Effect of thalidomide in patients with chronic heart failure
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Published on: July 18, 2014
Lars Gullestad1, Anne Grete Semb, Even Holt
1Department of Internal Medicine, Baerum Hospital, Aker Hospital, Oslo, Norway. lars.gullestad@broadpark.no
Insights
Thalidomide treatment reduced tumor necrosis factor-alpha (TNF-alpha) and improved cardiac function in patients with congestive heart failure (CHF). This pilot study suggests thalidomide may be a beneficial immunomodulating agent for CHF.
Area of Science:
- Cardiology
- Immunology
- Pharmacology
Background:
- Congestive heart failure (CHF) is linked to heightened immune activation, potentially driving disease progression.
- Investigating immunomodulatory therapies is crucial for managing CHF.
Purpose of the Study:
- To assess the efficacy of thalidomide, an immunomodulating drug, in improving cardiac performance in CHF patients.
- To evaluate the impact of thalidomide on tumor necrosis factor-alpha (TNF-alpha) levels in CHF.
Main Methods:
- A 6-week open-label pilot study involving nine CHF patients with left ventricular ejection fraction (LVEF) <40%.
- Patients received 200 mg of thalidomide daily alongside optimal conventional cardiovascular treatment.
- Measurements included plasma TNF-alpha levels and LVEF at baseline and study completion.
Main Results:
- Thalidomide therapy led to a significant decrease in elevated TNF-alpha levels.
- LVEF significantly improved from 26% to 34% in patients receiving thalidomide.
- Sedation was a common side effect, necessitating dose reduction in most participants.
Conclusions:
- Thalidomide demonstrated potential in reducing TNF-alpha and enhancing cardiac performance in CHF patients.
- Further investigation of thalidomide as an immunomodulating agent for CHF is warranted.
- The study highlights the role of immune pathways in CHF pathogenesis.
Background:
Congestive heart failure (CHF) is characterized by enhanced immune activation, which possibly plays a pathogenic role in this disorder. We therefore examined whether immunomodulation with thalidomide could improve cardiac performance in patients with CHF.
Methods:
Nine patients with chronic symptomatic CHF and left ventricular ejection fraction (LVEF) <40%, who were receiving "optimal" conventional cardiovascular treatment, were given 200 mg thalidomide daily in an open design for a period of 6 weeks. Tumor necrosis factor (TNF)-alpha and LVEF were measured at baseline and on completion of the study.
Results:
Two patients withdrew because of side effects. Sedation was common and required dose reduction in 6 of 7 patients completing the study. Plasma levels of TNF-alpha were elevated at baseline compared with levels in healthy control patients, but decreased significantly from 33.9 +/- 10.1 pg/mL to 19.3 +/- 6.1 pg/mL during therapy (P <.05). LVEF increased in all patients from 26% +/- 9% to 34% +/- 10% at the end of the observation period (P <.05).
Conclusions:
In this pilot study, therapy with thalidomide in patients with CHF resulted in decreased TNF-alpha levels and increased cardiac performance. Although few patients were included, our results suggest that thalidomide should be further investigated as an immunomodulating agent in CHF.
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