Management of heart failure

Management of heart failure requires a multimodal approach. It involves a combination of lifestyle modifications, medications, and possibly the use of devices or surgery. People with CHF are educated to undertake various non-pharmacological measures to improve symptoms and prognosis. Such measures include: 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. 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. Drugs used include: diuretic agents, vasodilator agents, positive inotropes, ACE inhibitors, beta blockers, and aldosterone antagonists (e.g., spironolactone). Some drugs which increase heart function, such as the positive inotrope milrinone, lead to increased mortality, and are contraindicated. Unless contraindicated or not tolerated, ACE inhibitor (ACE) therapy is recommended for all patients with systolic heart failure, irrespective of symptomatic severity or blood pressure. 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 or cardiovascular mortality RR 0.93 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. Diuretic therapy is indicated for relief of congestive symptoms. Several classes are used, with combinations reserved for severe heart failure: