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PHARMACOLOGICAL TREATMENT OF HEART FAILURE (HF) - page 7 / 48

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CLASS IIB recommendations

Placement of an implantable cardioverter-defibrillator might be considered in patients without HF who have non-ischemic cardiomyopathy and an LVEF less than or equal to 30% who are in NYHA functional Class I with chronic optimal medical therapy and have a reasonable expectation of survival with good functional status for more than 1 year. (Level of Evidence: C)

CLASS III recommendations

Digoxin should not be used in patients with low EF, sinus rhythm, and no history of HF symptoms, because in this population, the risk of harm is not balanced by any known benefit. (Level of Evidence: C)

Use of nutritional supplements to treat structural heart disease or to prevent the development of symptoms of HF is not recommended. (Level of Evidence: C)

Calcium channel blockers with negative inotropic effects may be harmful in asymptomatic patients with low LVEF and no symptoms of HF after MI (Level of Evidence: C)

PATIENTS WITH LEFT VENTRICULAR DYSFUNCTION WITH CURRENT OR PRIOR SYMPTOMS (STAGE C)

General Measures

Measures listed as class I recommendations for patients in stages A and B are also appropriate for patients with current or prior symptoms of HF.

In addition, moderate sodium restriction is indicated, along with daily measurement of weight, to permit effective use of lower and safer doses of diuretic drugs.

Immunization with influenza and pneumococcal vaccines may reduce the risk of a respiratory infection. Although most patients should not participate in heavy labor or exhaustive sports, physical activity should be encouraged, except during periods of acute decompensation or in patients with suspected myocarditis, because restriction of activity promotes physical deconditioning, which may adversely affect clinical status and contribute to the exercise intolerance of patients with HF13.

Three classes of drugs can exacerbate the syndrome of HF and should be avoided in most patients:

13 Chati Z, Zannad F, Jeandel C, et al. Physical deconditioning may be a mechanism for the skeletal muscle energy phosphate metabolism abnormalities in chronic heart failure. Am Heart J 1996;131:560–6.

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