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Review of Current Treatment Strategies in Heart Failure

Am Fam Physician. 1999 Jan 15;59(2):443-444.

The prevalence of heart failure is increasing in most developed countries because of aging populations. Older patients are also likely to have more concomitant diseases, complicating treatment. Recently, the goals of therapy have shifted from improving hemodynamic measurements to delaying death and improving the patient's quality of life. Cleland and associates reviewed treatment modalities for patients with heart failure and emphasized the importance of implementing treatment strategies proven effective in clinical trials into community practice.

Diuretics are the most popular form of treatment for heart failure, as they relieve symptoms of fluid overload, such as dyspnea and edema. Studies have shown that these symptoms recur in patients with moderate heart failure when diuretics are withdrawn or an angiotensin converting enzyme (ACE) inhibitor is substituted. Withdrawing diuretics for an extended period of time and substituting an ACE inhibitor may be appropriate in selected patients with mild heart failure, but more research is needed to clarify the optimal use of diuretics. Specifically, should diuretics be used regularly or intermittently, guided by weight gain and evidence of fluid retention? The development of new classes of diuretics and loop diuretics with high bioavailability may renew interest in the use of diuretic therapy for heart failure.

The effectiveness of digoxin therapy in the management of heart failure remains unclear. Findings from one study showed that, in standard dosages, digoxin appears to be safe and was associated with a modest reduction in hospital admissions. Standard dosages, however, may not achieve plasma concentrations in the generally accepted therapeutic range. The therapeutic range for digoxin is narrow, and increasing plasma concentrations are clearly linked to mortality.

The use of ACE inhibitors has been shown to effectively control symptoms, reduce hospital admission and lower the risk of myocardial infarction in patients with left ventricular systolic dysfunction. The benefit of ACE inhibitors has been shown to be dosage-related. Higher dosages appear to be more effective than lower dosages. Many patients with heart failure who should be receiving ACE inhibitors are not, and those who are may be receiving a dosage that is too low. More than one half of the patients with apparent heart failure have normal systolic function in the left ventricle, and the role of ACE inhibitors in these patients is unclear. Beta blockers have been shown to reduce morbidity and mortality in patients with heart failure. However, they can cause an initial exacerbation of heart failure, so they are not currently recommended for use in patients who have severe heart failure or New York Heart Association class IV heart failure. Beta blockers are also contraindicated in patients who have asthma, and their safety in patients older than 75 years who have heart failure has not been established. Beta blockers should be started at a low dosage and gradually titrated to effective levels.

Studies of older calcium-channel blockers showed no benefit in patients with heart failure. More recent studies of newer calcium channel blockers, especially those of felodipine and amlodipine, suggest symptomatic benefit. Other studies have suggested benefit when verapamil or diltiazem is used in conjunction with an ACE inhibitor. Much more research is needed to determine which subgroups of patients, if any, benefit from the use of calcium channel blockers in the management of heart failure related to left ventricular diastolic dysfunction.

The authors conclude that many agents are currently available, enabling physicians to tailor therapy for heart failure more appropriately for individual patients. Ongoing research should overcome many of the current uncertainties and ambiguities in treating this common condition.

Cleland JG, et al. Successes and failures of current treatment of heart failure. Lancet (Suppl 1). August 1998;352:19–28.


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