Diuretics in Diastolic Heart Failure Patients
Abstract & Commentary
Synopsis: Furosemide withdrawal is almost always successful and is associated with improved diastolic filling and improved blood pressure homeostasis.
Source: van Kraaij DJ, et al. Am J Cardiol 2000; 85:1461-1466.
There is controversy regarding the role of diuretics in heart failure due to diastolic dysfunction. Although reducing pulmonary or systemic congestion, if present, may be desirable, reducing preload could lower cardiac output and exacerbate symptoms of fatigue or cause orthostatic intolerance. Thus, van Kraaij and associates hypothesized that in stable patients with heart failure and normal systolic function, withdrawal of furosemide therapy would be safe and have positive effects on functional and hemodynamic status. To test this hypothesis, they performed a placebo-controlled trial of furosemide withdrawal in 32 elderly patients (mean age, 75 years) with a history of congestive heart failure (CHF) on furosemide (20-80 mg/d) but currently without evidence of congestion; and an ejection fraction of more than 40% (mean, 60%). Evaluations of the patients were done three months after withdrawal of furosemide. Recurrent CHF occurred in two of the 21 patients in the withdrawal group (10%) and in one of the 11 patients in the continued furosemide group (9%). Two patients in the withdrawal group restarted furosemide for ankle edema and one because of hypertension. Symptom scores, blood pressure, six-minute walk test, and quality of life were not different at three months between the two groups. In those successfully withdrawn, Doppler E/A ratio increased from 0.68 to 0.79 (P < 0.01) and the decrease in standing systolic blood pressure changed from -8 to +5 mmHg (P < 0.05). Van Kraaij et al conclude that furosemide withdrawal is almost always successful and is associated with improved diastolic filling and improved blood pressure homeostasis.
Comment by Michael H. Crawford, MD
This study suggests that many patients with a history of CHF and normal systolic left ventricular function are being overtreated with diuretics. It may be that diuretics were started during an episode of CHF and then just continued. In such cases, a re-examination of the need for diuretics seems appropriate and relatively safe based upon this study. Although van Kraaij et al claim that 90% did not need continuation of diuretics, if pedal edema and hypertension are included with CHF as appropriate indications for diuretics, then 75% did not need continued diuretics.
It should be pointed out that this was a highly selected, small group of patients that was studied. There were no NYHA class IV patients; no hypertensive patients; all were in sinus rhythm; none had more than mild angina; and all had negative stress tests for ischemia. Also, the follow-up interval was short (3 months). In addition, no data on left ventricular size were given. This would have been of interest since an enlarged left ventricle may be an indication for diuretics despite an ejection fraction of more than 40%, to reduce left ventricular size and hence wall stress. Finally, it is unclear how many patients were on angiotensin-converting enzyme inhibitors (ACEI) or other drugs that could affect blood pressure, left ventricular filling, and diastolic flow velocity parameters.
In addition to the failure to relapse into CHF in 90% of those with furosemide withdrawn, there were objective improvements in diastolic mitral velocity flow characteristics and orthostatic blood pressure homeostasis. However, these measured benefits did not translate into improved symptoms or exercise time. Thus, the clinical effect of withdrawing diuretics is unclear. Eliminating diuretics in 75-90% of patients should save some money and reduce the complexity of the patients’ treatment regimen. Consequently, an attempt to eliminate diuretics in stabilized diastolic heart failure patients seems a reasonable thing to do. Also, I would suggest re-evaluating the need for ACEI in such patients is appropriate as well.
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