Heart-Lung Transplantation

Abstract

We report our initial experience with three patients who received heart-lung transplants. The primary immunosuppressive agent used was cyclosporin A, although conventional drugs were also administered. In the first patient, a 45-year-old woman with primary pulmonary hypertension, acute rejection of the transplant was diagnosed 10 and 25 days after surgery but was treated successfully; this patient still had normal exercise tolerance 10 months late. The second patient, a 30-year-old man, underwent transplantation for Eisenmenger's syndrome due to atrial and ventricular septal defects. His graft was not rejected, and his condition was markedly improved eight months after surgery. The third patient, a 29-year-old woman with transposition of the great vessels and associated defects, died four days postoperatively of renal, hepatic, and pulmonary complications. We attribute our success to experience with heart-lung transplantation in primates, to the use of cyclosporin A, and to the anatomic and physiologic advantages of combined heart-lung replacement. We hope that such transplants may ultimately provide an improved outlook for selected terminally ill patients with pulmonary vascular disease and certain other intractable cardiopulmonary disorders.

Systemic hypertension in heart transplant recipients

“…It was observed that cyclosporine diminishes prostaglandin levels 5,11,15,22 and increases the synthesis of thromboxane A2 11,19,22,39 , a powerful vasoconstrictor and platelet aggregation factor 2 . However, selective antagonists for thromboxane A2 partially reverse the vasoconstriction caused by cyclosporine 15,21 , increasing the glomerular filtration rate, but do not change blood pressure levels 22 .…”

“…Cardiac denervation due to cardiac transplantation causes an increase in the sensitivity of beta-adrenergic receptors 11 , which results in an increment of sympathetic activation caused by cyclosporine 24 . Studies using intraneural microelectodes inserted selectively into muscle nerve fascicles of the fibular nerve Hypertension in heart transplant recipients…”

“…Even though most of the patients develop SH, despite using cyclosporine in low doses, this drug does not seem necessarily associated with renal function injury 9,25 . Decrease in glomerular filtration rate causes sodium and water retention, resulting in expansion of the extracellular liquid volume and BP increase 3,9,11,12,14,19,20,31,32 . The presence of normal cardiac output and ventricular filling pressure is an indirect argument against the hypothesis that hypervolemia would be the cause of cyclosporine-induced SH 9 .…”

“…It is a powerful immunosuppressive drug, representing the basis of current immunosuppressive therapy in organ transplant recipients [11][12][13] . Its use, however, is related to several adverse effects, such as SH 2,5-10,14-23 , nephrotoxicity 2,[5][6][7][8][11][12][13][14][15][16][17][20][21][22][23] , hepatotoxicity 8,11 , neurotoxicity 1 , myocardial fibrosis 6,8,12 , hirsutism, hypertrichosis and gingival hyperplasia 11,23 . SH and nephrotoxicity are the most common adverse effects 9,13 , more frequent in organ transplant recipients using cyclosporine than in those treated with azathioprine and prednisone 1,4,7 .…”

Asystole after intravenous neostigmine in a heart transplant recipient

“…1 Heart rate responses to exercise and medications early after transplant have demonstrated the denervated character. 2 More recently, there have been more studies of patients who are years posttransplantation showing consistent evidence of reinnervation.…”