Search

Case Report, A 51-year-old man who had undergone a modified Carpentier procedure at age 32 years for Ebstein anomaly later developed chronic heart failure due to severe tricuspid regurgitation and atrial flutter with right heart dysfunction. Findings from indocyanine green fluorescence angiography were helpful in avoiding an unnecessary additional procedure of one and one half ventricle repair. At a 6-month follow-up examination, the patient was asymptomatic and had a normal sinus rhythm without administration of an antiarrhythmic agent.

Case Report, A 64-year-old woman was admitted for weakness and coldness in her right upper arm. She had undergone a right mastectomy for breast carcinoma 32 years before presentation and radiotherapy for clavicular metastasis of breast cancer 3 years before presentation. After thorough investigation, post-radiotherapy axillary artery occlusion was diagnosed. She underwent right external carotid-brachial artery bypass and was discharged without postoperative cerebral complications. Herein, we describe treatment for post-radiotherapy axillary artery occlusion.

Impaired myocardial metabolism after cardioplegic arrest results in persistent anaerobic lactate production. Insulin may protect the heart from ischemia and reperfusion by enhancing myocardial metabolic recovery. However, the stimulation of glycolysis during ischemia may be detrimental because of an accumulation of metabolic end-products. We examined the effect of insulin on quiescent human ventricular cardiomyocytes subjected to simulated cardioplegic ischemia and reperfusion. Methods: Primary cardiomyocyte cultures were established from patients undergoing corrective repair of tetralogy of Fallot. Cells were exposed to varying concentrations of glucose and insulin during 30 minutes of stabilization in 10 mL of phosphate-buffered saline solution. Ischemia was simulated by exposing the cells to a low volume (1.5 mL) of deoxygenated phosphate-buffered saline solution for 90 minutes followed by 30 minutes of simulated reperfusion in 10 mL of normoxic phosphate-buffered saline solution. Cell viability was assessed by trypan blue exclusion. The activity of mitochondrial pyruvate dehydrogenase was measured in 3 states: stabilization, ischemia, and reperfusion. In addition intracellular lactate, adenine nucleotides, extracellular lactate, pyruvate, and acid release were measured. Results: Higher ambient glucose concentrations resulted in greater cellular injury although insulin-treated cells displayed less injury after ischemia and reperfusion. Insulin increased the pyruvate dehydrogenase activity by 31% in cardiomyocytes and reduced extracellular lactate production by 40%. Intracellular adenosine triphosphate was improved by 75% in cells exposed to high glucose concentrations in the presence of insulin. Conclusions: Insulin protected human ventricular cardiomyocytes from ischemia and reperfusion. This protection may be due to a stimulation of pyruvate dehydrogenase activity which resulted in improved aerobic metabolism. (J Thorac Cardiovasc Surg 1998;116:485-94)