Kuei-Ton Tsai

Protection of the brain by retrograde cerebral perfusion during circulatory arrest

Hypothermic circulatory arrest is commonly used to facilitate repair of complex congenital heart defects and aortic lesions and for complex neurosurgical procedures. However, extended periods of circulatory arrest may impair cerebral metabolism and cause ischemic injury. Retrograde cerebral perfusion has been applied recently in aortic surgery to protect the brain. From January 1991 to December 1993, 29 patients underwent emergency operations to repair acute type A aortic dissection with the aid of hypothermic circulatory arrest. Six patients received hypothermic circulatory arrest without retrograde cerebral perfusion with a rectal temperature of 16.4 degrees +/- 0.9 degrees C (mean +/- standard error of the mean, group 1). Retrograde cerebral perfusion during hypothermic circulatory arrest was performed in 15 patients with a rectal temperature of 15.9 degrees +/- 0.5 degrees C (group 2) and in eight patients with a rectal temperature of 21.7 degrees +/- 0.8 degrees C (group 3). The hypothermic circulatory arrest times were 25 +/- 4, 42 +/- 4, and 63 +/- 6 minutes, respectively (p < 0.05). The cardiopulmonary bypass times were 173 +/- 5, 184 +/- 7, and 143 +/- 6 minutes, respectively (p < 0.05). All patients survived the operation and regained consciousness with no neurologic defects. Follow-up (mean 23.2, 14.5, and 5.1 months, respectively) was complete in all patients except one. This patient, from group 2, was killed in a road traffic accident 12 months after the operation. Our experience suggests that retrograde cerebral perfusion can effectively protect the brain from ischemic injury and extend the safe period of hypothermic circulatory arrest. With the aid of retrograde cerebral perfusion, prolonged circulatory arrest can probably be performed safely with moderate hypothermia.

Surgical management of thrombotic disc valve

Thrombotic obstruction, a rare but often fatal complication of cardiac valve prostheses, appears to occur more frequently in tilting-disc valves than in other valve designs. Its diagnosis and surgical treatment remain a challenge. Ten consecutive patients who had thrombosis of a tilting-disc valve prosthesis were treated in Chang Gung Memorial Hospital from November 1982 to August 1990. Preoperative clinical features, including exertional dyspnea, new murmur, and absence of a metallic click from the prosthetic valve, occurred in all of the patients. Symptoms were present for 1 week or more before reoperation in 70% of the patients; nevertheless, many patients were referred only after acute exacerbation of heart failure and development of pulmonary edema. Echocardiography confirmed prosthetic valve malfunction in 90% of the patients. One unconfirmed case was later documented by cardiac catheterization. Anticoagulant therapy was in the therapeutic range for only half of the patients at the time of admission. Prompt reoperation was performed for thrombectomy (8 patients, all survived) or valve replacement (2 patients, one death). Long-term outcome was satisfactory in all survivors with a mean follow-up of 31.6 months. These findings emphasize the importance of considering the diagnosis of thrombosis in patients with mechanical heart valve prostheses who are first seen with nonspecific symptoms and minor changes of their physical findings. The diagnosis could be easily made by echocardiography. Thrombectomy is an easy, fast, and safe procedure, especially for these critically ill patients.

Endothelium-dependent contraction of canine coronary artery is enhanced by crystalloid cardioplegic solution ☆ ☆☆ ★ ★★ ♢

Experiments were designed to determine whether hyperkalemic crystalloid cardioplegic solution enhances endothelium-dependent contraction of coronary arteries. Segments of canine coronary arteries (n = 8 in each group) were preserved in cold (4 degrees C) crystalloid cardioplegic solution (group 1) and physiologic solution (group 2) for 60 minutes. Segments of preserved and control (group 3) coronary arteries with or without endothelium were suspended in organ chambers to measure isometric force. Perfusate hypoxia (oxygen tension 35 +/- 5 mm Hg) caused endothelium-dependent contraction in the arteries of all three groups. However, vascular segments with endothelium of group 1 exhibited hypoxic contraction (68.5% +/- 15.3% of the initial tension contracted by prostaglandin F2 alpha 2 x 10(-6) mol/L, p < 0.05) that was significantly greater than contraction of the group 2 and group 3 segments with endothelium (26.6% +/- 5.6% and 20.6 +/- 4.4%). The hypoxic contraction in arteries of group 1 could be attenuated by NG-monomethyl-L-arginine, the blocker of endothelial cell synthesis of the nitric oxide from L-arginine. The action of NG-monomethyl-L-arginine could be reversed by L-arginine but not D-arginine. Thus after preservation with cardioplegic solution, augmented endothelium-dependent contraction, occurs by L-arginine-dependent pathway, would favor coronary vasospasm after cardiac operation.

Continuous antegrade warm blood cardioplegia attenuates augmented coronary endothelium–dependent contraction after cardiac global ischemia and reperfusion

BACKGROUND Experiments were designed to evaluate the effect of warm blood cardioplegia on endothelium-dependent contraction of the coronary endothelium after cardiac global ischemia and reperfusion. METHOD Dogs (n = 12 in each group) were exposed to extracorporeal circulation with the body temperature at 37 degrees C (group 1) or 28 degrees C (groups 2 and 3). The ascending aorta was crossclamped for 120 minutes while continuous infusion of warm blood cardioplegec solution (group 1) or intermittent infusion of cold (4 degrees C) crystalloid cardioplegic solution (group 2) was performed via the coronary arteries through the aortic root. Cardioplegic solution was not used in group 3 animals. The heart was then allowed to function for 60 minutes of reperfusion. Reperfused (groups 1, 2, and 3) and control (group 4) coronary arteries were then harvested for study. RESULTS Perfusate hypoxia caused endothelium-dependent contraction in the arteries of all four groups that could be attenuated by NG-monomethyl-L-arginine (L-NMMA) or L-NMMA plus D-arginine, but not by L-NMMA plus L-arginine or endothelin receptor A and B antagonist PD 145065. The endothelium-dependent contraction results in groups 2 and 3 (75% +/- 4% and 80% +/- 5%, respectively) were significantly greater than those in groups 1 and 4 (15% +/- 3% and 18% +/- 5%, respectively). Scanning electron microscope studies showed that platelet adhesion and aggregation, areas of microthrombi, disruption of endothelial cells, and separation of the intercellular junction could be found in coronary segments from groups 2 and 3, but not in vessels from groups 1 and 4. CONCLUSION These experiments suggest that global ischemia and reperfusion enhances hypoxia-mediated endothelium-dependent contraction of the coronary endothelium and damages the ultrastructure. These kinds of changes can be prevented by continuous antegrade infusion of warm blood cardioplegic solution during global ischemia.

Conduit-on-valve replacement of a degenerated mitral bioprosthesis with a bioprosthesis

Explantation of a degenerated mitral bioprosthesis with reimplantation of a new bioprosthesis is time-consuming and can be associated with several life-threatening complications. We developed a technique to simplify this procedure and avoid the complications by attaching a new bioprosthesis supported by a pericardium-covered Dacron tube to the intact stent.