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Prolonged extracorporeal membrane oxygenation (PEMO) was performed in 6 adult ponies with the membrane oxygenator in vein-to-artery bypass circuit. A flow rate equal to 46 per cent of control cardiac output was diverted through the PEMO circuit of 10 to 24 hours. Three of the 6 ponies were perfused for at least 20 hours and developed no complications. Immediately following initiation of PEMO, left ventricular output decreased; however, in the interval between 6 and 24 hours, left ventricular output was increased above control levels. Aortic pressure and left ventricular work were markedly elevated during PEMO. Pulmonary ventilation and oxygen uptake also decreased initially but were elevated during later stages of bypass. Pulmonary compliance did not change, except in those studies in which problems were encountered with perfusion techniques. Hepatic glycolysis and hyperglycemia occurred and were more severe in ponies with catheter-produced thrombi. Marked diuresis, which could be attributed only partially to the hyperglycemia, was present throughout PEMO. Based on the minimal morphologic changes observed in the ponies, extracorporeal circulation diverting one half of the cardiac output through a membrane oxygenator can be safely performed for up to 24 hours.

Tweleve patients with the complete form of persistent atrioventricular (AV) canal were operated upon at the University of Wisconsin between May, 1972, and November, 1975. The technique originally described by Rastelli and his associates was used. All 12 patients are asymptomatic and well, with no hospital or late deaths. Postoperative cardiac catheterization in 8 patients showed a return to near normal dynamics, with minimal residual mitral insufficiency. Half of these children had type A and half type C malformations; both types could be repaired without the need for valve replacement. Since 3 of these patients were less than 2 years of age, we now feel that complete repair of the AV canal can be undertaken in children between 12 and 18 months of age for optimal management.

Heart and kideny allografts showed markedly prolonged survival in unrelated mongrel dogs following total lymphoid irradiation (TLI) and donor bone marrow without any other immunosuppression. In every animal the heart survived longer than the kidney; genetic disparity was ruled out, since the heart and kidney from the same donor were placed into one recipient. Placing the kidney allograft in the abdomen with the bone marrow given intraperitoneally doubled kidney survival over placement in the neck, but heart survival was equally prolonged in the abdomen or neck. Splenectomy before TLI or after TLI, but just before transplantation, almost completely eliminated the prolonged survival of both heart and kidney allografts. Thus there is suggestive evidence from the work of Slavin and his colleagues and from our study that TLI plus bone marrow from the donor may be valuable for transplantation in man, particularly heart transplantation.

Hearts preserved for 2 hours at 15 degrees C were evaluated for maximum function with the use of an isolated working dog heart subjected to stress. We determined left ventricular function by controlling aortic flow resistance and flow into the left atrium. Groups studied were hypothermia alone (H), hypothermia with a modified extracellular solution (H + DKS), hypothermia with a modified Collins solution (H + C), six periods of 20 minutes of hypoxic hypothermia followed by 10 minutes of blood reperfusion (H20 + R10) and blood cardiplegia (BC). Hypothermia alone for 1 hour was also evaluated. Functions were studied for 2 1/2 hours following reperfusion by determining Starling's curves for each heart. Our data show that H alone gave adequate myocardial protection for only 1 hour but not for 2 hours. H20 + R10 was better than H, but function was depressed. Use of H + C provided protection equal to H20 + R10, but the hearts recovered function slowly. Only hearts preserved by H + DKS and BC for 2 hours had normal function. Hearts from all groups except H + DKS and BC became edematous. Excellent function was obtained with DKS or BC following 2 hours of ischemia at 15 degrees C. Initial clinical use of BC supported these laboratory findings.

Eighty-six patients admitted with evolving myocardial infarction within 6 hours of symptom onset were treated with streptokinase. Thirty-nine received intracoronary streptokinase, and 47 received intravenous streptokinase. There were no streptokinase-related complications. Twenty-three patients treated with intracoronary streptokinase and 28 patients receiving intravenous streptokinase underwent coronary artery bypass grafting. On admission, 16 patients receiving intracoronary streptokinase had electrocardiographic evidence of anterolateral evolving myocardial infarction and seven had evidence of inferior evolving myocardial infarction. Time from first symptom to intracoronary streptokinase was 4.4 +/- 1.6 hours. In seven patients, intracoronary streptokinase failed to open the obstructed coronary. All developed severe left ventricular hypokinesia in the area supplied by that coronary artery. In spite of recanalization, nine of 14 patients developed severe hypokinesia in the supplied area, and one an apical aneurysm. Four patients developed mild to moderate hypokinesia, and one had no left ventricular damage. On admission, 14 patients receiving intravenous streptokinase had electrocardiographic evidence of anterolateral evolving myocardial infarction and four had evidence of inferior evolving myocardial infarction. Time from first symptom to intravenous streptokinase was 3.2 +/- 1.5 hours. In seven patients, intravenous streptokinase failed to open the coronary, and all developed severe hypokinesia of the supplied area, with formation of apical left ventricular aneurysm in three. In 21 patients, intravenous streptokinase opened the artery. Eighteen angiographies performed 9.6 +/- 7.9 days after therapy showed a normal left ventricle in eight patients, moderate hypokinesia in seven, and severe hypokinesia in three. Time from first symptom to therapy was shorter in the patients receiving intravenous therapy (p less than 0.01). Coronary artery bypass grafting and four resections after left ventricular aneurysm were performed without operative death. Two patients receiving intracoronary therapy died in the hospital, and one died 2 months later from arrhythmias. Freedom from angina and rehabilitation (New York Heart Association Class I) were achieved in 69.5% of patients receiving intracoronary streptokinase and in 75% of patients receiving intravenous streptokinase. Thus streptokinase-induced thrombolysis salvages myocardium, and the intravenous route seems as effective as the intracoronary. Advantages of the former are earlier administration that might increase myocardial salvage, no invasive procedure, and lesser cost.

Quinidine syncope is an unpredictable side effect of quinidine administrateion which has a mortality rate of 11.5 per cent when managed with conventional drugs and direct-current countershock. In 2 patients with quindine syncope, the arrhythmias were effectively controlled within 30 minutes following the slow infusion of 150 mg. of bretylium tosylate. This control is contrasted with 2 cases managed in the conventional manner. Bretylium tosylate is a quaternary amine with unique antifibrillatory properties and appears to have a significant role in the management of these arrhylmias.