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a Cardiothoracic
Surgical Unit, Queen Elizabeth Hospital, Birmingham, UK, b University Department
of Cardiovascular Medicine, Queen Elizabeth Hospital, c Department of Histopathology, Papworth
Hospital, Cambridge, UK, d MRC
Cyclotron Unit, Imperial College School of Medicine, Hammersmith
Hospital, Du Cane Road, London W14 0NN, UK
Correspondence to: Professor Camici email: paolo.camici{at}csc.mrc.ac.uk
Accepted 1 November
1999
BACKGROUND
In
patients with postischaemic left ventricular dysfunction, segments
recovering function after revascularisation (hibernating myocardium)
may not respond during dobutamine echocardiography, despite preserved
[18F] 2-fluoro-2-deoxy-D-glucose (FDG) uptake at positron
emission tomography.
OBJECTIVETo
investigate whether this lack of response might reflect the degree of
ultrastructural change in hibernating myocardium.
METHODSTransmural
biopsies were obtained from 22 dysfunctional segments in 22 patients
during coronary artery bypass grafting and examined by light and
electron microscopy. Wall motion scores and coronary vasodilator
reserve were assessed before and after coronary artery bypass grafting (CABG).
RESULTSMean (SD)
wall motion score improved in all segments following CABG (from 2.24 (0.4) to 1.55 (0.4); p < 0.0001), confirming hibernating myocardium.
In these segments myocardial blood flow (positron emission tomography
with H215O) before CABG was similar to that in
normal volunteers (1.02 (0.24) v 1.02 (0.23)
ml/min/g), while the coronary vasodilator reserve was blunted (1.26 (0.7) v 3.2 (1.6); p < 0.0001).
Myocardial blood flow was unchanged after CABG, whereas coronary
vasodilator reserve increased to 2.10 (0.90) (p < 0.0007). In
hibernating myocardium myofibrillar loss, interstitial fibrosis, and
glycogen-rich myocytes were more marked than in control donor hearts.
On the basis of the response to dobutamine before CABG, two functional groups were identified: group A, segments with inotropic reserve (n = 15); group B, segments without inotropic reserve (n = 7). FDG
uptake was similar in group A and group B (0.40 (0.1)
v 0.44 (0.1) µmol/min/g). In group B there
was more myofibrillar loss (26 (8)% v 11 (5)%; p = 0.0009) and glycogen-rich myocytes (28 (11)%
v 17 (10)%; p = 0.02), whereas
interstitial fibrosis, myocardial blood flow, and coronary vasodilator
reserve were similar in the two groups. Myofibrillar loss was the only
independent predictor of inotropic reserve (p = 0.01).
CONCLUSIONSHibernating
myocardium is characterised by a reduced coronary vasodilator reserve
which improves on revascularisation and shows a spectrum of
ultrastructural changes that influence the response to dobutamine,
while FDG uptake is invariably preserved.
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