. Some medications which increase heart function, such as the positive inotrope milrinone, lead to increased death, and are contraindicated.
Angiotensin-modulating agents Unless contraindicated or not tolerated, ACE inhibitor (ACEi) therapy is recommended for all patients with systolic heart failure, irrespective of symptomatic severity or blood pressure.National Institute for Clinical Excellence. Chronic heart failure: management of chronic heart failure in adults in primary and secondary care. Clinical Guideline 5. London: National Institute for Clinical Excellence; 2003 Jul. Available from: www.nice.org.uk/pdf/CG5NICEguideline.pdf ACE inhibitors improve symptoms, decrease mortality and reduce ventricular hypertrophy. Angiotensin II receptor antagonist therapy (also referred to as AT1-antagonists or angiotensin receptor blockers), particularly using candesartan, is an acceptable alternative if the patient is unable to tolerate ACEi therapy. ACEIs and ARBs decrease afterload by antagonizing the vasopressor effect of angiotensin, thereby decreasing the amount of work the heart must perform. It is also believed that angiotensin directly affects cardiac remodeling, and blocking its activity can thereby slow the deterioration of cardiac function.
A number of studies have been done to investigate whether ACEi plus ARB is better than an ACEi treatment alone in reducing death, disability or hospital admission in CHF with systolic dysfunction. The two largest studies were CHARM-Added and Val-HeFT. The conclusion of a Cochrane Database systematic review, which included these two studies and five others, was that combining ACEi treatment with ARB was not effective in reducing total mortality RR 0.98 [95% CI 0.9, 1.06] or cardiovascular mortality RR 0.93 [95% CI 0.84, 1.03] when compared with single therapy of an ACEi. Combined therapy did reduce HF-related hospital admissions with an absolute risk reduction of 4.4% but also increased discontinuation of medication due to adverse effects with an absolute risk increase of 3.7%. In plain English, 23 people would need to be treated to reduce one hospitalisation for HF while treating 27 people would harm one person with adverse effects. Thus, combined therapy does not improve mortality and may slightly increase morbidity.
Diuretics Diuretic therapy is indicated for relief of congestive symptoms. Several classes are used, with combinations reserved for severe heart failure: Loop diuretics (e.g. furosemide, bumetanide) – most commonly used class in CHF, usually for moderate CHF Thiazide diuretics (e.g. hydrochlorothiazide, chlorthalidone, chlorthiazide) – may be useful for mild CHF, but typically used in severe CHF in combination with loop diuretics, resulting in a synergistic effect. Potassium-sparing diuretics (e.g. amiloride) – used first-line use to correct hypokalaemia. Spironolactone is used as add-on therapy to ACEI plus loop diuretic in severe CHF. Eplerenone is specifically indicated for post-MI reduction of cardiovascular risk.
If a heart failure patient exhibits a resistance to or poor response to diuretic therapy, ultrafiltration or aquapheresis may be needed to achieve adequate control of fluid retention and congestion. The use of such mechanical methods of fluid removal can produce meaningful clinical benefits in patients with diuretic-resistant heart failure and may restore responsiveness to conventional doses of diuretics.
Newly emerging evidence showed that glucocorticoids could be used in the treatment of decompensated heart failure to potentiate renal responsiveness to diuretics, especially in heart failure patients with refractory diuretic resistance with large dose of loop diuretics. Glucocorticoids induce a potent diuresis in heart failure because they could improve renal responsiveness to atrial natriuretic peptide by upregulating natriuretic peptide receptor A NPR-A expression in the renal inner medullary collecting duct, inducing a potent diuresis.
Beta blockers Until recently (within the last 20 years), β-blockers were contraindicated in CHF, owing to their negative inotropic effect and ability to produce bradycardia – effects which worsen heart failure. However, current guidelines recommend β-blocker therapy for patients with systolic heart failure due to left ventricular systolic dysfunction after stabilization with diuretic and ACEI therapy, irrespective of symptomatic severity or blood pressure. As with ACEI therapy, the addition of a β-blocker can decrease mortality and improve left ventricular function. Several β-blockers are specifically indicated for CHF including: bisoprolol, carvedilol, nebivolol and extended-release metoprolol. The antagonism of β1 inotropic and chronotropic effects decreases the amount of work the heart must perform. It is also thought that catecholamines and other sympathomimetics have an effect on cardiac remodeling, and blocking their activity can slow the deterioration of cardiac function.
Positive inotropes Digoxin (a mildly positive inotrope and negative chronotrope), once used as first-line therapy, is now reserved for control of ventricular rhythm in patients with atrial fibrillation; or where adequate control is not achieved with an ACEI, a beta blocker and a loop diuretic. There is no evidence that digoxin reduces mortality in CHF, although some studies suggest a decreased rate in hospital admissions. It is contraindicated in cardiac tamponade and restrictive cardiomyopathy.
The inotropic agent dobutamine is advised only in the short-term use of acutely decompensated heart failure, and has no other uses.
Phosphodiesterase inhibitors such as milrinone are sometimes utilized in severe cardiomyopathy. The mechanism of action is through inhibiting the breakdown and thereby increasing the concentration of cAMP similar to beta adrenoreceptor agonism, resulting in inotropic effects and modest diuretic effects.
Alternative vasodilators The combination of isosorbide dinitrate/hydralazine is the only vasodilator regimen, other than ACE inhibitors or angiotensin II receptor antagonists, with proven survival benefits. This combination appears to be particularly beneficial in CHF patients with an African American background, who respond less effectively to ACEI therapy.
Aldosterone receptor antagonists The RALES trial showed that the addition of spironolactone can improve mortality, particularly in severe cardiomyopathy (ejection fraction less than 25%.) The related medication eplerenone was shown in the EPHESUS trial to have a similar effect, and it is specifically labelled for use in decompensated heart failure complicating acute myocardial infarction. While the antagonism of aldosterone will decrease the effects of sodium and water retention, it is thought that the main mechanism of action is by antagonizing the deleterious effects of aldosterone on cardiac remodeling.
Recombinant neuroendocrine hormones Nesiritide, a recombinant form of B-natriuretic peptide, is indicated for use in patients with acute decompensated heart failure who have dyspnea at rest. Nesiritide promotes diuresis and natriuresis, thereby ameliorating volume overload. It is thought that, while BNP is elevated in heart failure, the peptide that is produced is actually dysfunctional or non-functional and thereby ineffective.
Vasopressin receptor antagonists Tolvaptan and conivaptan antagonize the effects of antidiuretic hormone (vasopressin), thereby promoting the specific excretion of free water, directly ameliorating the volume overloaded state, and counteracting the hyponatremia that occurs due to the release of neuroendocrine hormones in an attempt to counteract the effects of heart failure. The EVEREST trial, which utilized tolvaptan, showed that when used in combination with conventional therapy, many symptoms of acute decompensated heart failure were significantly improved compared to conventional therapy alone although they found no difference in mortality and morbidity when compared to conventional therapy.
SGLT2 inhibitors