Why the study?
The study aimed to follow changes in myocardial function and physiology in patients awaiting CABG and relate these changes to post-revascularisation functional response.
Does delayed revascularisation reduce myocardial function and post-operative contractile improvement in patients with CAD and LV dysfunction?
Cohort (n=21)
Does delayed revascularisation reduce myocardial function and post-operative contractile improvement in patients with CAD and LV dysfunction?
Absolute Event Rate: 31% vs 58%
p-value: p=0.0002
Delayed revascularization in patients with ischemic cardiomyopathy leads to progressive decline in LV function and reduces the likelihood of myocardial recovery after CABG.
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, p=0.0001) and the LV ejection fraction decreased (30.6 +/- 11.1% vs. 27.3 +/- 11.5%, p<0.001). LVEF fell in 14 patients (28.7 +/- 9.4 vs. 23.8, p<0.0001). 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, [p=0.004] and 1.9 +/- 0.75 vs. 1.33 +/- 0.6, [p=0.005], respectively). Such myocardium displayed attenuated recovery postoperatively (21/68 [31%] LV segments) versus 'waiting-time' stable myocardium (98/169 [58%], p=0.0002). CONCLUSION: Delayed revascularisation in ischaemic left ventricular impairment results in declining function and a reduced likelihood of contractile improvement.
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Michael Pitt (2004) conducted a cohort in Coronary artery disease and left ventricular dysfunction (n=21). Delayed revascularisation (waiting time) vs. Stable myocardium during waiting time was evaluated on Postoperative contractile recovery of LV segments (p=0.0002).
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