PubMed · 10908078
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J N Cohn. 2000. Lumpers versus splitters.. https://doi.org/10.1016/s1071-9164(00)90006-x
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CONTEXT: Advanced heart failure, defined as persistence of limiting symptoms despite therapy with agents of proven efficacy, accounts for the majority of morbidity and mortality in heart failure. OBJECTIVE: To review current medical therapy for advanced heart failure. DATA SOURCES: We searched MEDLINE for all articles containing the term advanced heart failure that were published between 1980 and 2001; EMBASE was searched from 1987-1999, Best Evidence from 1991-1998, and Evidence-Based Medicine from 1995-1999. The Cochrane Library also was searched for critical reviews and meta-analyses of congestive heart failure. STUDY SELECTION: Randomized controlled trials of therapy for 150 patients or more were included if advanced heart failure was represented. Other common clinical situations were addressed from smaller trials as available, trials of milder heart failure, consensus guidelines, and both published and personal clinical experience. DATA EXTRACTION: Data quality was determined by publication in peer-reviewed literature or inclusion in professional society guidelines. DATA SYNTHESIS: A primary focus for care of advanced heart failure is ongoing identification and treatment of the elevated filling pressures that cause disabling symptoms. While angiotensin-converting enzyme inhibitors and beta-adrenergic agents can slow disease progression and prolong survival, titration and tolerability often present challenges. Most patients are not eligible for surgical intervention but do benefit from a medical regimen tailored to individual clinical and hemodynamic profiles and from heart failure management programs that reduce rehospitalization. Survival ranges from 80% at 2 years for patients rendered free of congestion to less than 50% at 6 months for patients with refractory symptoms, in whom end-of-life options may include hospice care and inactivation of implantable defibrillators. CONCLUSIONS: Current management of advanced heart failure is based more on consensus than on randomized trials. Systematic investigation should address not only new therapies but also strategies for selecting and optimizing therapies already available.
The aim of this study was to determine if it was possible to decrease the number of boluses of indomethacin for the treatment of patent ductus arteriosus. This retrospective study included 46 preterm neonates (<34 weeks' GA) who had had an ultrasound diagnosis predictive of subsequent symptomatic patent ductus arteriosus. All patients had received a daily intravenous doses of indomethacin, 0.1 mg/kg. Mean age at initiation of treatment was 4.5 +/- 3.1 days. Patency of the ductus arteriosus was controlled echocardiographically each day and treatment was discontinued as soon as the ductus arteriosus was closed. The initial success rate was 84.7%, of which 6.5% reopened. The mean cumulative dose of indomethacin was 0.35 mg/kg. There was no correlation between gestational age or birth weight and total cumulative dose. Overall tolerance was satisfactory with only one case of transient acute renal failure. A weak correlation between the cumulative dose of indomethacin and natremia (r = -0.43) or weight gain (r = 0.35) was noted, and none with serum creatinine or blood urea nitrogen levels. We confirm that lower indomethacin treatment of patent ductus arteriosus in premature neonates are as effective as standard protocols.