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Published on: June 14, 2020
Chronic stable ischaemia protects against myocyte damage during beating heart coronary surgery
Gerald Carr-White1, Tat Koh, Anthony DeSouza
1Department of Academic Cardiac Surgery, Royal Brompton and Harefield Hospitals NHS Trust, Sydney Street, London, UK. g.carr-white@virgin.net
Insights
Chronic stable angina patients with resting ischemia showed reduced heart muscle damage during beating heart surgery. This natural protection differs from surgical preconditioning, highlighting a protective effect of pre-existing ischemia.
Area of Science:
- Cardiology
- Cardiac Surgery
- Myocardial Ischemia Research
Background:
- Coronary artery disease (CAD) patients often exhibit chronic resting myocardial dysfunction.
- The impact of pre-existing ischemia on myocardial damage during cardiac surgery is not fully understood.
Purpose of the Study:
- To investigate if chronic resting ischemia influences myocardial damage during beating heart surgery.
- To compare the protective effects of natural ischemia versus surgical preconditioning.
Main Methods:
- Studied 33 patients with chronic stable angina and normal ejection fraction.
- Assessed myocyte injury via Troponin T release and evaluated functional ischemia using echocardiograms and left ventricular pressure.
- Included a subset of 10 patients with a surgical preconditioning protocol.
Main Results:
- Patients with resting ischemia had lower preoperative regional peak power and work.
- Postoperative Troponin T levels were significantly lower at 48 and 72 hours in patients with preoperative resting ischemia.
- Longer ischemic time and increased cycle efficiency were independent determinants of reduced troponin release.
Conclusions:
- Stable preoperative ischemia may offer natural myocardial protection, reducing Troponin T release after beating heart surgery.
- This protective effect is distinct from classical ischemic preconditioning.
- Findings suggest a potential therapeutic role for managing pre-existing ischemia in CAD patients undergoing surgery.
Objectives:
Many patients with coronary artery disease demonstrate chronic resting ischaemic myocardial dysfunction. We have investigated whether this ischaemia influences the myocardial damage caused by the period of coronary occlusion involved in beating heart surgery.
Methods:
Thirty-three patients with chronic stable angina and normal left ventricular ejection fraction were studied. To make our model clinically appropriate, we included patients with a wide range of ischaemic times, ages and in a subset of 10 patients a surgical preconditioning protocol. Myocyte injury was assessed from venous Troponin T release measured on days 1, 2, and 3. We used intraoperative transoesophageal M mode echocardiograms and simultaneous high-fidelity left ventricular pressure to assess whether patients were demonstrating the functional effects of ischaemia (asynchronous regional contraction with reduced mechanical function).
Results:
Patients demonstrated the functional effects of resting ischaemia and 17 did not. Patients with resting ischaemia had lower preoperative values of regional peak power and work and all three variables increased significantly with surgery. Venous Troponin T levels at 48 and 72 h postoperatively were lower in those with preoperative resting ischaemia (median (interquartile range) 0.13 (0.08-0.20) vs 0.21 (0.13-0.69) for 48 h and 0.10 (0.08-0.19) vs 0.26 (0.12-0.51) for 72 h). Stepwise multiple linear regression of total postoperative troponin release (measured as the area under the curve of troponin release) demonstrated two independent determinants (R squared for model 0.40): longer ischaemic time, and increasing values of cycle efficiency. The surgical ischaemic preconditioning protocol and preoperative collaterals were not independent determinants.
Conclusions:
In patients with chronic coronary artery disease, stable preoperative ischaemia may thus represent a naturally occurring form of myocardial protection, whose presence reduces Troponin T release after beating heart surgery. This protection is different in nature from classical ischaemic preconditioning.
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