From the Departments of Medicine and Pathology, The Montreal General
Hospital and McGill University (S.C.Y.W., M.F., P.M., A.G.); GenPath
Laboratories (A.G.); and Merck Frosst Laboratories (I.R.), Montreal, Quebec,
Canada.
Correspondence to Dr Adel Giaid, Suite L3–314, The Montreal General Hospital, 1650 Cedar Ave, Montreal, Quebec, Canada H3G 1A4. E-mail mdga{at}musica.mcgill.ca
Abstract
Background—Chronic heart failure is
associated with induction of secondary inflammatory mediators,
including prostanoids. The latter exert diverse functional and
morphological effects on cardiac myocytes. Induction of
cyclooxygenase (COX), the enzyme responsible for
generating prostanoids, requires activation of nuclear factor-
Methods and Results—Myocardial tissue from 27 patients with
end-stage heart failure (various etiologies: ischemic heart
disease, n=16; idiopathic dilated cardiomyopathy,
n=10; and valvular heart disease, n=1), 2 septic patients, and
8 normal control subjects was immunostained with antisera
to COX-2 and NF-
Conclusions—We demonstrate induction of COX-2 and activation of
NF-
© 1998 American Heart Association, Inc.
Brief Rapid Communication
Induction of Cyclooxygenase-2 and Activation of Nuclear Factor-
B in Myocardium of Patients With Congestive Heart Failure
B
(NF-B). The aim of the present study was to determine the
expression of COX-2 and activation of NF-B in the failing human
heart. B. Western blotting was performed and showed high
anti–COX-2 antibody specificity and the presence of COX-2 protein in
the sample tissues. In situ hybridization and immunohistochemistry
showed little or no expression of COX-2 and NF-B in the control
hearts. In contrast, there was abundant expression of COX-2 mRNA and
protein in myocytes and inflammatory cells in areas of fibrotic scar
compared with regions of normal morphology in all cases of heart
failure, except the cases with sepsis, which showed an abundance of
COX-2 throughout the myocardium. Sites of NF-B
activation were associated with those of COX-2 expression. B in the myocardium of failing human hearts.
Induction of both molecules appears to be associated with the presence
of inflammation and scar formation.
Key Words: heart failure • myocardium • infarction • cardiomyopathy
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