Background. In patients with chronic coronary artery disease (CAD) and
left ventricular dysfunction, flow/metabolic studies of the myocardiu
m with positron emission tomography (PET) are able to distinguish viab
le but dysfunctional myocardium from irreversible ischemic injury and
scar tissue. In this study, PET findings of blood flow and metabolism
in chronically hypoperfused myocardium were correlated with histology.
Methods and Results We studied 33 patients suffering from CAD, In eac
h patient, myocardial blood flow and metabolism were measured with PET
1 or 2 days before revascularization. During surgery, transmural biop
sies were taken from the left ventricular anterior wall and planimetri
cally scored for the degree of myolysis (sarcomere loss). The amount o
f connective tissue was calculated using morphometric techniques. Cont
rast ventriculography demonstrated abnormal wall motion in 23 patients
. Fourteen patients with a mismatch pattern (decreased flow with prese
rved metabolism) in the biopsy region after quantitative analysis of t
he PET data showed 11+/-6 vol% fibrosis and 25+/-13% cells with sarcom
ere loss. The space formerly occupied by sarcomeres was mainly replace
d by glycogen and mitochondria. A significant wall motion improvement
was noted 3 months after surgery. Nine patients showed a match pattern
(concordant flow/metabolism defects). The biopsies revealed 35+/-25%
fibrosis and 24+/-115% glycogen-storing cells. The biopsies of the 10
patients with normal anterior wall motion showed 8+/-4% fibrosis and 1
2+/-8% glycogen-accumulating cells. Conclusions It can be concluded th
at areas with impaired wall motion and a PET match pattern show extens
ive fibrosis. Regions with reduced flow and preserved FDG metabolism,
however, contain predominantly viable cells. In these regions, signifi
cant recovery of wall motion is found after revascularization. Regions
with normal wall motion contain predominantly viable cells. Cells wit
h reduced contractile material and increased glycogen content are main
ly found in areas with wall motion impairment but are also present in
areas with normal wall motion and a severe stenosis of the coronary ve
ssel.