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From the Department of Medicine,* Section ofCardiovascular Sciences, the Section ofCardiology, and the Department ofSurgery, Baylor College of Medicine, theMethodist Hospital, and the DeBakey Heart Center, Houston, Texas
Myocardial hibernation refers to a state of prolonged impairment of
left ventricular function in the presence of coronary artery
disease, which may be reversed by revascularization. In this
study we present evidence for a local inflammatory reaction in
hibernating myocardial segments from patients undergoing coronary
revascularization. We obtained transmural myocardial biopsies guided by
transesophageal echocardiography from patients with ischemic
ventricular dysfunction undergoing bypass surgery. Among the 28
biopsied segments included in the study, 23 showed evidence of
systolic dysfunction. The majority of dysfunctional segments (85.7%)
were viable (201Tl uptake 
60%). The samples were
stained with markers for mast cells, mature resident
macrophages, and the monoclonal antibody Mac387 that labels
newly recruited myeloid cells. Dysfunctional segments showed more
extensive fibrosis and higher macrophage density than normal segments.
Among the 23 dysfunctional segments, 12 recovered function as
assessed with echocardiograms 3 months after revascularization.
Segments with postoperative functional recovery had comparable
macrophage and mast cell density with those showing persistent
dysfunction. However, biopsied segments that subsequently
recovered function contained significantly higher numbers of newly
recruited Mac387-positive leukocytes (18.7 ± 3.1
cells/mm2, n = 12
versus 8.6 ± 0.9 cells/mm2,
n = 11; P = 0.009). In
addition, monocyte chemotactic protein-1, a potent
mononuclear cell chemoattractant, was predominantly expressed
in segments with recovery of function. Myocardial hibernation is
associated with an inflammatory response leading to active leukocyte
recruitment. Dysfunctional myocardial segments that show an active
inflammatory reaction have a greater potential for recovery of function
after revascularization. We postulate that revascularization may
promote resolution of the ongoing inflammation,
preventing further tissue injury and fibrosis.
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