effects are observed in the proximal portion of the contra- lateral coronary artery and thus are not selective when administered as in our protocol. Hackett et al* administered intracoronary ergonovine to a maximum cumulative dose of 50 pg in 6 patients with variant angina and in 9 patients similar to the group included in the current study. In the latter group, intra- coronary ergonovine produced vasoconstriction of a simi- lar magnitude as seen in our study; however, proximal, mid- and distal segment responses were not compared and the contralateral coronary artery was not measured. Fournier et al2 administered single or repeated intracoro- nary bolus doses (25 pg) of ergonovine to 108 patients with normal coronary angiography. Again, ergonovine caused vasoconstriction but no contralateral coronary ar- tery effects were measured. In general, our data show a dose-dependent ergono- vine-mediated vasoconstriction, although in 1 patient all right coronary artery segments revealed vasodilation af- ter 10 fig (Figure 2), which was overcome with higher doses of ergonovine. Mohri et al4 described a similar case, in which a dilator response of both the left and right coronary arteries was observed with 20 PLg intracoronary ergonovine followed by a constrictor response when an additional 35 pg intracoronary ergonovine was adminis- tered. These results are similar to observations of the effect of intravenously administered ergonovine on coro- nary arterial diameter in dogs. This response has been shown to be biphasic, in the form of an initial dilating action followed by a constricting action.5 The magnitude of mean proximal right coronary ar- tery constriction (69%) after administration of 60 pg ergonovine into the left main coronary artery was greater than the effect seen when ergonovine was administered directly into the right coronary artery (44%). When ergo- novine was administered into the right coronary artery, a 19% mean decrease in left main coronary artery area was observed, whereas a 33% decrease was seen when ergono- vine was given directly into the left main. Although these measurements cannot be directly compared because they were obtained from different patients, the magnitude of the responses observed in the proximal contralateral ar- tery is impressive. The mechanism by which intracoro- nary ergonovine affects the contralateral coronary artery in its most proximal segment cannot be deduced from this observational study. One obvious possibility includes spilling of ergonovine during systole into the contralateral sinus despite precautions taken to prevent this by careful catheter placement and slow injection. Other potential mechanisms include recirculation of ergonovine, preresis- tance vessel or collateral shunting of blood or local reflex- es. In any event, the assumption that one is safely getting a selective unilateral coronary vasoconstrictor effect dur- ing intracoronary ergonovine administration is not sup- ported by the data presented herein. Whether this repre- sents a cause for concern clinically must await further studies. Contralateral coronary angiograms should prob- ably always be recorded after intracoronary administra- tion of ergonovine so as not to miss important coronary vasoconstriction that may occur. 11.Hackett D, Larkin S, Chierchia S, Davies G, Kaski JC, Mascri A. Induction of coronary artery spasm by a direct local action of ergonovine. Circulation 1987;75:577-582. 2. Fournier JA, Cortacero JAP, Tura A, Hernandez-Aparicio C, Granada C, Vallejo J. Effects of intracoronary injection of ergonovine on angiographic normal coronary arteries: study of 108 consecutive patients. Chin Cardiol 1989;12:56 I - 568. 3. Silver KH, Buczec JA, Esser PD, Nichols AB. Quantitative analysis of con- nary angiograms by microprocessor cinc-videodensitomctry. C&et Cardiouasc Diagn 1987;13:291-300. 4. Mohri M, Okamatsu S, Nakamura M. Case report: biphasic response of coronary arterial diameter to intracoronary ergonovine. Clin Cardiol 1988; 11:710-714. 5. Holtz J, Held W, Sommcr 0, Kuehne G, Bassenge E. Ergonovine-induced constrictions of epicardial coronary arteries in conscious dogs: alpha-adrenoccp- tars are not involved. Basic Res Cnrdiol 1982;77:278-283. Karen &ark, RN, Pm, Dermis Crowley, MD, Louise Callow, Mm, and Edward Bove, MD ince the 1985s a steadily increasing number of chil- dren have undergone cardiac transplantation. Al- though graft rejection and complications of immunosup- pressive therapy are the leading causes of death in chil- dren and adults after cardiac transplantation, coronary atherosclerosis is a significant cause of late mortality.1,2 Our first pediatric heart transplant patient died suddenly 17 months after transplantation at 3 years of age with severe coronary atherosclerosis. Transplant coronary ath- erosclerosis may be the result of immune endothelial inju- ry, with a response characterized by proliferation of -- From the University of Michigan Medical Center, Division of Pediatric Cardiology and Division of Thoracic Surgery, Room F1126, Box 0204, 1500 East Medical Center Drive, Ann Arbor, Michigan 48109-0204. Manuscript received April 23, 1990; revised manuscript received and accepted July 18, 1990. myoi~timal cells, thrombus formation, and ultimate in- traarterial deposition of lipid material.3-5 The develop- ment of atherosclerosis in transplanted hearts may be enhanced by the presence of hyperlipidemia, both hyper- triglyceridemia and hypercholesterolemia. We measured serial lipid levels in 14 children after heart transplanta- tion to assess the prevalence of lipid abnormalities and the usefulness of niacin therapy in children with significant hypercholesterolemia after transplantation. The study sample comprised 14 children (aged 6 months to 16 years [mean S]) who underwent cardiac transplantation. There were 5 girls and 9 boys. Eight of I4 children (57%) received transplants for cardiomyop- athy, 1 restrictive, 7 of the dilated type, and 1 caused by anthracyclines. The remaining6 children had severe ven- tricular dysfunction with congenital heart disease-4 with complex cyanotic heart disease, 1 with severe aortic THE AMERICAN JOURNAL OF CARDlOLOGY DECEMBER 1, 1990