Chest
Volume 110, Issue 4, October 1996, Pages 992-995
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Clinical Investigations: Heart Failure: Articles
The Clinical Relevance of Circulating Tumor Necrosis Factor-α in Acute Decompensated Chronic Heart Failure Without Cachexia

https://doi.org/10.1378/chest.110.4.992Get rights and content

Study objective

To evaluate the clinical relevance of circulating tumor necrosis factor-α (TNFα) 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 TNFα 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. TNFα 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 TNFα 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 TNFα 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 TNFα compared with healthy control subjects, no significant reduction or alteration in circulating TNFα is noted in the short-term follow-up despite clinical improvement.

Section snippets

Study Population

The study population consisted of 29 noncachectic patients (20 men and 9 women; age range, 27 to 79 years; mean 56±13 years) with advanced CHF who demonstrated acute decompensation while receiving adequate oral medical therapy, thus requiring admission to the hospital for therapeutic intervention. Patients were excluded if they exhibited any evidence of cachexia or infectious, inflammatory, or neoplastic disease. Cachexia was considered to be present if the percentage of ideal body weight was

TNFα in CHF Patients and Control Subjects

The mean concentration of TNFα in the normal control subjects was 0.89±0.40 pg/mL (range, 0.5 to 9.7 pg/mL) and was above the limit of detection (≥0.5 pg/mL) in 8 subjects. Plasma concentrations of TNFα in acutely decompensated CHF patients were significantly higher (p<0.002) at 3.0±0.4 pg/mL (range, 0.5 to 6.8 pg/mL) and were above the detection limit of the assay in 22 patients (Fig 1). Furthermore, by χ2 analysis, heart failure patients demonstrated a significantly higher frequency of any

Discussion

The findings of this investigation allow us to make two important clinical observations. First, as in other reports,13 our results allude to the higher elucidation of TNFα in patients with chronic heart failure, even in the absence of cachexia. Second, and more importantly, we were unable to demonstrate a significant improvement in elaboration of TNFα following clinical resolution of acute decompensation. Thus, in the short-term recovery period (1 to 2 weeks), no significant reduction of TNFα

CONCLUSION

This investigation demonstrates that although noncachectic patients with chronic heart failure who suffer acute decompensation elaborate significantly higher circulating levels of TNFα compared with healthy control subjects, no significant reduction or alteration in circulating TNFα is noted in the short-term follow-up despite clinical improvement.

The authors appreciate the technical expertise of Barbara Hand and Christiane Haslberger.

References (16)

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