Serial circulating concentrations of c-reactive protein, interleukin (il)-4, and il-6 in patients with acute left heart decompensation



Background: Interleukin (IL)-6 has recently been shown to have negative inotropic effects, and several studies have reported increases in circulating concentrations of this cytokine in patients with depressed left ventricular ejection fraction and chronic left heart failure. However, most previous clinical studies have measured cytokines in compensated chronic heart failure.

Hypothesis: The purpose of this study was to examine the temporal evolution of circulating concentrations of C-reactive protein (CRP) and cytokines in patients with cardiomyopathy and acute cardiac decompensation, free of infection and unstable angina.

Methods: The time course of circulating concentrations of CRP, an anti-inflammatory cytokine interleukin (IL)-4, and a proinflammatory cytokine IL-6 were studied in eight patients with cardiomyopathy and acute cardiac decompensation in the absence of infection or unstable angina. Control samples were obtained from eight age-matched asymptomatic subjects.

Results: Increased circulating concentrations of CRP (2.6 ± 0.8 mg/dl), IL-4 (164.6 ± 36.5 pg/ml), and EL-6 (17.1 ± 5.1 pg/ml) were found in all eight patients during acute cardiac decompensation; these values decreased significantly with the resolution of symptoms of cardiac decompensation (0.5 ±0.1 mg/dl, 77.8 ± 23.6 pg/ml, 2.3 ± 0.1 pg/ml, respectively, p< 0.05 for both). There was a significant correlation between peak CRP and peak IL-6 (p<0.05).

Conclusions: In patients with acute left heart decompensation in the absence of infection or coronary events, CRP, IL-4, and IL-6 increased and returned toward normal levels as the symptoms of heart failure resolved. Since the changes in concentrations of CRP, IL-4, and IL-6 in patients with heart failure are dynamic, the distinction between compensated and decompensated state is important when discussing the significance of acute reactive proteins or cytokines in the pathogenesis of heart failure.