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8. Charmer K, Bukis E, Hartnell G, et al. Myocardial bridging of the coronary arteries. Clin Radio1 1989;40:355-9.

9. Angelini P, Trivellato M, Donis J, Leachman RD. Myocardial bridges: a review. Prog Cardiovasc Dis 1983;26:75-88.

10. Laif’er LI. Weiner BH. Percutaneous transluminal coronarv angioplasry of a coronary stenosis at the site of myocardial bridging. Cardiology 1991;79:245-8.

11. Edwards JC, Burnsides CH, Swarm RL, et al. Arteriosclerosis in the intramural and extramural portions of coronary arte- ries in the human heart. Circulation 1956;13:235-42.

12. Ishii T, Asuwa N, Masuda S, et al. Atherosclerosis suppression in the anterior descending coronary artery by the presence of a myocardial bridge: an ultrastructural study. Mod Path01 1991;4:424-31.

13. Stehbens WE. The lipid hypothesis and the role of hemody- namics in atherogenesis. Prog Cardiovasc Dis 1990;2:119-36.

14. Stehben WE. Hemodynamics and the blood vessel wall. Springfield, IL: Charles C Thomas, 1979.

Coronary atherectomy complicated by coronary embolus in a cardiac transplant recipient

Calvin Bell, MD, Morton J. Kern, MD, Frank Aguirre, MD, Leslie Miller, MD, Richard Bach, MD, Thomas Donohue, MD, and Frederick Dressler, MD St. Louis, MO.

Coronary atherectomy is now commonly performed for fo- cal, noncalcified atherosclerotic coronary artery narrow- ings.id4 To date, there has been only one reported study of this procedure being employed for obstructive coronary arteriopathy in cardiac transplant recipients.s We present a unique case of directional atherectomy complicated by coronary embolus in a patient with an orthotopic heart transplant. This patient example indicates the potential complications and benefits of direcbional endoluminal tis sue excision as a means to treat and advance our under- standing of transplant-related coronary artery disease.

A 63-year-old man underwent orthotopic cardiac trans- plant in 1987. A recent routine yearly surveillance angiog- raphy demonstrated a high-grade left anterior descending lesion (80% diameter narrowing by visual estimate). Be- cause of advanced coronary arteriopathy, he was subse- quently admitted for atherectomy of the proximal left an- terior descending coronary artery lesion. During the Z-week interim between the diagnostic and interventional proce- dures, the patient remained asymptomatic despite devel- oping new electrocardiogram changes that showed sinus tachycardia, bifascicular block (right bundle branch block

From the Cardiology Division, St. Louis University Hospital.

Reprint requests: Morton J. Kern, MD, Director, J. G. Mudd Cardiac Cath- eterization Laboratory, St. Louis University Hospital, 3635 Vista Ave. at Grand Blvd., St. Louis, MO 63110-0250.

A.% Hwm’r J 1993;125:1172-1175.

Copyright ” 1993 by Mosby-Year Book, Inc. 0002-870:~/93/$1.00 + .I0 4/4/44070

and left anterior fascicular block). and anteroseptal myo- cardial infarction. These findings were not present on the electrocardiogram obtained after the diagnostic study. Be- fore the procedure, the blood pressure was IlO/ mm IIg, pulse was 98/min, respiratory rate was 16/min, and tem- perature was 97.2” F. Cardiac examination was normal ex- cept for a summation gallop. The examination of the lungs, abdomen, and extremities was unremarkable. The labora- tory profile was normal except for a creatinine of 1.9 mg/ dl. A chest roentgenogram was also normal with t,he excep- tion of the sternal wires from the previous surgery. Coro- nary angiograph y immediately before atherectomy revealed minimal irregularities of the right coronary artery and moderate (61 ‘C narrowing) disease involving the sec- ond obtuse marginal branch, with an otherwise normal cir- cumflex artery. There was total occlusion of the left ante- rior descending artery, which was a new finding compared with a study performed 2 weeks earlier (Fig. I). Left ven- triculography revealed anterolateral akinesis and severe apical hypokinesis, with an ejection fraction of 31’,:. (Two-dimensional echocardiographic left ventricular wall motion at the previous admission indicated only mild an- terior hypokinesis. Contrast ventriculography had been deferred.) After consultation with the attending transplan- tation service physicians and because of the recent total occlusion of the left anterior descending artery, angioplasty and atherectomy were elected. A 10,000 unit bolus and continuous intravenous infusion of heparin were adminis- tered. A 2.0 Magnum balloon system Schneider (USA), Inc., Plymouth, Minn. was initially used, leaving a patent vessel with a residual lesion of 62”, . A 7F atherocatheter device (Atherocath, Devices for Vascular Intervention, Redwood City, Calif.) was then introduced over an 0.014 inch guide wire into the proximal left anterior descending artery. Eight directional cuts were performed with an inflation pressure of 10 to 1:j psi. A total of 12.0 gm of tis- sue was obtained and was transferred to specially prepared media for histologic and immunopathologic staining. The final diameter narrowing was 15”,, (Fig. 2). However, shortly after withdrawal of the atherocatheter, total occlu- sion of the proximal circumflex branch was observed, pre- sumably caused by embolization of thrombotic or athero- sclerotic material (Fig. 3). There were no symptoms, elec- trocardiographic, or hemodynamic changes associated with the new obtuse marginal branch occlusion. The obtuse marginal and circumflex arteries were immediately dilated with a 3.0 mm balloon catheter (Shadow, Scimed, Inc., Minneapolis, Minn.) without difficulty, leaving a residual circumHex narrowing of 3’, The second obtuse marginal branch had a residual lesion of 18’~’ (Fig. 4). The patient remained asymptomatic during and after the procedure. Following the procedure, a continuous intravenous heparin infusion (1000 units/hr) was maintained for an additional 48 hours. The remainder of the hospital course and a s-month follow-up were uneventful, and the patient’s ar- teries remained angiographically patent. The typical fea- tures of classic at.heroscierosis usually demonstrate fibro- sis, lipid, and atherosclerotic inclusion material. Trans-

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American Heart Journal Bell et at. 1173

plant arteriopathy is I usually characterized by proliferative endot thelial cells, thro lmbus (old and new), fibroblasts, and collag ;en.5 Tissue frag :ments of the endoluminal excisions were fixed in 10% fo Irmalin, sectioned, and stained with

Fig. 1. Total occlusion of the left anterior descending artery (white arrow) and a moderate lesio second obtuse marginal artery (black arrow).

mn in the

Fig. 2. Left anterior descending coronary artery post atherectomy.

hematoxylin/azoflaxin and eosin stains and were examir led under light microscopy (original magnificat ,ion X 400) (I cig. 5). The atherectomy core consisted main1 iy of loose 0 on- nective tissue with collagen predominatir ng. Alpha-ac :tin

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Fig. 3. Occluded circumflex artery after successful left anterior descending artery atherectomy.

Fig. 4. Circumflex/obtuse marginal arteries post coronary angioplasty.

staining (not shown) revealed scattered smooth muscle noted. The endothelium was replaced by atherosclerc cells mostly concentrated in the more cellular portions of proliferative changes. The patient did well over a 4-mar the specimen. No section had evidence of elastic membrane follow-up period with only minimal left anterior descer or adventitia. Sporadic intermixed myofibroblasts were ing (<30’,. ) restenosis on follow-up angiography.

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Fig. 5. Histology of the atherectomy specimen. See text for description.

This case illustrates several important points regarding the management of transplant coronary artery disease with interventional techniques. Focal angiographic lesions are commonly observed in patients >3 years after donor organ implantation. The presence and progression of the coro- nary obstructions are often asymptomatic, but recent studies of cardiac reinnervation indicate that the occa- sional patient with chest pain may be experiencing true angina pectoris.6 The occlusive coronary disease in the left anterior descending artery was likely thrombus superim- posed on atherosclerosis and was recanalized by primary coronary angioplasty. The atherectomy procedure was used to debulk the lesion and allowed the procurement of tissue for study. Although thrombolytic therapy was con- sidered, the angiographic result after angioplasty sug- gested resolution of thrombus. As demonstrated here, some thrombus or atherosclerotic debris can remain in situ and may be dislodged by the atherectomy procedure. Careful consideration of this sequence of coronary interventions and their complications should be made before proceeding in patients with compromised ventricular function. The complication rates of routine coronary angioplasty for cor- onary arteriopathy of cardiac transplant recipients are comparable to those of nontransplant patients.7 Major events of advanced coronary arteriopathy in such patients include death, retransplantation, repeat angioplasty, and myocardial infarction in approximately 38% (19 of 51) of patients.7 The examination of tissue from these patients provides one of the first opportunities to study the in vivo manifestations of transplant coronary arteriopathy. How- ever, the silent embolization to the circumflex branches was a known but unanticipated complication of the atherec- tomy procedure. Fortunately, the transplanted heart was unaffected electrocardiographically or hemodynamically by this additional potentially ischemic burden, with stan- dard angioplasty restoring the normal blood flow.

The major differences in histologic findings between atherosclerotic and arteriopathic lesions appear in the greater degree of endothelial proliferation of the arterio- pathic lesions compared with de novo atherosclerotic lesions. Recent reports of coronary luminal tissue excised from the few transplant patients having atherectomy pro- vide similar data.5 The use of atherectomy with tissue analysis will greatly contribute to our understanding of coronary disease progression in the ever-increasing trans- plant recipient population.

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Simpson JB, Johnson DE, Thapliyal HV, Marks DS, Braden LJ. Transluminal atherectomy: a new approach to the treat- ment of atherosclerotic vascular disease [Abstract]. Circula- tion 1985;72:111-146. Simpson JB. Future interventional techniques. In: Califf RM, et al., eds. Acute coronary care in the thrombolytic era. Chi-

cago: Year Book Medical Publishers, 1988:392-404. Hinohara T, Robertson GC, Selmon MR, Simpson JB. Trans- luminal atherectomy: the Simpson atherectomy catheter. In: Moore WS, Ahn SS, eds. Endovascular surgery. Philadelphia: WB Saunders, 1989:310-22. Robertson GC, Hinohara T, Selmon MR, Johnson DE, Simp- son JB. Textbook of interventional cardiology: Directional coronary atherectomy. Philadelphia: WB Saunders, 1990:563- 79. Strikwerda S, Umans V, van der Linden M, van Suylen RJ, Balk AH, de Feyter PJ, Serruys PW. Percutaneous directional atherectomy for discrete coronary lesions in cardiac transplant patients. AM HEART J 1992;123:1686-90. Stark RP, McGinn AL, Wilson RF. Chest pain in cardiac- transplant recipients: evidence of sensory reinnervation after cardiac transplantation. N Engl J Med 1991;324:1791-4. Halle A, DiSciascio G, Wilson R, Massin E, Johnson M, Sta- dius M, Wray R, Young J, Davies R, Walford G, Deligonul U, Rincon G, Bourge R, Crandall C, Cowiey M, Vetrovec G. Cor- onary angioplasty in cardiac transplant patients: results of a multicenter study [Abstract]. J Am Co11 Cardiol 1991;17: 103A.