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Cardiac dysfunction and inefficiency after substrate-enriched warm blood cardioplegia.
C Korvald1, O P Elvenes, T Myrmel
1Department of Thoracic and Cardiovascular Surgery, University Hospital in Tromsø, Tromsø, Norway. christian.korvald@rito.no
Summary
Prolonged warm continuous antegrade blood cardioplegia (WCBC) severely depressed cardiac function and efficiency, even with added substrates. Sustained normothermic hyperkalemic perfusion poses significant risks to heart mechanical performance.
Area of Science:
- Cardiovascular Physiology
- Cardiac Surgery
- Myocardial Protection
Background:
- Warm continuous antegrade blood cardioplegia (WCBC) is used in cardiac surgery.
- Substrate enrichment aims to improve myocardial protection during cardioplegia.
- Understanding the impact of prolonged WCBC on cardiac function is crucial.
Purpose of the Study:
- To assess the mechanical performance and mechanoenergetic efficiency after prolonged WCBC with substrate enrichment.
- To compare the effects of WCBC alone, WCBC with glucose-insulin-potassium (GIK), and WCBC with L-glutamine (GLN).
Main Methods:
- Three groups of pigs (n=7 each) received 3 hours of WCBC: alone, +GIK, or +GLN.
- Cardiac function (systolic/diastolic), pressure-volume area (PVA), and myocardial oxygen consumption (MVO(2)) were measured.
- Measurements were taken before and twice after WCBC using advanced hemodynamic monitoring.
Main Results:
- All groups showed significant decreases in left ventricular developed pressure, dP/dt(max), and preload recruitable stroke work post-WCBC.
- Mechanoenergetic efficiency (PVA/MVO(2)) significantly decreased in all groups.
- End-diastolic stiffness increased in WCBC and +GLN groups, but not in the +GIK group.
Conclusions:
- Prolonged WCBC, even with substrate enrichment, severely impairs cardiac contractile function and mechanoenergetic efficiency.
- Sustained normothermic hyperkalemic perfusion carries significant risks for myocardial performance.
- The glucose-insulin-potassium (GIK) substrate may offer some protection against increased end-diastolic stiffness.