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in Acute Decompensated Chronic Heart Failure Without Cachexia
1 From the Department of Internal Medicine, Klinikum Innenstadt, University of Munich, Germany
2 From the Section on Cardiology; Department of Pathology, Klinikum Innenstadt, University of Munich, Germany
3 From the Department of Ochsner Medical Institutions, New Orleans; and Medizinische Klinik, Klinikum Innenstadt, University of Munich, Germany
Study objective: To evaluate the clinical relevance of circulating tumor necrosis factor-
(TNF) in subjects with advanced acutely decompensated congestive heart failure (CHF) and to determine the modulatory effect of clinical interventions on short-term elaboration of this cytokine.
Design: Prospective, case-controlled study.
Setting: Inpatient and outpatient (hospital and clinic), at regional academic medical center.
Patient interventions: Plasma concentrations of TNF were determined in 25 healthy, normal control subjects and in 29 noncachectic patients with advanced CHF (mean ejection fractions 16±6%) who required hospitalization for IV diuretic and/or inotropic therapy despite optimization of oral medical regimens. CHF patients were divided into two groups: diuretic responsive (group A; n=6) and diuretic resistant requiring inotropic support (group B; n=23). Group B was randomly allocated to receive either IV dobutamine (n=13) or milrinone (n=10) for 72 h. TNF levels in CHF patients were measured serially at baseline, at 6 h, at 48 h, at 72 h, and at 1-week follow-up after hospital discharge.
Results: Plasma TNF levels at baseline in CHF patients were 4.0±1.1 pg/mL (range, 0.5 to 6.5 pg/mL) and 2.5±0.6 pg/mL (range, 0.5 to 6.8 pg/mL) in groups A and B, respectively, which were significantly different (p<0.002) from normal subjects (0.89±0.40 pg/mL; range, 0.5 to 9.7 pg/mL). Despite clinically successful therapy with IV diuretics, dobutamine, or milrinone, plasma levels of this cytokine remained unchanged. Plasma TNF in CHF patients measured in recovery (1 week after hospital discharge) was 5.1±1.2 pg/mL (range, 1.0 to 9.9 pg/mL) and 3.9±0.8 pg/mL (range, 0.5 to 8.7 pg/mL) in groups A and B, respectively.
Conclusion: These findings suggest that although noncachectic patients with chronic heart failure who suffer acute decompensation elaborate significantly higher circulating levels of TNF compared with healthy control subjects, no significant reduction or alteration in circulating TNF is noted in the short-term follow-up despite clinical improvement.
Key Words: cytokines • heart failure • inotropes • tumor necrosis factor
Submitted on October 26, 1995
Accepted on May 7, 1996
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