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From the Section of Clinical Immunology and Infectious Diseases (P.A.,
F.M., I.N., S.S.F.) and Research Institute for Internal Medicine (P.A., F.M.,
I.N., S.S.F.), Medical Department A, and the Section of Cardiology (T.U.,
A.K.A., H.A., J.K., S.S., L.G.), Medical Department B, University of Oslo,
Rikshospitalet, Oslo, Norway.
Correspondence to Pål Aukrust, MD, PhD, Section of Clinical Immunology and Infectious Diseases, Medical Department A, Rikshospitalet, N-0027 Oslo, Norway. E-mail pal.aukrust{at}klinmed.uio.no
Background—Immunologic and
inflammatory responses appear to play a pathogenic role in the
development of congestive heart failure (CHF). Activation and migration
of leukocytes to areas of inflammation are important factors in these
immunologic responses. Because the C-C chemokines are potent
chemoattractants of monocytes and lymphocytes and can modulate other
functions of these cells (eg, generation of reactive oxygen species),
we measured circulating levels of three C-C chemokines in CHF.
Methods and Results—Levels of macrophage chemoattractant
protein-1 (MCP-1), macrophage inflammatory protein-1
Conclusions—This first demonstration of increased circulating
levels of C-C chemokines in CHF with particularly high levels in
patients with severe disease may represent previously
unrecognized pathogenic factors in CHF.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Elevated Circulating Levels of C-C Chemokines in Patients With Congestive Heart Failure
(MIP-1), and RANTES (regulated on
activation normally T-cell
expressed and secreted) were measured by
enzyme immunoassays in 44 patients with CHF and 21 healthy control
subjects. CHF patients had significantly elevated levels of all
chemokines with the highest levels in New York Heart Association class
IV, and MCP-1 and MIP-1 levels were significantly inversely
correlated with left ventricular ejection fraction.
Elevated C-C chemokine levels were found independent of the cause of
the heart failure, but MCP-1 levels were particularly raised in
patients with coronary artery disease. Studies on cells
isolated from peripheral blood suggested that
platelets, CD3+ lymphocytes, and in particular, monocytes, might
contribute to the elevated C-C chemokine levels in CHF. The increased
MCP-1 levels in CHF were correlated with increased monocyte activity
reflected in an enhancing effect of serum from CHF patients on
O2- generation in monocytes, which was
inhibited by neutralizing antibodies against MCP-1.
Key Words: heart failure • coronary disease • chemokines • free radicals • monocytes
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