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Protection of the hypertrophied myocardium by crystalloid cardioplegia
N A Munfakh1, J B Steinberg, J S Titus
1Department of Surgery, Massachusetts General Hospital, Boston.
Insights
Hearts with left ventricular hypertrophy (LVH) show better recovery after cardiac surgery using cold, oxygenated cardioplegia. This protection is maintained even with calcium in the cardioplegia, suggesting hypertrophied hearts are well-protected.
Area of Science:
- Cardiology
- Physiology
- Biochemistry
Background:
- Left ventricular hypertrophy (LVH) is associated with poorer outcomes post-cardiac surgery.
- Understanding myocardial protection strategies for LVH patients is crucial.
Purpose of the Study:
- To evaluate the protective effects of multidose, cold, oxygenated cardioplegia on hypertrophied rat hearts.
- To assess the impact of calcium in cardioplegia on the recovery of LVH hearts.
Main Methods:
- Left ventricular hypertrophy (LVH) was induced in rats by abdominal aorta banding.
- Isolated rat hearts underwent cold, oxygenated cardioplegia with varying calcium concentrations.
- Cardiac output, myocardial energy metabolites (ATP, PCr), glycogen, and oxygen consumption were measured.
Main Results:
- LVH hearts demonstrated significantly higher cardiac output recovery (82%) compared to controls (66-69%) after cardioplegia.
- Myocardial efficiency was best preserved in LVH hearts post-reperfusion.
- Calcium in cardioplegia depressed recovery and energy metabolites in all groups but did not preferentially harm LVH hearts.
Conclusions:
- Standard cold, oxygenated cardioplegia effectively protects the hypertrophied myocardium.
- Calcium in cardioplegia does not exacerbate functional decline in LVH hearts.
- LVH hearts exhibit enhanced resilience to ischemic arrest and reperfusion injury with current cardioplegia protocols.
Abstract:
Patients with left ventricular hypertrophy (LVH) have a worse outcome after cardiac surgery than those without hypertrophy. We studied protection of hearts with LVH in an isolated rat heart model using multidose, cold, oxygenated cardioplegia. LVH was produced by banding the abdominal aorta in young rats. Six weeks after banding, this produced a 31% increase in the left ventricular dry weight/body weight ratio compared to two age-matched control groups comprising sham-operated and nonoperated animals. The recovery of cardiac output after arrest was higher in LVH (82 +/- 4% of prearrest) than in sham-operated (69 +/- 4%) or nonoperated (66 +/- 3%) control groups. The improved functional recovery in LVH occurred although there were no differences among the groups in myocardial adenosine triphosphate (ATP) and phosphocreatine (PCr) prior to arrest, at the end of arrest, or after reperfusion. Glycogen levels were also similar among the three groups prior to arrest and after reperfusion but were highest in LVH after arrest. Myocardial oxygen consumption (MVO2) and efficiency, expressed as cardiac output/MVO2, were similar among the groups prior to arrest. Myocardial efficiency after reperfusion declined in all groups but was best preserved in LVH. We also compared the sensitivity of hypertrophied and control hearts to the deleterious effects of calcium in cardioplegia. Calcium in the cardioplegia increased myocardial lactate production during arrest in a dose-related fashion and depressed myocardial levels of ATP, PCr, and glycogen at end arrest in all groups. Cardiac output recovery was also depressed by calcium but was still best in LVH. We conclude that the hypertrophied myocardium is well protected by standard cardioplegia and that calcium in cardioplegia does not preferentially depress recovery in LVH.