A significant reduction in plasma free triiodothyronine (T3) (P less than 0.0001) has been observed in patients undergoing open heart surgery. The beneficial effect of T3 would appear to be associated with increased synthesis and utilization of myocardial high energy stores. We have therefore administered T3 (4-10 micrograms iv) to 10 patients either when difficulty was being experienced in weaning from cardiopulmonary bypass (CPB) support (n = 5), or when myocardial function remained extremely poor (n = 5), despite inotropic and intraaortic balloon pump support. Mean preoperative NYHA functional class of the 10 patients was 3.2, left ventricular enddiastolic pressure (LVEDP) 20 mm Hg and ejection fraction (EF) 40%. The mean myocardial ischaemia time was 72 min (range 40-120 min). Within 1 h of T3 administration the mean plasma free T3 level had risen from 1.03 to 3.56 micrograms/ml and CPB was discontinued in all 5 cases. Balloon pump support (n = 2) was no longer essential within 3 h. At 1 h, the mean arterial pressure (MAP) had risen from 42 to 78 mm Hg, and heart rate (HR) from 90 to 104 beats/min; the left atrial pressure (LAP) had fallen from 30 to 14 mm Hg, and the central venous pressure (CVP) from 20 to 11 cm H2O. (All changes significant at P less than 0.0001.) Inotropic support had been significantly reduced or discontinued. To our knowledge, T3 has not been administered previously as an inotropic agent to patients who have undergone cardiac surgery. We believe that T3 may have an important role in the rescue of failing hearts following a period of myocardial ischaemia in patients who have undergone open heart surgery.
Corrected transposition of the great vessels is a congenital anomaly first described by von Rokitansky in 1875. In its most common form it consists of transposition and inversion of the great vessels and inversion of the ventricles, while the atria and their venous connections are normally situated. The right atrium connects with the left ventricle via a bicuspid valve on the right side and this right-sided, but anatomically left, ventricle joins the pulmonary trunk arising posteriorly and to the right of the aorta. Similarly, the left atrium connects via a tricuspid valve to an anatomically right ventricle on the left side, from which arises the aorta anteriorly and to the left of the pulmonary trunk. The great vessels then ascend side by side without crossing over in the normal manner. In this way the aorta receives oxygenated blood and the pulmonary artery desaturated blood. In addition the coronary arteries show inversion and transposition. The plane of the interventricular septum is rotated through 180 degrees so that it runs from the back to the front and from left to right (De La Cruz et al., 1959). The interior of the right ventricle has all the anatomical features of a normal left ventricle, while the left-sided ventricular chamber has the features of a right ventricle. Walmsley (1931) has demonstrated the reversal of the usual pattern of the conduction system in that the atrio-ventricular bundle and its branches proceed along the septal wall of the right-sided ventricle. Cardell (1956) and Anderson et al. (1957) have reviewed the various types of corrected transposition that may occur. These types depend on the presence of sinu-atrial, ventricular, and bulbar inversion in various combinations.Various embryological explanations have been given in an attempt to understand the mechanism of development of this abnormality. Spitzer's (1929) conception of the role of torsion and detorsion has been accepted by some, while others like Walmsley (1931) (1942), Davis (1927), Streeter (1948), andLicata (1954) who have studied a large number of human embryos at the Department of Embryology of the Carnegie Institute, Washington and other universities. They conclude that corrected transposition, in any of its varieties, is a complex malformation in which two embryonic elements are involved, namely the bulbo-ventricular loop and the cono-truncal septum. They propose an embryological explanation of the defect in a normally situated heart, in mirror image dextrocardia, and in dextro-rotation.Corrected transposition rarely exists as an isolated abnormality. Cardell (1956) mentions two patients without associated abnormalities, one of whom had heart block. Edwards et al. (1954) quote a patient, in whom the defect existed as an isolated asymptomatic lesion. More recently Schaefer and Rudolph (1957) reported a patient who died in congestive heart failure at the age of 36 with heart block, but there was no other abnormality. The vast majority of cases have some associated lesion, an atrial septal defect, ventricular s...
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