Akihiko Ohkado

Clinical Assessment of Prolonged Myocardial Preservation for Patients With a Severely Dilated Heart

BACKGROUND The purpose of this study was to compare the myocardial protective effect of histidine-tryptophan-potassium and glucose-insulin-potassium cardioplegic solutions in patients with a dilated heart (left ventricular diastolic diameter > 55 mm, left ventricular systolic diameter > 45 mm) associated with prolonged cross-clamp time (longer than 200 minutes). METHODS We selected 20 patients with dilated hearts due to severe aortic regurgitation. Glucose-insulin-potassium cardioplegia was used in 11 patients and histidine-tryptophan-potassium cardioplegia was used in 9 patients. RESULTS After operation, the cardiac index was significantly increased in the histidine-tryptophan-potassium group (p < 0.05). Postoperative percent fractional shortening was 13.4% +/- 3.1% in the glucose-insulin-potassium group and 23.6% +/- 2.6% in the histidine-tryptophan-potassium group (p < 0.05). Creatine kinase levels were significantly lower in the histidine-tryptophan-potassium group than that in the glucose-insulin-potassium group (p < 0.05). The incidence of ventricular arrhythmia (higher than Lowns grade 2) was lower in the histidine-tryptophan-potassium group. CONCLUSIONS These data support the superiority of the histidine-tryptophan-potassium method over the glucose-insulin-potassium method for protection of the dilated heart during prolonged ischemia in open heart operations.

Prolonged preservation of the blood-perfused canine heart with glycolysis-promoting solution

BACKGROUND Prolonged ischemia and inadequate myocardial preservation remain significant perioperative risk factors in cardiac transplantation. Long-term preservation techniques that have been effective in small rodent hearts have not been as effective in larger animal models or in clinical studies. We developed a cardioplegia solution formulated to promote high-energy phosphate production from glycolysis and determined its efficacy in a blood perfused canine heart model subjected to 24 hours of ischemia. METHODS Hearts harvested from adult dogs (n = 6 per group) were flushed with a histidine-buffered cardioplegia solution containing glucose or University of Wisconsin solution. The hearts were maintained at 4 degrees C for 24 hours then reperfused with autologous blood. After reperfusion, left ventricular pressures were measured with an intracavitary balloon at varying balloon volumes and compared with control nonischemic hearts. Predicted stroke volume and ejection fraction were calculated at an end-systolic pressure of 70 mm Hg and end-diastolic pressure of 15 mm Hg. RESULTS Developed pressure was better preserved in the hearts that received histidine-buffered solution (93+/-9 versus 38+/-7 mm Hg, p<0.05), along with a higher end-diastolic volume at 15 mm Hg (31+/-3 versus 22+/-2 mL histidine-buffered versus University of Wisconsin solutions, respectively, p<0.05). Stroke volume and ejection fraction were also higher in the histidine group (17+/-2.5 versus 2.3+/-1.2 mL and 50%+/-3.5% versus 9% +/-4.5%, respectively) in the presence of dobutamine. CONCLUSIONS The highly buffered glycolysis-promoting cardioplegia solution provided effective preservation of the blood perfused canine heart with superior recovery of pump performance after 24 hours of hypothermic ischemia compared with University of Wisconsin solution in this model.

Effectiveness of ischemic preconditioning on long-term myocardial preservation.

BACKGROUND This study was designed to assess whether the protective effect of ischemic preconditioning can be adapted for myocardium undergoing 6 hr of ischemia. METHODS Eighteen isolated rat hearts were perfused with oxygen-bicarbonated Krebs-Henseleit buffer in the Langendorff mode for 35 min (group A, controls) or perfused in the Langendorff apparatus for 20 min, followed by 5 min of global normothermic ischemia and 10 min of buffer perfusion (group B, preconditioning) or followed by two cycles of 2.5 min of global normothermic ischemia plus 5 min of buffer perfusion (group C, preconditioning). The hearts were then arrested and preserved for 6 hr with Bretschneiders histidine-tryptophan-potassium cardioplegic solution at 4 degrees C, followed by 30 min of reperfusion. Recovery of cardiac function, postischemic enzyme leakage, and intracellular calcium concentration were compared. RESULTS After 6 hr of ischemia, the hearts that underwent preconditioning in groups B and C showed better recovery of left ventricular developed pressure (P<0.05), a lower end-diastolic pressure level (P<0.05), less leakage of creatine kinase, and a lower intracellular calcium concentration than those in group A. There were no statistical differences in the rate of recovery of coronary flow. CONCLUSIONS Our study demonstrated that ischemic preconditioning improves myocardial functional recovery after 6 hr of hypothermic preservation in the isolated rat heart. Preconditioning might be useful for preserving the heart against long-term ischemia/reperfusion injury.

Delayed diagnosis of anomalous origin of the left coronary artery 16 years after mitral valve replacement

Mitral insufficiency caused by ischemia is frequently found in anomalous origin of the left coronary artery from the pulmonary artery. We report a case of a 25-year-old woman who was diagnosed to have anomalous origin of the left coronary artery from the pulmonary artery and had successful left internal mammary artery bypass grafting 16 years after mitral valve replacement for mitral insufficiency of an unknown cause in her childhood.

Should the Aortic Valve Homograft Be Recryopreserved

BACKGROUND The number of homograft donors is limited and the once-thawed homograft may be unsuitable for the recipient and obliged to be wasted. The purpose of this study was to investigate the possibility of recryopreserving and using the once-thawed homograft for another patient. METHODS Canine aortic valve leaflets were frozen to -80 degrees C by a programmed freezer, stored in liquid nitrogen, and thawed after 1 week. A subgroup of leaflets was left at 4 degrees C for 15 minutes, re-cryopreserved, and thawed after 1 week. Pathologic and flow cytometric evaluations were performed. RESULTS After thawing, by pathology, alignment of the fibers was acceptably maintained but the membrane and cytoplasm of the fibroblast were damaged. These findings were not significantly aggravated even after rethawing. By flow cytometry, fibroblast viability was 90.7%+/-1.7% immediately after thawing, 87.6%+/-1.0% after thawing for 15 minutes at 4 degrees C, 63.7%+/-2.7% during refreezing at 0 degrees C, and 39.4%+/-4.3% after rethawing. CONCLUSIONS From the standpoint of fibroblast viability, it is not possible to recryopreserve the once-cryopreserved and thawed aortic valve homograft.

Cardioprotective efficacy of ischemic preconditioning on long-term myocardial ischemia

This study was designed to assess whether the protective effect of ischemic preconditioning can be adapted for myocardium undergoing 6 h of no-flow ischemia. Twelve isolated rat hearts were either perfused with oxygen-bicarbonated Krebs-Henseleit buffer in the Langendorff mode for 35 min (n=6), or perfused in the same way for 20 min, following 5 min of global normothermic ischemia and 100 min of buffer-perfusion (n=6). The 12 hearts were then preserved for 6 h in HTK solution at 4 degrees C, followed by 30 min of reperfusion. Recovery of cardiac function, metabolic activity and intracellular free calcium concentration were compared between the two groups. After 6 h ischemia, the hearts that underwent preconditioning showed better recovery of left ventricular developed pressure (P<0.01), a lower end-diastolic pressure level (P<0.05), less creatine kinase leakage and a lower calcium concentration. There was no statistical difference in the recovery rate of coronary flow and leakage rate of LDH between the two groups. In conclusion, this experiment demonstrates that ischemic preconditioning improved myocardial functional recovery after 6 h of hypothermic ischemic preservation in the isolated rat heart. Preconditioning might be a potential mechanism for preserving the heart against long-term ischemia/reperfusion injury.

Mechanisms of Exercise Response in Denervated Heart After Transplant

Mechanisms through which the denervated heart responds to supine exercise were assessed in various ways in seven cardiac transplant recipients, 1–37 months after surgery. The results were compared with those in 15 normal subjects. The heart rate at rest and after exercise in transplant patients was 30% higher than normal (P < 0.01). Although cardiac output at rest was similar in both groups, early in exercise the means by which cardiac output increased in the transplant patients differed from normal. In the transplant recipients during the early stage of exercise, the blood norepinephrine level was significantly elevated, and the percent fraction shortening and velocity of circumferential fiber shortening (Vcf) was also higher than in normal subjects with an approximately similar heart rate. The level of atrial natrium diuretic peptide was also significantly increased during exercise by augmented preload (P < 0.01). These results support the concept that in the transplanted heart, there are increases in cardiac output via mechanisms different from those in normal hearts.

Transdiaphragmatic drainage of pericardial effusion with severe pericardial adhesions

We describe a method to perform successful drainage of pericardial effusion by incising the diaphragm via the peritoneal cavity assisted by transesophageal echocardiography. This transdiaphragmatic approach is a remarkably simple and useful method for pericardial drainage when the conventional transsubxiphoid approach is difficult and dangerous because of intractable adhesions between the heart and the pericardium.