Abstract

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. 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-alpha) (decompensation vs recompensation: 25 +/- 23 pg.ml-1 vs 26 +/- 17 pg.ml-1) and interleukine 6 (IL-6) (decompensation vs recompensation: 27 +/- 24 pg.ml-1 vs 20 +/- 18 pg.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, 90 s after forearm cuff deflation, increased significantly during reactive hyperaemia at the time of admission (3.4 +/- 0.7 mm vs 4.0 +/- 0.5 mm; P = 0.014) and following recompensation (3.4 +/- 0.5 mm vs 3.8 +/- 0.2 mm; 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-alpha 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). 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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