Surgical Treatment of Variant Angina:Use of Plexectomy with Aortocoronary Bypass

MICHEL E. BERTRAND, JEAN M. LABLANCHE, MICHEL F. ROUSSEAU,HENRI H. WAREMBOURG, JR., CZESLAS STANKOWTAK, AND GEORGES SOOTS

SUMMARY Aortocoronary bypass surgery, widely accepted in the treatment of patients with coronaryartery disease, is controversial in the management of variant angina. Persistence of attacks, occlusion of thegraft or postoperative infarction have been described and could be explained by a persistent spasm frequentlyobserved in variant angina that might occlude the distal part of the grafted vessel.

It has been suggested that plexectomy might be added to the aortocoronary graft procedure in order to pre-vent the spasm. Our study includes 35 patients with variant angina who had surgery. They were divided into twogroups. Group 1 (n = 13) had aortocoronary bypass alone; the patients in group 2 had plexectomy in additionto the myocardial revascularization. The average follow-up period was 37 months in group 1 and 20 months ingroup 2. The results were assessed by clinical study, stress testing, control of patency of the grafts andprovocative test with an ergot alkaloid (methergine).

Despite the difficulties of evaluating the effects of the various treatments in these patients with a wide spon-taneous variability of symptoms, these data suggest that a complete plexectomy associated with aortocoronarybypass gives better results (86%) than bypass alone (61%) in variant angina. The recurrence rate of attacks waslower (5%) when plexectomy was associated with bypass than with bypass alone (18%).

IN 1959 Prinzmetal et al.' described a variant form ofangina characterized by attacks at rest and during thenight, rather than with exercise, and associated withST-segment elevation. The ECG changes are transientand disappear without further enzymatic or electricalevidence of myocardial infarction. The authorspostulated that this clinical syndrome was due to cor-onary artery spasm. The development of coronaryarteriography provided a clue to confirm that spasmwas indeed an important, if not predominant, factor invariant angina.2-8 Although aortocoronary bypass sur-gery has been widely accepted in the treatment ofpatients with coronary artery disease, its role is con-troversial in variant angina. A review of theliterature9' 10 has shown poor results with coronaryartery grafting: persistence of spontaneous pain inspite of patent grafts, high incidence of occlusion ofthe grafts or postoperative myocardial infarction. Itwas even suggested that surgery was not the most ap-propriate treatment for these cases. An explanation ofthe failure of surgical therapy could be the persistenceof spasm that was not suppressed and can eitherocclude the distal part of the grafted vessel or narrowanother vessel that was apparently normal duringpreoperative coronary arteriography. Therefore, itwould seem feasible to add denervation to the aor-tocoronary bypass procedure in order to prevent therecurrent spasm. In this report we describe the resultsof coronary bypass surgery in 35 patients with variant

From the Divisions of Cardiology and Hemodynamics and Car-diovascular Surgery, University Hospital, Lille, France.

Dr. Rousseau's present address: Division of Cardiology, Univer-sity of Louvain, 1200 Brussels, Belgium.

Address for correspondence: Dr. M. E. Bertrand, Service de Car-diologie et Hemodynamique, H6pital Cardiologique 59037 Lille,Cedex, France.

Received March 20, 1979; revision accepted October 20, 1979.Circulation 61, No. 5, 1980.

angina, 22 of whom had a plexectomy associated withmyocardial revascularization.

Materials and MethodsFrom January 1974 to November 1978, 53 patients

with variant angina were admitted to our institution.Variant angina was defined according to classiccriteria.1

Left-heart catheterization, left ventriculographyand coronary arteriography were undertaken in allpatients. Left ventriculography was performed in the30° right anterior oblique projection using 35-mm filmtaken at 50 frames/sec. Coronary arteriography wasperformed with the Judkins method using Bo'urassa'scatheter. Thirteen patients had angiographically nor-mal coronary arteries and were medically treated witha calcium antagonist or long-acting nitrates. Thearteriograms in the other 40 patients revealed severeorganic obstructive disease. In this group, five patientswere technically unsuitable for surgery because ofdiffuse distal coronary vascular disease. The remain-ing 35 patients were considered to be surgical can-didates and they were divided into two groups. Group1 included an initial series of 13 consecutive patientsobserved from 1974 to December 1976. They had aor-tocoronary bypass alone. Group 2 consisted of a sec-ond series of 22 consecutive patients who were studiedafter January 1977. In these patients, a plexectomywas performed together with coronary artery graft-ing.Plexectomy was performed at the onset of operation

and included four steps:1) In order to avoid spasm induced by manipulat-

ing Wrisberg's ganglion (as it was observed intwo patients) a large bolus of lidocaine was in-filtrated under the aortic root.

2) The adventitia overlying the aorta from the leftvagus nerve laterally to the most anterior aspectof the ascending aorta medially was peeled.

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3) Meticulous resection of all the ganglia andnerves located under the aortic root in theWrisberg's quadrilateral space was performed.This included resection of the entire triangulararea of tissue located between the tracheaposteriorly and the ascending aorta medially.

4) Dissection of the space located between the de-scending aorta and the main pulmonary trunk,where a nerve goes to the right coronary artery.This nerve must be resected. Therefore, we per-formed a resection as large as possible of themajor cardiac plexus located anteriorly near thebase of the aorta and under the aortic root.Histologic examination of the resected tissuewas done after the plexectomy. Extracorporealcirculation was started and conventional aorto-coronary bypass grafting was carried out.

Postoperative follow-up data, including com-plications and functional status, were obtained duringthe last 3 months of 1978 in all patients who survivedoperation. In 16 patients, the patency of the grafts wasassessed. Provocative testing with methergine, anergot alkaloid, was undertaken in 23 patients toattempt induction of spasm.

Patients

Clinical FeaturesTable 1 summarizes the clinical presentation. Each

patient of group 1 had angina at rest from 1 week to 5months duration. Two patients had angina in themorning when awakening. Three experienced syn-copal episodes and two had frequent palpitations.

All the patients of group 2 experienced angina atrest from 2 weeks to 4 years duration. In four patientsangina at rest was associated with pain during exer-cise. Eight patients had syncope and three hadpalpitations. All 22 patients had one to four risk fac-tors for coronary artery disease (about 2.2 perpatient).ECGs obtained during angina in group 1 showed

TABLE 1. Clinical Presentation of Patient PopulationGroup 1 Group 2

(13 patients) (22 patients)

Male/female 11/2 20/2

Age (years) 56.2 (45-71) 50.3 (40-70)

Patients withangina at rest 13 22

Patients withsyncopal episodes 3 8

Patients with risk factorsfor coronary artery disease 10 22

Patients with ST-segmentelevation during attacks

Anterior leads 9 14Inferior leads 4 8

ST-segment elevation in precordial leads in ninepatients and in inferior leads in the four patients; ST-segment depression was never observed. One patienthad ventricular tachycardia during pain. Only onepatient who had angina during exertion had an exer-cise stress test that showed ST-segment elevation. Ingroup 2, 14 patients had ST-segment elevation duringpain in the precordial leads and eight subjects hadthese ECG changes in leads II, III, aVF. No patienthad ST-segment depression during angina; one patienthad bradycardia during pain. Two had short runs ofventricular tachycardia and two others had multiplepremature ventricular contractions. All patients wereadmitted to the coronary care unit. An exercise testwas performed in only four patients: Only one had ST-segment depression and the other three had ST-segment elevation, suggesting that exercise per sebrought on coronary spasm.

Arteriographic Findings

Coronary arteriograms were read separately by twoobservers. The lesions were judged to be anatomicallysignificant when they reduced the diameter of thevessels by at least 75%.The number of diseased vessels is shown in table 2.

In group 1, four patients had a one-vessel disease, sixpatients had two-vessel disease and three had three-vessel disease. Five patients had spasm; it occurredspontaneously in three and was induced by metherginein two. Spasm was located in the right coronary arteryin three patients; one patient had a spasm of the leftanterior descending artery and another had spasmsimultaneously in the right coronary artery and leftanterior descending artery.Ten patients of group 2 had one-vessel disease;

seven had two-vessel disease and five had three-vesseldisease. Twelve patients had spasm, which was locatedmost often in the left anterior descending artery (sevenpatients). It occurred in the right coronary artery infour patients. The remaining patient had spasm in twovessels, the left anterior descending and right coronaryarteries.

Hemodynamic and Cineangiographic Findings

The comparative values of the left ventricular end-diastolic pressure (LVEDP), cardiac index (CI), leftventricular end-diastolic index (LVEDVI) and ejec-tion fraction (EF) are shown in figure 1. The meanvalues for groups 1 and 2 were, respectively, LVEDP

13.8 and 11.2 mm Hg (normal value in our

laboratory 10.5 ± 3.2 mm Hg); CI 3.36 and 2.76

TABLE 2. Coronary Arteriographic Findings

One- Two- Three-vessel vessel vessel

n disease disease disease Spasm

Group 1 13 4 6 3 5

Group 2 22 10 7 5 12

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GROUP I GROUPII GROUP I GROUP II GROUP I GROUP II

FIGURE 1. Individual values for left ventricular end-diastolic pressure (L VEDP), cardiac index, and leftventricular end-diastolic volume index (LVEDV) in each group.

1/min/m2 (normal value 3.5 ± 0.62 1/min/M2);LVEDVI 92.7 and 80.6 mI/M2 (normal value81 ± 15 mI/rM2) and EF 57% ± 10% and60% ± 12% (normal value 68% ± 8.8%). Althoughthe LVEDVI and the EF appeared to be worse ingroup 1, differences between the two groups were notstatistically significant.

ResultsDuring the immediate postoperative period, two

patients died in each group (surgical mortality: 15.3%in group 1 and 9% in group 2). Two deaths (one ineach group) were related to a low cardiac output. Onepatient in group 2 died with an intractable arrhythmiaand the other (group 1) died from an air embolism. Ofthe 31 patients who survived surgery, all were alive atthe end of the follow-up period. The survivors have amean follow-up period of 36.8 ± 11.4 months (21-57months) in group 1 and 20 ± 9 months (6-38 months)in group 2. All the patients in the two groups tookdipyridamole. At the end of the follow-up period,patients underwent clinical, x-ray and ECG in-vestigations. In 16 patients a new coronaryarteriogram was performed to assess the patency ofthe grafts. In 23 patients, provocative testing by injec-tion of 0.4 mg of methergine was undertaken after afull explanation of the procedure and after informedconsent was obtained. The protocol of provocativetesting varied, depending on whether the patient hador did not have repeat coronary arteriography toassess the patency of aortocoronary bypass. In the 16patients restudied, provocative testing included ECGand aortic pressure monitoring, opacification of thegrafted vessel and the bypass and was repeated 1, 3and 5 minutes after injection of the drug. If spasm hadbeen observed before operation in a vessel, theopacification of this artery was obtained after ad-ministration of methergine to determine if spasmcould still be observed. In the seven remainingpatients, provocative testing was performed in the cor-

onary care unit according to the method published by

Nelson et al.'1 and the effects of the drug were

followed only from ECG changes.Results for each group are presented below.

Group 1 (n = 11)

Nine patients were free of pain and were clinicallyimproved. They experienced no syncope and had noheart failure. One patient who had bypass of the leftanterior descending artery suffered an inferior infarc-tion after operation that was rather unexpected,because the right coronary and circumflex arterieswere normal before operation.An exercise test was performed in these nine

patients. Their maximal heart rate during exercise was95 4.5% of the age-predicted maximal heart rate.The exercise ECG was negative in all but one patient.

Six patients (10 grafts) were restudied by coronaryarteriography. Nine of 10 grafts were patent.Provocative testing with methergine was performed inthe nine patients (six provocative tests during repeatcoronary arteriography). The test induced spasm andECG changes in one patient.

Finally, there were two poor results (two of 11,18%); two patients remained symptomatic andsuffered from severe attacks similar to those observedbefore operation. In one patient, a severely narrowed(75%) right coronary artery with a spontaneous spasmsuperimposed on the lesion was bypassed. Thepostoperative catheterization showed that graft waspatent. However, provocative testing induced spasmon that part of the right coronary artery distal to thegraft. The second patient had a 95% narrowing of theleft anterior descending artery before surgery. Spasmwas also spontaneously observed at the site of the le-sion. After operation, the graft was patent but spon-taneous spasm again occurred in two vessels. Spasmoccluded the part of the left anterior descending arterydistal to the graft and was also observed in the mid-portion of the right coronary artery, which was

previously normal. Therefore, these two patients weretreated with a calcium antagonist drug and are

presently asymptomatic.

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Group 2 (n = 20)

All patients but one are asymptomatic; they are freeof pain, and they had neither syncope nor heartfailure. No patient had peri- or postoperative infarc-tion. An exercise test was performed in nine patientsand they were able to reach 91 ± 8.9% of the age-predicted maximal heart rate. In all patients exceptone, ECG exercise test was negative. In the threepatients with preoperative ST-segment elevation, thetest became negative, suggesting that spasm broughton by exercise was alleviated by the combination ofbypass surgery and plexectomy.Ten patients had recatheterization and all the grafts

(n = 12) were patent. Provocative tests were per-formed in 14 patients (10 during the restudy and fourin the coronary care unit). In these 14 patients, ofwhom eight had spasm previously demonstratedbefore operation, methergine did not induce spasm orECG changes in 13. However, this test was positive inone patient. This 45-year-old man had variant anginarelated to a severe (95%) stenosis of the proximal partof left anterior descending artery. Spontaneous spasmwas superimposed on the lesion, totally occluding thevessel. He was operated on 2 days after coronaryarteriography. A plexectomy was performed togetherwith venous bypass of the left anterior descendingartery. He immediately improved, but 3 months laterhe had repeated angina. ST-segment elevation wasobserved in precordial leads after injection ofmethergine. He was restudied by left-heartcatheterization. The graft was patent; however, spasmwith ST-segment elevation could be induced by theprovocative test, and when it occurred the bypass wasineffective. He received nifedipine (40 mg orally)together with isosorbide dinitrate. He became asymp-tomatic and further provocative testing could not in-duce the ECG changes previously observed. The poorresults are not related to an occlusion of the grafts butto the persistent spasm.

DiscussionThe overall results of surgical treatment in variant

angina are usually not as good as in other forms ofangina pectoris, either stable or unstable. In 1974,Gaasch et al.9 reported from the literature a 12.5%rate of operative deaths, 19% postoperative myocar-dial infarction and a 57.1% rate of graft occlusion.More recently, Grondin and Limet'O reviewed the sur-gical literature and found that only 56% of patientswith variant angina showed good results.

This difference in the overall outcome between thetwo forms of angina might be explained by the spasmfrequently observed in the variant angina. Previousworks12, 13 have demonstrated that attacks of variantangina are not induced by an increase of myocardialoxygen demands, but by a sudden reduction ofmyocardial supply. Myocardial scintigraphy14-6 andcoronary sinus flow measurement17 by thermodilutionhave shown that myocardial blood flow declinesdrastically during episodes of spontaneous variantangina and returns to normal after the attacks. At the

same time, the widespread use of coronaryarteriography shows that spasm is indeed an essentialfactor in the pathogenesis of variant angina. In ourdata, 30 of the 53 patients with variant anginademonstrated evidence of coronary artery spasm. Inpatients with otherwise angiographically normal cor-onary arteries, artery grafting is contraindicated.Most often, spasm is superimposed on fixedarteriosclerotic coronary artery disease. Although agraft will bypass the narrowing, the spasm can persistand the bypass may be inefficient if spasm occurs dis-tally to a patent graft, occluding the distal runoff. Thiswas demonstrated in three of our patients.

Moreover, we observed in one patient that spasmcan appear on another vessel that had not been graftedbecause it was previously angiographically normal.Therefore, it appears that the treatment of variantangina with organic narrowing should have two aims:to bypass the organic narrowing and to suppress thespasm. If these two factors cannot be treated, poorresults should be expected, with persistence of attacksor myocardial infarction or sudden death.The studies of Yasue et al.18 suggested that

enhanced activity of the parasympathetic nervoussystem is involved in the initiation of the attack bystimulation of the sympathetic nerve, which can in-duce coronary arterial spasm by activating alpha(vasoconstrictors) receptors. More recently, Ricci etal.'9 showed that coronary spasm is a manifestation ofaltered autonomic activity. The observation of spasmduring manipulation of Wrisberg's ganglion noted intwo of our cases, can be considered also as suggestive.Nervous system factors are certainly not the onlycause of spasm, but one can assume that they play animportant role. In light of this, it was logical to con-sider the usefulness of denervation.

In 1977, Clark et al.20 reported eight cases of aorto-coronary bypass followed by cardiac denervation. Thedenervation was partial (stripping of the great vessels)in three cases. One patient died at operation and twopatients were alive and well more than 2 years later.Two patients had total cardiac denervation byautotransplantation. One died, and the other one iswell 3 years after the operation. This latter patient wasrestudied after the operation and spasm of the cor-onary artery was again demonstrated by the ergotratestimulation test. With respect to this last observation,Clark et al.20 wrote that induced coronary spasm canoccur despite total denervation.

Cipriano et al.21 demonstrated that ergonovinemaleate can induce the same degree of coronaryarterial narrowing in heart transplant recipients and inpatients with normally innervated hearts who did notdevelop coronary spasm. Thus, the normal phar-macologic response to ergonovine maleate was due toa direct vasoconstriction action of the drug, and thisaction was independent of neural extrinsic control.Ergot alkaloid did not provoke spasm after operationin 14 patients of group 2 who had plexectomy; the factthat eight of them had spasm before operationsuggests strongly that plexectomy is beneficial.

However, we do not know why ergot alkaloid in-

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duced spasm after total denervation (autotransplanta-tion) and not after plexectomy. This technique wasfirst described by Arnulf.22 According to this author,the heart is innervated from both the parasympatheticand the sympathetic systems. They emit fibers thatform the superior, middle and lower cardiac nervesand they converge to form the cardiac plexus; theyform a rich network of fibers surrounding the aorticroot and are divided into three main plexus: the pre-aortic plexus is located anteriorly to the aortic root,the second plexus is located in the subepicardial regionof the left atrium, the third is located in the spacedelineated laterally by the pulmonary artery,posteriorly by the trachea and medially by the ascend-ing aorta, including the large and inconsistentganglion of Wrisberg.The location of these plexus explains the difficulty in

achieving a good plexectomy. First, the approach tothis area is difficult. Second, because of bleeding in-duced by the heparinization, the plexectomy had to beperformed before starting extracorporeal circulation,and before performing the saphenous graft thatcrosses the area of plexectomy. Third, the richnetwork of fibers explains why plexectomy can be in-complete, especially as far as the posterior plexus isconcerned. The evidence of a good plexectomy seemsto be a change in heart rate during the resection andespecially the appearance of tachycardia: all thepatients of group 2 with good results have shown asignificant increase in heart rate. The only one whohad poor results with persistent spasm had a bradycar-dia during and immediately after resection.

Plexectomy associated with coronary artery graft-ing in variant angina was first performed by Grondinand Limet'O in two patients with organic narrowing ofcoronary arteries. These patients remained asymp-tomatic over 18 and 12 months respectively. To ourknowledge, there are no other publications on thissubject. The results obtained in our series of 22 casesseem to confirm the preliminary report of Grondinand Limet'0: the overall outcome, taking into accountperioperative deaths, infarction and persistent attacks,suggests that plexectomy associated with bypass graft-ing gives better results (86%) than bypass alone (61%)(table 3). Moreover, it is important to observe thatthere was only 5% of persistent recurrent attacks ingroup 2 while this recurrence rate was 18% in group 1.

Nevertheless, these preliminary results should be in-terpreted with caution because of obvious difficultiesin evaluating the effects of treatment in patients whohave a wide spontaneous variability of symptoms.

However, these results do suggest that plexectomyassociated with aortocoronary bypass improves theresults of surgical treatment in variant angina withorganic narrowing. Considering these encouragingpreliminary results, plexectomy was attempted inthree other patients who had severe variant anginarelated to spasm alone with otherwise angi-ographically normal coronary arteries. Consideringthe failure of medical therapy to give even a slightrelief of attacks, plexectomy alone was performed. Amean of 35 months later (range 12-58 months) thethree patients are free of pain. Various continuousECG recordings have not shown any ECG changesand provocative testing with methergine was unable toreproduce the ST-segment elevation that waspreoperatively observed after injection of this drug.Obviously, the small number of cases does not permitus to draw any conclusions, but such observations areencouraging and the validation of this approach re-quires further confirmation.

References

1. Prinzmetal M, Kennamer R, Merliss R: Angina pectoris. 1. Avariant form of angina pectoris: preliminary report. Am J Med27: 375, 1959

2. Dhurandar RW, Watt DL, Silver MD, Trimble ASA, DelmanAG: Prinzmetal's variant form of angina with arteriographicevidence of coronary arterial spasm. Am J Cardiol 30: 902,1972

3. Oliva PB, Potts DE, Pluss RG: Coronary arterial spasm inPrinzmetal angina: documentation by coronary arteriography.N Engl J Med 288: 745, 1973

4. Cheng TO, Bashour T, Kelser GA, Weiss L, Bacos J: Variantangina of Prinzmetal with normal coronary arteriograms. Avariant of the variant. Circulation 47: 476, 1973

5. MacAlpin RN, Kattus AA, Alvaro AB: Angina pectoris at restwith preservation of exercise capacity. Circulation 47: 946,1973

6. Higgins CB, Wexler L, Silverman JF, Schroeder JS: Clinicaland arteriographic features of Prinzmetal's variant angina:documentation of etiologic factors. Am J Cardiol 37: 831, 1976

7. Meller J, Pichard A, Dack S: Coronary arterial spasm inPrinzmetal's angina. A proved hypothesis. Am J Cardiol 37:938, 1976

8. Wiener L, Kasparian H, Duca PR, Walinsky P, Gottlieb RS,Hanckel R, Brest AN: Spectrum of coronary arterial spasm-clinical, angiographic and myocardial metabolic experiences in29 cases. Am J Cardiol 38: 945, 1976

9. Gaasch WH, Lufschanowskii R, Leachman RD: Surgicalmanagement of Prinzmetal's variant angina. Chest 66: 614,1974

10. Grondin CM, Limet R: Sympathetic denervation in associationwith coronary artery grafting in patients with Prinzmetal'sangina. Ann Thorac Surg 23: 111, 1977

11. Nelson C, Nowak B, Childs H, Weinrauch L, Forwand S:Provocative testing for coronary arterial spasm: rationale, risk

TABLE 3. Overall Outcome

Follow-up Postoperative Persistent Persistentn (months) deaths Infarction attacks spasm

Group 1 13 36.8 11.4* 2 1 2 2(21-57)

Group 2 22 20 =E9* 2 1 1(6-31)

*Mean = SD.

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and clinical illustrations. Am J Cardiol 90: 624, 197812. Guazzi M, Polese A, Fiorentini C, Magni F, Bartorelli C: Left

ventricular performance and related haemodynamic changes inPrinzmetal's variant angina pectoris. Br Heart J 33: 84, 1971

13. Maseri A, Mimmo R, Chierchia S, Marchesi C, Pesola A,L'Abbate A: Coronary artery spasm as a cause of acutemyocardial ischemia in man. Chest 68: 625, 1975

14. Berman MD, McLaughlin PR, Huckell VF: Prinzmetal'sangina with coronary artery spasm: angiographic, phar-macologic, metabolic and radionuclide perfusion studies. Am JMed 60: 727, 1975

15. Maseri A, Parodi 0, Severi S: Transient transmural reductionof myocardial blood flow, demonstrated by thallium 201 scin-tigraphy as a cause of variant angina. Circulation 54: 280, 1975

16. McLaughlin PR, Doherty PW, Martin RP: Myocardial imag-ing in a patient with reproducible variant angina. Am J Cardiol39: 126, 1977

17. Ricci DR, Orlick AE, Doherty PW: Reduction of coronaryblood flow during coronary artery spasm occurring spon-

taneously and after provocation by ergonovine maleate. Cir-culation 57: 392, 1978

18. Yasue H, Touyama M, Shimamoto M, Kato H, Tanaka S,Akiyama C: Role of autonomic nervous system in thepathogenesis of Prinzmetal's variant form of angina. Circula-tion 50: 534, 1974

19. Ricci DR, Orlick AE, Cipriano PR, Guthaner DF, HarrisonDC: Coronary artery spasm: a manifestation of alteredautonomic activity. (abstr). Circulation 56 (suppl III): 111-32,1977

20. Clark DA, Quint RA, Mitchell RL, Angell WW: Coronaryartery spasm. Medical management, surgical denervation andautotransplantation. J Thorac Cardiovasc Surg 73: 332, 1977

21. Cipriano PR, Guthaner DF, Orlick AE, Ricci R, Wexler L,Silverman JF: The effects of ergonovine maleate on coronaryarterial size. Circulation 59: 82, 1979

22. Arnulf G: Chirurgie des coronaires: bases anatomiques,physiologiques et pathologiques: coronarographie. M6thodeschirurgicales et indications (Masson, ed), Paris 1965

Myocardial Perfusion as an Indicator of GraftPatency after Coronary Artery Bypass SurgeryALBERT J. KOLIBASH, M.D., THOMAS D. CALL, M.D., CHARLES A. BUSH, M.D.,

MARC R. TETALMAN, M.D., AND RICHARD P. LEWIS, M.D.

SUMMARY Stress and resting myocardial perfusion were assessed in 38 patients who received 96 grafts.Stress perfusion was evaluated with thallium-201 and resting myocardial blood flow distribution withradiolabeled particles. When both stress and rest perfusion were normal, graft patency was 82% (51 of 62grafts). Graft patency was also high (81%, 13 of 16) in areas where stress perfusion abnormalities resolved orbecome less apparent at rest. However, when stress perfusion defects remained unchanged at rest, the graftwas likely to be occluded (73%, 11 of 15). Maintenance of normal rest perfusion or improvement of rest perfu-sion postoperatively was also associated with a high graft patency rate (80%, 35 of 44), whereas the develop-ment of new rest perfusion defects postoperatively implied graft occlusion (86%, six of seven).

CORONARY ARTERY bypass grafting to po-tentially ischemic areas of myocardium is widely usedto treat patients with coronary artery disease.1 2Because success or failure of such surgery seemslargely determined by graft patency, it has becomecommon in many institutions to restudy postop-erative patients with a cardiac catheterization.

Until recently, a postoperative catheterizationappeared to be the only reliable method of assessinggraft patency. However, developments in nuclear car-diology imaging techniques have provided reliable

From the Divisions of Cardiology and Nuclear Medicine, TheOhio State University Hospitals, The Ohio State University,Columbus, Ohio.

Supported in part by NIH grant 5T01-HL0598-04 and by theCentral Ohio Heart Chapter of the American Heart Association.

Dr. Call's present address: Hague Medical Center, Norfolk,Virginia.Address for correspondence: Albert J. Kolibash, M.D., 657

Means Hall, 466 West 10th Avenue, Columbus, Ohio 43210.Received May 7, 1979; revision accepted October 25, 1979.Circulation 61, No. 5, 1980.

methods of evaluating myocardial perfusion.315Thallium-201, the radionuclide most commonly usedto assess myocardial perfusion, may provide useful in-formation concerning graft patency in patients whohave undergone myocardial revascularization.6' 7

Another useful technique in evaluating myocardialblood flow distribution is the instillation of radio-labeled particles directly into the coronary circula-tion.8-10 Because two radionuclides are used, it is possi-ble to distinguish the blood flow distribution fromgrafts and that from the native circulation, thusproviding information not always obtainable fromthallium studies.-1'13 Total myocardial blood flow dis-tribution is indicated by the dual image, which is acombination of both graft and native vessel perfusion.Therefore, the dual or combined image, which is com-parable to a resting thallium image,5' 14 can be com-pared with a stress thallium study to distinguish stress-induced defects from defects that represent fibrosis.'5We assessed both stress and rest myocardial perfu-

sion after myocardial revascularization and correlatedpostoperative perfusion characteristics with graftpatency and native vessel anatomy to predict thesuccess or failure of coronary bypass surgery.

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SootsM E Bertrand, J M Lablanche, M F Rousseau, H H Warembourg, Jr, C Stankowtak and GSurgical treatment of variant angina: use of plexectomy with aortocoronary bypass.

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1980 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation doi: 10.1161/01.CIR.61.5.877

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