The purpose of this study was to determine the effects of the addition of amino acids to blood cardioplegic solution and the value of terminal cardioplegia enhancement techniques in routine myocardial protection. Forty-five open-chest adult dogs were instrumented with sonomicrometry crystals to measure left ventricular long axis, midequatorial short axis, and wall thickness. The aorta was clamped for 120 minutes of cardiopulmonary bypass. Animals were randomly separated into four myocardial protection groups: (1) blood cardioplegic solution with amino acids and no terminal cardioplegia (n = 12); (2) blood cardioplegic solution with amino acids and warm amino acid terminal cardioplegia (n = 11); (3) blood cardioplegic solution with amino acids and cold amino acid terminal cardioplegia (n = 12); and (4) blood cardioplegic solution plus cold terminal cardioplegia (no amino acids, n = 10). Data for preload recruitable stroke work were obtained by inflow occlusion before bypass (baseline) and at 30 and 60 minutes after reperfusion and analyzed for changes in x-intercept and slope. A significant rightward shift in x-intercept did not occur in any group. When cardiac function was expressed as a percentage of baseline preload recruitable stroke work slope, improved functional recovery was seen at both 30 and 60 minutes in groups 2 (88.6 % and 91.8%), 3 (85.8% and 86.9%), and 4 (88.6% and 92.6%) compared with group 1 (77.3% and 79.2%, p < 0.05). No significant difference was found in the degree of functional recovery among groups 2, 3, and 4. These results suggest that for myocardial protection of 2 hours in nonischemic hearts, a terminal dose of blood cardioplegic solution before unclamping is beneficial, but this positive effect is independent of amino acid supplementation and temperature.
A 23-year-old African American woman with a past medical history of systemic lupus erythematous (SLE), secondary hypertension, and end stage renal disease (ESRD) on hemodialysis for eight years was stable until she developed symptomatic severe mitral regurgitation with preserved ejection fraction. She underwent a bioprosthetic mitral valve replacement (MVR) at outside hospital. However, within a year of her surgery, she presented to our hospital with NYHA class IV symptoms. She was treated for heart failure but in view of her persistent symptoms and low EF was considered for heart and kidney transplant. This was a challenge in view of her history of lupus. We presumed that her stenosis of bioprosthetic valve was secondary to lupus and renal disease. We hypothesized that her low ejection fraction was secondary to mitral stenosis and potentially reversible. We performed a dobutamine stress echocardiogram, which revealed an improved ejection fraction to more than 50% and confirmed preserved inotropic contractile reserve of her myocardium. Based on this finding, she underwent a metallic mitral valve and tricuspid valve replacement. Following surgery, her symptoms completely resolved. This case highlights the pathophysiology of lupus causing stenosis of prosthetic valves and low ejection cardiomyopathy.
