The relationship of the erythrocyte sedimentation rate to inflammatory cytokines and survival in patients with chronic heart failure treated with angiotensin-converting enzyme inhibitors

OBJECTIVES The object of the study was to assess the relationship between e rythrocyte sedimentation rate (ESR) and inflammatory cytokine production in chronic heart failure (CHF). Our findings lead us to re-evaluate the progn ostic value of the ESR in assessing patients with CHF. BACKGROUND The search for simple prognostic markers in CHF that can be asse ssed anywhere at low cost is important. Increases in ESR are related to the acute phase response in states of inflammation and infection. METHODS Initially, we studied ESR in relation to plasma levels of inflammat ory cytokines in 58 CHF patients. The findings prompted us to analyze the m ortality predictive power of ESR compared with established risk factors in these patients and (retrospectively) in a second group of 101 clinically st able CHF patients who had ESR measured. RESULTS In all 159 CHF patients (age 62 +/- 2 years, New York Heart Associa tion [NYHA] class 2.7 +/- 0.1), ESR ranged from 1 to 96 mm/h (median 14 mm/ h). The ESR nas correlated with tumor necrosis factor (TNF)-alpha (r = 0.31 , p < 0.05), soluble TNF receptor-1 (r = 0.48, p < 0.0005), soluble TNF rec eptor-2 (r = 0.39, p < 0.005) and interleukin 6 (r = 0.45, p ( 0.005) level s. High ESR levels indicated a poor prognosis (p < 0.0001), and this was in dependent of age, NYHA class, ejection fraction and peak oxygen consumption (p < 0.005). Patients with ESR above median (greater than or equal to 15 m m/h) compared with patients with ESR <15 mm/h had an impaired survival (haz ard ratio 2.62, 95% confidence interval 1.58-4.36, p < 0.0001). CONCLUSIONS Our study demonstrates that in CHF a high ESR is an unfavorable prognostic sign, independent of patients' symptomatology and ventricular f unction. These results are in diametrical contrast to previous results. Thi s may reflect a change in the underlying pathophysiology due to today's tre atment with angiotensin-converting enzyme inhibitors, (C) 2000 by the Ameri can College of Cardiology.