tions

of coronary

b

Agop ~~~r~ta~~ia~, Robert I. Hamby, Robert J. Kramer, M.D. l3. George M&off, M.D. New Hyde

Park

and

Stony

Brook,

N. Y.

Since the advent of coronary bypass surgery, each year an increasing number of patients are subjected to this procedure with good results.‘, 2 Reported complications of saphenous vein bypass surgery have included pulmonary emboli and myocardial infarction or postoperative apathologic new & waves, associated at times with det~~oration of the left ventricular function due to closure of the graft or trauma caused by left ventricular apical venting.“. 4 A few case reports described post-bypass appearance of new systolic5 or continuous murmurs due to normal or stenosed graft,“, i or to anastomoses of the gaft to coronary vein6 and in one case to a coronary ateriovenous fktula.8 Other complications include: false aneurysm of the vein graft,” intimal tear with or without dissecting aneurysm of the aorta,lO. I1 and transmyocardial left-toright shunt.” Here we report five eases, three of whom developed post-bypass apical thrombus, one developed a moderate degree of new mitral regurgitation, and in the other patient there was stagnation of angiographic contrast material around the distal anastomat~~ site. To our knowledge, these complications have not been described. &worn the Department of Medicine, Division of Cardiology, Long Island Jewish-Hillside Medical Center,New Hyde Park, N. Y., and Department of Medicine, School of Medicine, Health Sciences Center, State University of New York at Stony Brook, Stony Brook, N. Y. Received Accepted

for publication for pubtication

Reptim requests to: Agop Long Island Jewish-Hillside 11cMQ.

May Aug.

23, 1977. 19, 1977.

Aiitablian, Medical

M.D., Center,

Division of Cardiology, New Hyde Park, N. Y.

, and Febzmry, :91K, 900 patients underwent surgery. Postoperative an&yams were formed in 585 patients. Among these patients, in three (Cases 1, 2, and 3f, postoperative angiograms showed new apicali thromb.i, which were not present prior to surgery. la one patient (Case

e teft anterior descending artery. The fifth petier,t (Case 5): developed new mitral ~e~~~~ita~~~. aae All patients bad reverse saphenous vein aortocoronary bypass utilizing ota1 ~~rd~o~~lrn5~a~~7 support. Priming solution was 5 per cent dextrose in one-third normal saline. Flow rates were 40 to 55 mI./Kg. using a b~~~l~ o~~~~~e~~t~~~with mean arterial pressures of at least 561mm. The left ventricle was vented through the r superior ~~~o~ary vein. None of these patients ‘had apical venting. Moderate ~~~~~~e~rn~~ was achieved by cooling the ~a~~e~t to 32” C. After total cardiopulmonary bypa , the ventricle was occasionally electrically de6bri!.lated and aorta was intermittently clamped for the distal anastomoses. 1 .4 %-year-ok3 white female who had documented antexjor wali myocardial infarction 14 months and doubie saphenous vein bypass surgery fonr months earlier, was admitted to the hospital for the second time in Aug;isi, 2376, with recurrent

Aintablian

et al.

E

YSTBlE

PRE-OP

Fig. 1. Pre- and postoperative left ventricular angiograms of Case No. 1 as viewed in the right anterior oblique projection. Prior to surgery (R-e-op) she had prolapsed mitral valve and apical akinesia (arrow in end-&stole); postoperatively (post-op), not only prolapsed mitral valve remained unchanged (upper arrozu), but the patient also developed apical thrombus (lower arrow). angina pectoris. On her first admission in April, 1976, she gave a history of typical angina pectoris initially on exertion, then at rest and nocturnally for the last three months, not well controlled with long acting nitrates and propranolol. Her blood pressure was 140/80 mm. Hg with a regular heart rate of 75 per minute. Physical examination was within normal limits, except for a systolic ejection murmur Grade ll/Vl and a S, gallop best heard at the apex. The electrocardiogram revealed regular sinus rhythm and pathoIogic Q waves in Leads 1, aVL, V, to V, consistent with anterior wall infarction. Chest x-ray revealed minimal cardiomegaly. The first cardiac catheterization and coronary angiography revealed normal cardiac output and normal pressures in the right heart, with slight elevation of pulmonary wedge pressure (15 mm. Hg) and left ventricular end-diastolic pressure (16 mm. Hg). The left ventricular angiogram revealed akinesia of the apex of the left ventricle with a prolapsed mitral valve (Fig. 1, pre-op). The coronary angiograms demonstrated over 50 to 75 per cent narrowing of the right coronary artery at the crux, slight irregularities of the circumflex artery, and 80 to 90 per cent proximal narrowing of the left anterior descending artery with good distal run-off. On the day of cardiac catheterization, she underwent saphenous vein bypass graft surgery to the right

18

coronary and the left anterior descending arteries. IIer postoperative course was uneventful except for mental depression. She was discharged two weeks after surgery on no medication and remained asymptomatic for three months. On her second admission for recurrent angina pectoris, a repeat left heart cardiac catheterization and left ventricular angiogram revealed again apical akinesia with a prolapsed mitral valve; however, there was a new large apical filling defect (Fig. 1, post-op), which was not present prior to surgery. The saphenous vein bypass graft angiograms revealed a patent graft to the left anterior de&ending artery and closure of the graft to the right coronary artery. A year after surgery she continues to have occasional exertional angina, despite antianginal therapy.

Case 2 A 44-year-old white male, with history of exertional precordial pain for one year, sustained a transmural inferior infarction three months prior to admission. In the last three months he continued to have precordial pressure radiating to the left arm occurring only on exertion and excitement, relieved by sublingual nitroglycerin. Because of these symptoms and his job as a truck driver, he was advised to take a treadmill stress

July, 1978, Vol. 96, No. 1

Fig. 2. XPre- and postoperative projection. Prior to surgery not only is there deterioration

left ventricuiar angiograms of Case No. 3 as viewed in tbe right anterior a:s&;ue left ventricular contraction is normal {’ and B). Postoperatively @~&o;o)? of left ventricular contraction, baut also new apical tkn-ombus (arms in 22).

(WET-op)the

test during which he developed 3 mm. ST segment depression and angina pectoris at a heart rate of 133/minute (‘70 per cent of predicted maximum). On admission he was comfortable -with a blood pressure of 130180 mm. Hg and a regular pulse rate of 85 per minute. He looked older than his age with extensive graying of his hair. On physical examination the only positive finding was the presence of an S, gallop. His electrocardiogram showed an old inferior wall infarction. Cardiac catheterization performed on ,December 3, 1976 revealed normal cardiac output and normal pressures in both left and right heart. The left ventriculogram revealed an inferior wall aneurysm. Selective coronary angiograms showed almost complete occlusion of the right coronary artery at its midportion with a good distal run-off. The left anterior descending artery had a 70 to 80 per cent proximal stenosis w&h good run-off. The circumflex artery was almost completely occluded proximally with good distal delayed filling. Because of his symptoms and the finding5 on coronary angiography, he underwent left anterior descending and right coronary bypass surgery. Bypass graft to the marginal branch could not be performed. His postoperative course was uneventful and ten days after surgery a postbypass graft angiogram showed patency of both grafts, but the left ventriculogram revealed a new apical filling defect, consistent with

apical thrombus, aot present prior after surgery he was asymptomatic

to surger\ Four o3 no thenapy.

months

Gas A ii6-year-old white male with a 3 week history of progressive resting and nocturnal angina not weii controlled vtith antianginal drugs, was admitted for coronary angiography and possible bypass surgery. He was fonnd to have hypertension 6 months earlier for which be received &&de, Physical examination on admission was entirely within normal limits. His chest x-ray and electrocardiogram did not reveal arly abnormalities. Cardiac catheterization done on January 4, 1977 revealed normal cardiac output and norma.!l pressures in the right and ieft heart except for slight elevation of left ventricular end-diastolic pressure (16 mm. Hg). The !eft ventricular wall motion, as well as vakular fui?arct.ions, were ail normal. Selective coronary angiograms demonstrated almost complete proximal occlusion of the right coronary artery with good run-off, the left anterior descending anal eircumdex arteries also showed over 70 per cent praxima! steno& with fair run-off. A similar lesion was noted on the d~~~~~~~~ branch of the left anterior descending artery. Four days later he underwent saphenrjus vein bypass surgery to the abovementioned arteries. On the fourth postoperative day, be

Aintablian

et al.

Fig. 3. Selective saphenous vein opacification to the diagonal branch of the left anterior descending artery. A, In right anterior oblique projection, upper large arrow points to patent graft and lower large arrow points to the leakage of angiographic material around distal anastomatic with good visualization of native vessel (small arrows). B, The angiographic material continued to stagnate around the anastomatic site while the bypass graft and coronary artery already has been emptied. C, The graft (upper large arrow), the native vessel (small arrow), and the extravasated angiographic material (lower large arrow) are seen in left anterior oblique projection.

complained of severe retrosternal pain and lightheadedness and his electrocardiogram revealed a new anterior wall infarction. He was digitalized and treated as an acute myocardial infarction. One month after surgery and just before discharge, he had bypass angiograms which revealed deterioration of left ventricular contraction with impaired movement of the lower anterior and apical segment. There was also a new apical filling defect consistent with thrombus (Fig. 2). The saphenous vein grafts were patent to the left anterior descending, right coronary, and left circumflex arteries but the graft to the diagonal branch of the left anterior descending artery was closed.

Case 4 A 65year-old white female was admitted for evaluation because of refractory exertional angina. Her resting electrocardiogram was normal. Cardiac catheterization performed on October 7, 1976 revealed normal left ventricular contractile pattern, normal cardiac output, and normal pressures in the left and right heart. Coronary angiograms revealed a severe degree of proximal stenosis of all three coronary arteries and also of the diagonal branch of the left anterior descending artery. She underwent triple saphenous vein bypass grafts with five distal anastomoses; the graft to the posterior descending artery and two marginal branches of circumflex artery was a “snake” (side-to-side) graft. Her postoperative course was uneventful and her electrocardiogram remained normal. Angiogram two weeks after bypass revealed no

change in the normal left ventricular contractile pattern and normal left ventricular end-diastolic pressure. The bypass grafts to the left anterior descending artery and its diagonal branch were patent but there was leakage with stagnation of angiographic material around the distral anastomatic site of the graft to the diagonal branch (Fig. 3). The “snake” graft was closed.

Case

5

A 52-year-old white male with a history of angina for 6 years which required two admissions for “coronary insufficiency” in the last two years, was admitted for coronary angiography because of progressive angina, not well controlled with high doses of propranolol and nitrates. He had a history of hypertension for twenty years treated with Aldomet. On admission his electrocardiogram and physical examination was normal and his blood pressure was 150/90 mm. Hg. On cardiac catheterization, cardiac output, right and left heart pressures, and left ventricular contractile pattern were all normal. There was no evidence of any mitral regurgitation (Fig. 4). His coronary angiogram showed 70 to 80 per cent narrowing of the main left, left anterior descending, and right coronary arteries. The circumflex artery was irregular. He underwent triple saphenous vein graft surgery. Prior to discharge left heart catheterization and post-bypass angiogram were performed, which showed normal left ventricular end-diastolic pressure with normal motion of the left ventricular walls, but there was significant mitral regurgitation.

July, 1978, Vol. 96, No. 1

Figi. 4. Comparison of pre- and postoperative significant angiographic evidence of mitral

left ventricular angiograrns of Case No. 5. ,4s shotiin 12 9, regurgitation (arrow) which was not present prior to surgery.

Because 3f possble catheter-induced mitral regurgitation, the catheter was repositioned and repeat left ventriculogram again demonstrated moderate degree of mitral regurgitation. Bypass angiogram showed patent grafts to a11 three arteries, but there was significant stenosis of the right coronary artery at its anastomatic site (Fig. 5). Auscultation at this time failed to reveal any heart murmur. Six months after surgery he is completely asymptomatic and does not have murmur.

The most common complications of saphenous vein bypass surgery are related to the stenosis or occlusion of the vein grafts with subsequent myocardial infarction or deterioration of the left ventricular contraction, whereas unusual complications are seldom related to the occlusion of the graft but rather due to surgical technique. Karpman” noted that a high percentage of patients with a patent bypass graft to the left anterior descending artery have a systolic murmur. auman and Tsagaris’ described a continuous murmur in two patients which appeared after

Americwn

Heart

Journal

ha:.e .is

bypass surgery and they speeul~W~ t murmur was produced by ~~rb.~i@~~,Bow related to the graft. In our previous reporr,8 as well as that of Vieweg and associates,” the continuous murmur was due to a fistula between coronary artery and right ventricle or between the vein graft and coronary vein. ~~t~o~2b we noted smalk false aneurysms of the vein grafts at the distal anastomatic site with patent graft33 in two patients on their two-weed postoperative angiograms, none of them had late repea.t graft angiograms to evaluate any det~~~~~a~~~~in these destructures. However, a&axe and LQVin" scribed a case with false aneurysm of the vein graft, whose initial patent graft was occluded during a second study, eight months after surgery. Accsrding TV these authors, the occlusion of the graft was caused by the c~~~~e~~~~~ of false aneurysm upon the bypass graft. Post-bypass formation of the apkaK Case 1 and 2 probably is related to t

2I

Aintablian

et al.

Fig. 5, Selective specification of vein graft (black arrow) to the right coronary artery of Case 5. The white arrow points to the significant stenosis just distal to t.he anastomatic site; probably this significant stenosis by causing papillary muscle dysfunction resulted in mitral regurgitation.

caused by the vent introduced through the right pulmonary vein to the endothelieum of the apex of the heart with subsequent fibrin deposition and formation of the thrombus, whereas in Case 3 apical thrombus may have been due to postoperative anterior wall infarction. None of these patients had left ventricular apical venting. It is conceivable that patients with left ventricular apical venting who develop localized apical contractile abnormalities due to stab wound may develop apical thrombus. However, none of our 104 early saphenous vein bypass cases in whom apical venting technique was used, demonstrated apical thrombus. It is well known that diffuse left ventricular dysfunction or multiple infarctions predispose to apical thrombus.‘” Since none of the first two patients had diffuse left ventricular dysfunction or multiple infarctions, it is improbable that apical akinesia in Case 1 and inferior wall aneurysm in Case 2 played any role in the genesis of apical thrombus. Nevertheless, these abnormal wall movements were present prior to surgery and did not predispose to the formation of thrombus. In our Case 4 patient, as a result of improper and incomplete suturing of distal anastomosis, there was leakage of angiographic material probably on the epicardial surface surrounding the anastomatic site, without compromising the flow to the distal vessel. Although this patient continued to be asymptomatic six months after surgery, we advised recatheterization a year after

22

surgery to re-evaluate the patency of the grafts. New post-bypass significant angiographic mitral regurgitation in our fifth patient was most likely due to papillary muscle dysfunction. Although the bypass graft to the right coronary artery was patent, there was significant stenosis just distal to the anastomatic site of the graft, possibly sufficient to compromise the blood supply of the papillary muscle. Lack of systolic murmur in the presence of significant angiographic mitral regurgitation, as in our case, is uncommon. In a few series not only was the intensity of the murmur poorly correlated to the degree of angiographic mitral regurgitation in patients with left ventricular dysfunction,‘” but silent mitral insufficiency of significant magnitude has been described in patients with coronaryI and rheumatic heart disease.16 Although our five patients had rare complications after bypass surgery and were asymptomatic, these complications should be considered in the entire spectrum of bypass surgical complications, because they are potential future sources of morbidity for these patients. Summary

Five patients after coronary bypass surgery developed unusual complications. Three developed new apical thrombi which are thought to be due to the trauma of the left ventricular vent or deterioration of the left ventricular contraction. Significant new mitral regurgitation in one patient probably is secondary to papillary muscle dysfunction as the result of stenosis distal to anastomoses. The leakage of angoigraphic material around distal anastomatic site is due to technical error. Although these unusual complications are very rare, however, they should be considered as potential source of morbidity in asymptomatic patients who leave the hospital after bypass surgery. REFERENCES Chatterjee, K., Matloff, J. M., Swan, H. J. C., Ganz, W., Sustaita, H., Magnusson, P., Buckbinder, N., Henis, M., and Forrester, J. S.: Improved angina threshold and coronary reserve following direct myocardial revascularization, Circulation 51 and 52 (Suppl. I): I,-81, 1975. Stile, Q. R., Lindesmith, G. G., Tucker, B. L., Hughes, R. K., and Meyer, B. W.: Long-term follow-up of patients with coronary artery bypass grafts, Circulation 54 (Suppl. III):III-32, 1976. Aintablian, A., Hamby, R. I., Hoffman, I., Hartstein, M. L., and Wisoff, B. G.: New Q waves after bypass grafting: Correlations between graft patency, ventriculogram and

July,

1978,

Vol.

96, No.

1

SiWgiCESi

‘t.

5. 6.

7.

8.

9.

10.

verting

technique,

J.

Eiectrocardiol.

9:321,

1976. Shaw, R. A., Kong, Y., Pritchett, C. L. C., Warren, S. G., Oldham, II. N., and Wagner, G. S.: Ventricular apical vents and postoperative focal contraction abnormalities in patients undergoing coronary artery bypass surgery, Circulation 86:34, 1977. Karpman, I.: The murmur of aortocoronary bypass, AM. HEART J. 83:179, 1972. Vieweg, W. V. R., Folkerth, L. T., and Hagan, A. D.: Saphenous vein graft from aorta to coronary vein with production of continuous murmur: A complication of coronary artery bypass surgery, Chest 68:377, 1975. Wauman, D. J., and Tsagaris, T. J.: Continuous heart murmur following aortocoronary bypass surgery, Chest 64:269, 1973. Tabrah, F., Aintablian, A., and Hamby, R. I.: Coronary arteriovenous f%tual complicating aortocoronary bypass surgery, AM. HEART J. 852534, 1973. Baltaxe, H. A., and Levin, D. C.: Angiographic demonstration of complications related to the saphenous aortocoronary bypass procedure, Am. J. Roentgenol. Radium Ther. Xucl. Med. 118484, 1973. Kimbiris, D.. Dreifus, L. S., Adam, A., Beanco, G., and Linhart, 6. W.: Dissection and rupture of the ascending

aorta:

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15.

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i~nUS?&i

1. !X~pLXX%~l5ns

3i

aJrtOi3?.

,33iy

!JypasS

surgery, Chest 68313, 1975. 3ouchow, I. B., Lyengar, R., and -Jude, J. R.: Injury to ascending aorta by partial occ!usion clamp during aortoxronary bypass, d. Thorac. Cardiovaso. Surg, 78303, 1977. Zbrahim, F., Minard, S. A., Schwartz, E. I,., and Dietreich, E. 3.: Transmyocardial left to right shunt complicating acute mferior wall myocardial infarction after aortocoronary bypass, Surgery 77:2SS, 1975. Hamby, R. I., Wisoff, El. G., Davison, E. ‘T., and IIartstem, M. L.: Coronary artery disease and left ventricular mural thrombi: Clinical, h~rnod~~ar~~~ and angiographic aspects, Chest 66488, 1974. Cheng, T. 0.: Incidence of ventricular aneurysm in coronary artery disease. An angiographic npprasiai, Am. J. Med. 50:340, 1971. Forrester, 3. S,, Diamond, G., Freedman, S., Allen, Il. N., Pannley, W. ha., Matloff, J., and Swan, H, J. 6.: Silent mitral insufliciency in acute myocardial infarction, Circulation 44:877, 1971. Sctie, V., Vogelpoel, L., Nellen, M., Swanepoel, A., and Beck, W.: Silent mitral incompebence, hb5. HEnET J. 81:723, 1961.