Abstract
Objectives. Normothermic hyperkalemic cardioplegia arrest (NHCA) may not effectively preserve hypertrophied myocardium during open-heart surgery. Normothermic normokalemic beating perfusion (NNBP), keeping hearts empty-beating, was utilized as an alternative to evaluate its cardioprotective role. Materials and Methods. Twelve hypertrophied pig hearts at 58.6 ± 7.2 days after ascending aorta banding underwent NNBP and NHCA, respectively. Near infrared myocardial perfusion imaging with indocyanine green (ICG) was conducted to assess myocardial perfusion. Left ventricular (LV) contractile function was assessed by cine MRI. TUNEL staining and western blotting for caspase-3 cleavage and cardiac troponin I (cTnI) degradation were conducted in LV tissue samples. Results. Ascending aortic diameter was reduced by 52.7% ± 0.4% at approximately fifty-eight days after banding. LV wall thickness was significantly higher in aorta banding than in sham operation. Myocardial blood flow reflected by maximum ICG absorbance value was markedly higher in NNBP than in NHCA. The amount of apoptotic cardiomyocyte was significantly lower in NNBP than in NHCA. NNBP alleviated caspase-3 cleavage and cTnI degradation associated with NHCA. NNBP displayed a substantially increased postoperative ejection fraction relative to NHCA. Conclusions. NNBP was better than NHCA in enhancing myocardial perfusion, inhibiting cardiomyocyte apoptosis, and preserving LV contractile function for hypertrophied hearts.
Highlights
Conventional cardioplegia confers sufficient myocardial protection for most patients with preserved ventricular function and leads to a complete postoperative recovery of cardiac function
In patients with compromised cardiac function, such as those with severe myocardial hypertrophy, conventional cardioplegia does not provide adequate myocardial preservation [1, 2]. This is because the hypertrophied hearts are more vulnerable to the detrimental effects of cardioplegia, such as coronary endothelial dysfunction, cardiomyocyte apoptosis, and myocardial stunning
Left ventricular (LV) hypertrophy occurred progressively as aortic constriction remained fixed with normal body growth
Summary
Conventional cardioplegia confers sufficient myocardial protection for most patients with preserved ventricular function and leads to a complete postoperative recovery of cardiac function. In patients with compromised cardiac function, such as those with severe myocardial hypertrophy, conventional cardioplegia does not provide adequate myocardial preservation [1, 2]. This is because the hypertrophied hearts are more vulnerable to the detrimental effects of cardioplegia, such as coronary endothelial dysfunction, cardiomyocyte apoptosis, and myocardial stunning. Myocardial hypertrophy is associated with an increase in coronary vascular resistance and a significantly decreased capillary numerical and volume density [3, 4]. Cardioplegia impairs the release of endothelium-derived relaxing factors from the coronary endothelium and damages the ultrastructure of the coronary endothelium [5, 6].
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