[A case of circumflex artery-coronary sinus fistula].
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Biomedical subjects
Publications and source records attributed to C Dubost.
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Persistent or recurrent hyperparathyroidism after total parathyroidectomy with forearm implant may be caused by hyperplastic grafted tissue, residual parathyroid tissue left in the neck or the presence of a supernumerary gland not found during surgery. A correct assessment of graft function is needed to localize the source of hormone excess and to avoid an unnecessary neck reoperation in cases of graft dependent hyperparathyroidism. In 12 patients with relapsing hyperparathyroidism after total parathyroidectomy with forearm implant, total ischemic blockade of the arm bearing the parathyroid graft produced a "transitory implantectomy" with a significant reduction of serum levels of intact PTH in those with graft hyperfunction. In 6 patients with proved supernumerary glands, total ischemia of the graft was not followed by significant changes in intact PTH. Hyperparathyroidism was reversed after surgical resection of the parathyroid implants in the 6 patients with positive responses to the ischemic maneuver. A repeat neck reoperation removing cervical or mediastinal supernumerary glands was followed by control of recurrent hyperparathyroidism in the 6 patients with a negative response to the ischemic blockade. Total ischemic blockade of the arm bearing the parathyroid graft is a valuable method for a correct assessment of graft function after total parathyroidectomy with forearm autotransplantation.
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Myocardial protection, in two parallel series of 100 consecutive valvular patients operated upon between June 1972 and July 1973 in Broussais Hospital, was afforded in two different ways: one withh hypothermic ischemia (H.I.) as it was advocated by N. Shumway, the other with coronary perfusion (C.P.) of a beating heart with consecutive ischemic periods limited to 20 minutes. Three parameters were used to evaluate the quality of protection: death with primary cardiogenic shock, post-operative myocardial infarction and acute cardiac insufficiency making it necessary to use post-operative inotropic support. Death was 1% (H.I.) and 5% (C.P.). Infarctions were 5% (H.I.) and 8% (C.P.). Acute cardiac insufficiency was: with cardiogenic shock 0% (H.I.) and 4% (C.P.), without cardiogenic shock 8% (H.I.) and 2% (C.P.). Peculiar aspects of myocardial infarction in each series are analyzed, and apparent absence of correlation between aortic cross-clamp time and ischemic complications is discussed. A "myocardial intrinsic factor" seems to be part of each valvular group and appears also to be an important factor in producing ischemic complications.