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. 2009 Feb 3;22(12):811–813. doi: 10.1002/clc.4960221211

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

Yukihito Sato 2,, Yoshiki Takatsu 2, Kazuaki Kataoka 2, Tasuku Yamada 2, Ryoji Taniguchi 2, Shigetake Sasayama 1, Akira Matsumori 1
PMCID: PMC6655929  PMID: 10626084

Abstract

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.

Keywords: C‐reactive protein, cytokine, heart failure, cardiomyopathy

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References

  • 1. Finkel MS, Oddis CV, Jacob TD, Watkins SC, Hattler BG, Simmons RL: Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science 1992; 257: 387–389 [DOI] [PubMed] [Google Scholar]
  • 2. Levine B, Kalman J, Mayer L, Fillit HM, Packer M: Elevated circulating levels of tumor necrosis factor in severe chronic heart failure. N Engl J Med 1990; 323: 236–241 [DOI] [PubMed] [Google Scholar]
  • 3. Matsumori A, Yamada T, Suzuki H, Matoba Y, Sasayama S: Increased circulating cytokines in patients with myocarditis and cardiomyopathy. Br Heart J 1994; 72: 561–566 [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4. Mohler ER, Sorensen LC, Ghali JK, Schocken DD, Willis PW, Bowers JA, Cropp AB, Pressler ML: Role of cytokines in the mechanism of action of amlodipine: The PRAISE heart failure trial. J Am Coll Cardiol 1997; 30: 35–41 [DOI] [PubMed] [Google Scholar]
  • 5. Tsutamoto T, Hisanaga T, Wada A, Maeda K, Ohnishi M, Fukai D, Mabuchi N, Sawaki M, Kinoshita M: Interleukin‐6 spillover in the peripheral circulation increases with the severity of heart failure, and the high plasma level of interleukin‐6 is an important prognostic predictor in patients with congestive heart failure. J Am Coll Cardiol 1998; 31: 391–398 [DOI] [PubMed] [Google Scholar]
  • 6. Haverkate F, Thompson SG, Pyke SDM, Gallimore JR, Pepys MB: Production of C‐reactive protein and risk of coronary events in stable and unstable angina. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Lancet 1997; 349: 462–466 [DOI] [PubMed] [Google Scholar]
  • 7. Richardson CP, McKenna RW, Bristow CM, Maisch B, Mauntner B, O'Connell J, Olsen E, Thiene G, Goodwin J, Gyarfas I, Martin I, Nordet P: Report of the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and Classification of Cardiomyopathies. Circulation 1996; 93: 841–842 [DOI] [PubMed] [Google Scholar]
  • 8. Yamauchi‐Takihara K, Ihara Y, Ogata A, Yoshizaki K, Azuma J, Kishimoto T: Hypoxic stress induces cardiac myocyte‐derived interleukin‐6. Circulation 1995; 91: 1520–1524 [DOI] [PubMed] [Google Scholar]
  • 9. Matsumori A, Ono K, Sato Y, Shioi T, Nose Y, Sasayama S: Differential modulation of cytokine production by drugs: Implications for therapy in heart failure. J Mol Cell Cardiol 1996: 28: 2491–2499 [DOI] [PubMed] [Google Scholar]

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