Pro-inflammatory cytokines and endothelium-dependent vasodilation in the forearm. Serial assessment in patients with congestive heart failure

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Abstract
Background In patients with heart failure endothelium-dependent vasodilation of the forearm conduit vessels is impaired possibly because of elevated plasma levels of pro-inflammatory cytokines. The effect of elevated plasma cytokines on endothelium-dependent vasodilation of forearm conduit vessels was therefore serially investigated in 16 patients with congestive heart failure during an episode of acute failure and at the time of recompensation. Methods and Results Pro-inflammatory cytokine levels and hyperaemic brachial artery diameters were obtained shortly after admission for an episode of acute heart failure and 11±3 days later at the time of recompensation, which was obtained using diuretic therapy without changing other cardiovascular medications. Serum concentrations (Mean±SD) of tumour necrosis factor alpha (TNF-α) (decompensation vs recompensation: 25±23pg.ml−1vs 26±17pg.ml−1) and interleukine 6 (IL-6) (decom-pensation vs recompensation: 27±24pg.ml−1vs 20±18pg.ml−1), determined in venous blood using immunoradiometric assays were elevated but remained unaltered following recompensation. Brachial artery diameter, derived from high-resolution ultrasound scans at rest and during reactive hyperaemia, 90s after forearm cuff deflation, increased significantly during reactive hyperaemia at the time of admission (3·4±0·7mm vs 4·0±0·5mm;P=0·014) and following recompensation (3·4±0·5mm vs 3·8±0·2mm;P=0·032). The brachial artery diameter during recompensation expressed as a percentage of the baseline value was similar at both intervals (decompensation vs recompensation: 117±14% vs 116±10%;P=ns). At the time of decompensation, the correlation between TNF-α and the percentage change in brachial artery diameter following reactive hyperaemia was absent (r=0·098;P=0·719). The same correlation became significant at the time of recompensation (r=0·750;P=0·001). Conclusions In patients with congestive heart failure, plasma levels of pro-inflammatory cytokines correlate with endothelium-dependent vasodilation of the brachial artery following recompensation, but not during an acute episode of heart failure.

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