The changes of circulating tumor necrosis factor levels in patients with congestive heart failure influenced by therapy.
Recent studies suggest that tumor necrosis factor-alpha (TNF-alpha) plays an important role in the pathogenesis of congestive heart failure and that drugs used in the treatment of heart failure have modulation effects on the production of TNF-alpha. To examine an alteration of circulating TNF-alpha concentration in patients with severe chronic heart failure after improving heart function and investigate the influence of agents on circulating TNF-alpha concentrations, we measured the plasma levels of TNF-alpha by enzyme linked immunoabsorbent assay in 31 patients and evaluated their heart functions before and after 72 h of therapy. The results showed that circulating TNF-alpha concentrations significantly decreased after therapy (from 124.36+/-14.85 pg/ml to 93.84+/-13.57 pg/ml, P<0.001). The circulating TNF-alpha concentrations of patients (n = 22) whose heart function was improved one class or more after therapy declined significantly (from 127.51+/-20.78 pg/ml to 91.54+/-18.56 pg/ml, P<0.01) but this situation did not exist in patients (n = 9) whose heart functions had no or little improvement. All patients were divided into three groups according to their management: 'group A' (n = 14) who received milrinone and angiotensin-converting enzyme inhibitors (ACEI), 'group B' (n = 6) who received milrinone but not ACEI and 'group C' (n = 11) who received ACEI and dobutamine but not milrinone. The circulating TNF-alpha concentration of patients in group A significantly declined (from 126.68+/-26.04 pg/ml to 95.92+/-24.79 pg/ml, P<0.01). No statistical significance of change of TNF-alpha concentration was found in patients in group B or group C, although a tendency of decline existed (from 119.92+/-34.72 pg/ml to 84.33+/-30.70 pg/ml and from 123.83+/-19.50 pg/ml to 96.37+/-16.62 pg/ml, respectively). These findings support that decreased plasma TNF-alpha level accompanies the improvement of heart function. This phenomenon may be explained by the special abilities of agents, such as ACEI and milrinone, to inhibit the TNF-alpha production.
Liu
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Department of Cardiology, The Second Affiliated Hospital, Human Medical University, Changsha, People's Republic of China.
Zhao
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D000293:Adolescent; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D004280:Dobutamine / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D005260:Female; D006333:Heart Failure / Q000097:blood* / Q000188:drug therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D020105:Milrinone / Q000627:therapeutic use*; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D000806:Angiotensin-Converting Enzyme Inhibitors; D002316:Cardiotonic Agents; D010726:Phosphodiesterase Inhibitors; D014409:Tumor Necrosis Factor-alpha; D004280:Dobutamine; D020105:Milrinone