Copyright © 2004 by the European Society of Cardiology.
Clinical research
The natural history of myocardium awaiting revascularisation in patients with impaired left ventricular function
a Department of Cardiology, Birmingham Heartlands Hospital, Bordesley Green East, Birmingham B9 5SS, UK
b Department of Cardiothoracic Surgery, Queen Elizabeth Medical Centre, Edgbaston, Birmingham, UK B15 2TH
c MRC Clinical Sciences Centre, Imperial College of Science and Medicine, Hammersmith Campus, DuCane Road, London W12 0NN, UK
Received February 14, 2003;
revised January 12, 2004;
accepted January 22, 2004
* Corresponding author. Tel.: +44-121-4243737; fax: +44-121-4241074
E-mail address: michael.pitt{at}heartsol.wmids.nhs.uk
Aims Our aim was to follow changes in myocardial function and physiology in patients awaiting coronary artery bypass surgery (CABG) and relate changes to post-revascularisation functional response.
Methods and results In 21 patients with CAD and LV dysfunction, myocardial glucose utilisation (MGU) and blood flow (MBF) were measured with positron emission tomography using F-18-fluorodeoxyglucose and oxygen-15-labelled water. Left ventricular function, MGU, and MBF were re-assessed after one year, immediately prior to CABG. At baseline, dysfunctional myocardium displayed a reduction in MGU, hyperaemic MBF, and coronary vasodilator reserve (CVR) compared to normally functioning muscle. In the year preceding CABG, the overall wall motion score index increased (2.09±0.65 vs. 2.3±0.7, 
) and the LV ejection fraction decreased (30.6±11.1% vs. 27.3±11.5%, 
). LVEF fell in 14 patients (28.7±9.4 vs. 23.8, 
). Aggregate regional wall motion worsened in 15 patients. In contrast to myocardium displaying stable function at echocardiography, myocardium with evidence of deterioration showed a parallel decrease in hyperaemic MBF and CVR (1.57±0.67 vs. 1.19±0.7 ml/min/g, [
] and 1.9±0.75 vs. 1.33±0.6, [
], respectively). Such myocardium displayed attenuated recovery postoperatively (21/68 [31%] LV segments) versus `waiting-time' stable myocardium (98/169 [58%], 
).
Conclusion Delayed revascularisation in ischaemic left ventricular impairment results in declining function and a reduced likelihood of contractile improvement.
Key Words: Coronary disease • Blood flow • Metabolism • Revascularisation
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