Surgical Management of Ventricular Septa1 Defects and Mitral Regurgitation Complicating Acute Myocardial Infarction

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1 Surgical Management of Ventricular Septa1 Defects and Mitral Regurgitation Complicating Acute Myocardial Infarction Mortimer J. Huckley, M.D., Eldred D. Mundth, M.D., Willard M. Daggett, M.D., Herman K. Gold, M.D., Robert C. Leinbach, M.D., and W. Gerald Austen, M.D. ABSTRACT Sixteen patients were studied subsequent to the development of acute ventricular septal rupture in 7 and severe mitral regurgitation in 9. These lesions occurred within two weeks of acute myocardial infarctions. Intraaortic balloon assistance was initiated when cardiovascular deterioration occurred, and hemodynamic improvement was obtained in all patients. Shunting through a ventricular septal perforation was reduced during balloon assistance, and mitral regurgitation, when present, was decreased. These effects were short-lived, and the patients were subsequently studied with coronary angiography and ventriculography. Two of 3 patients with anterior ventricular septal defect underwent successful surgical correction. Three patients had attempted closure of inferior ventricular septal defect without success. The fourth patient with an inferior ventricular septal defect died of his lesion without any attempt at surgical repair. Four patients with rupture of the papillary muscle were long-term surgical survivors. Coronary artery bypass grafting was carried out when indicated in these patients. Two of 5 patients with papillary muscle dysfunction who underwent operation during the acute period of their infarction were long-term survivors. The findings suggest that the mechanical lesions of mitral regurgitation and ventricular septal perforation are amenable to surgical intervention if a sufficient amount of residual functional muscle can be preserved in the left ventricle. Intraaortic balloon assistance allows a period of time to stabilize the condition of patients with these lesions, to reduce myocardial ischemia, and to carry out studies to determine the degree of associated coronary artery disease and the extent of irreversible myocardial damage. Based on the findings from these studies, surgical procedures may be selected. From the Surgical and Medical Services of the Massachusetts General Hospital and the Departments of Surgery and Medicine, Harvard Medical School, Boston, Massachusetts. Supported in part by U.S. Public Health Service Grant No. HE and Myocardial Infarction Research Unit Grant No. PH Presented at the Ninth Annual Meeting of The Society of Thoracic Surgeons, Houston, Tex., Nov , Address reprint requests to Dr. Buckley, Department of Surgery, Massachusetts General Hospital, Boston, Mass THE ANNALS OF THORACIC SURGERY

2 VSD and MR Complicating Acute Myocardial Znfarction T he appearance of acute mitral regurgitation secondary to dysfunction or rupture of a papillary muscle frequently leads to severe pulmonary congestion and cardiogenic shock in patients with acute myocardial infarction. Similarly, the onset of a large left-to-right shunt secondary to rupture of the interventricular septum may lead to biventricular failure and shock in the patient with an acute myocardial infarction. Recent reports [l, 91 have shown that these lesions can be successfully managed weeks to months after the acute infarction. A few successful repairs have been accomplished in the first two weeks after infarction [3, 4, 71. Intensive medical management with pressors, diuretics, oxygen, and similar measures in some circumstances has allowed the critically ill patient to stabilize and survive long enough to undergo correction of his defect at a later time. The addition of pressor agents, however, may increase left ventricular afterload in some patients who are in an acute, failing state and produce more mitral regurgitation or left-to-right shunting, leading to deterioration of the patient. Inotropic agents may increase cardiac output in these patients, but often at the expense of increased myocardial oxygen demand and extension of ischemia [6]. Counterpulsation, however, by reducing afterload and increasing diastolic aortic root pressure, can improve left ventricular function [2, 101. In order to determine if these beneficial effects would improve the hemodynamics and possibly survival in patients with the mechanical lesions of mitral regurgitation and acute ventricular septal perforation, intraaortic balloon pump assistance (IABPA) was applied to critically ill patients with these defects. Subsequently, cardiac catheterization was carried out and an operation was performed when indicated. The results of these interventions are outlined. Material and Methods Sixteen patients with acute myocardial infarction who developed acute septal rupture or severe mitral regurgitation within about two weeks of their infarction were admitted to the intensive study area. Infarction was documented by history, electrocardiogram, and serial enzyme studies. The appearance of an apical systolic murmur prompted further hemodynamic evaluation of the patients. Seven patients had ventricular septal rupture one to eleven days after the onset of their acute infarction (Table 1). In 3 the infarction was anterior, and in 4, inferior. Nine other patients developed acute mitral regurgitation one to eighteen days after their infarction (Table 2). In 3 the infarct was anterior, and in 6, inferior. Patients with ventricular septal perforation showed severe hypotension, venous desaturation, and reduced urine output. Chest films demonstrated marked pulmonary congestion. Patients with acute mitral regurgitation sim-

3 TABLE 1. SURGICAL INTERVENTION FOR VSD COMPLICATING ACUTE MYOCARDIAL INFARCTION IN 7 PATIENTS Duration of Balloon Assist (days) Patient, Infarct to VSD Before After Age, & Sex Location of Infarct (days) Opera tion Operation Operation Result 1, 62, M 2, 65, M 3, 62, M 4, 68, M 5, 63, M 6, 54, F 7, 63, F Inferior with 2 anterior ischemia Inferior Inferior Inferior Anteroseptal Anterior Anteroseptal CABG: RCA; infarct ec tomy; direct closure of VSD 2 CABG: RCA & LAD; infarctectomy ; direct closure of VSD 7 CABG: RCA & LAD; infarctectomy ; direct closure of VSD 0 No operation because of extensive ventricular damage 4 VSD direct closure of CABG: RCA; infarctectomy ; 5 CABG: LAD & RCA; infarctectomy; direct closure of VSD 3 CABG: none; infarctectomy; direct closure of VSD Death in O.R. from disruption Died 2 days postop. with low output & arrhythmia Died 21 days postop. of renal shutdown & sepsis; had residual 1.6 : 1 shunt Died 1 wk. after IABPA with low output; postmortem examination showed extensive ventricular damage Alive & well, 18 mo. Died 2 wk. postop. of sepsis & renal failure Alive & well, 22 mo.

4 c Duration of Balloon Assist (days) Patient, Infarct to MR Before After Age, & Sex Location of Infarct (days) Operation Operation Operation Result 1, 57, M Inferior with CABG: RCA & LAD; Alive & well, anterior ischemia MVR (papillary 6 mo. muscle dysfunction) 2, 62, M Inferior CABG: LAD; MVR Alive & well, (ruptured papillary 2 mo. muscle) 3, 54, M Anterior CABG: RCA & LAD; Death from low MVR (papillary output & renal muscle dysfunction) failure, 10 days 4, 56, M Inferior CABG: RCA & LAD; Alive & well, MVR (ruptured 14 mo. papillary muscle) 5, 45, M Inferior CABG: RCA & LAD; Death postop. from inf arctectomy ; low output with MVR (papillary renal failure c. m muscle dysfunction) 2 6, 39, F Anterior with CABG: RCA & LAD; Death immediately inferior ischemia infarctectomy ; postop. in shock P Q1 MVR (papillary muscle dysfunction) fz 7, 57, M Inferior CABG: RCA & LAD; Alive & well, n M 5 "j w s 05 MVR (ruptured 8 mo. papillary muscle) 8, 63, M Inferior CABG: RCA & LAD; Alive & well, MVR (ruptured 4 mo. papillary muscle) 9, 62, M Anterolateral CABG: none; Alive & well, infarctectomy; 3 mo. Q, MVR (papillary z muscle dysfunction) MR = mitral regurgitation; CABG = coronary artery bypass graft; RCA = right coronary artery; LAD = left anterior descending coronary artery; MVR = mitral valve replacement.

5 BUCKLEY ET AL. ilarly were hypotensive and had poor peripheral perfusion, together with pulmonary edema, by clinical examination and on chest film. Medical therapy with digitalis, diuretics, and oxygen was begun. Catecholamine infusions were initiated in all but 1 patient. Transvenous pacing was carried out when indicated. Radial artery pressure was monitored constant1.y. A flow-directed Swan-Ganz catheter was inserted transvenously and placed in the wedge position. Pulmonary artery pressures were monitored constantly, and the pulmonary capillary wedge pressure was measured intermittently. A central venous pressure catheter was inserted for both sampling and constant monitoring of central venous pressure. Pulmonary-to-systemic flow ratios were determined by oxygen saturation. In patients with acute mitral regurgitation, cardiac output was estimated by the dye-dilution technique with indocyanine green injected into the pulmonary artery and sampled from the radial artery. Because of persistent reduced peripheral perfusion as evidenced by decreased urine output and failure to respond to the medical program, intraaortic balloon assistance was initiated. The balloon was inserted retrograde from the femoral artery by a standard technique [lo]. During this period the patients received heparin, and low-molecular-weight dextran was infused at the rate of 10 to 25 ml. per hour. Once the patient s condition had stabilized, repeated on-off studies were performed to determine the effect of balloon assistance. Systemic and pulmonary artery pressures, pulmonary capillary wedge pressure, and electrocardiograms were recorded. Duplicate determinations of cardiac output and oxygen saturation were obtained. IABPA was then stopped. Three to ten minutes were allowed before repeat determinations of cardiac output or oxygen saturations or both were repeated. Arterial pressure, pulmonary wedge pressure, pulmonary artery pressure, and central venous pressure were monitored as before. IABPA was subsequently resumed, and after a period of five minutes the previous determinations were repeated. In order to determine the overall effect of IABPA on afterload, angiotensin was infused in 3 patients while balloon pump assistance was continued. The systolic arterial pressure was elevated to the level maintained by the patient prior to the institution of balloon assistance. At that time another set of measurements was obtained. After an average of 36 hours of IABPA, selective coronary artery and left ventricular cineangiography was performed by the Sones technique while uninterrupted circulatory assistance was maintained. Emergency cardiac operation was then carried out as indicated. Partial excision of the acute infarct. and closure of the ventricular septa1 defect (VSD) was attempted in 6 patients. All VSDs were closed by a direct suture technique [3, 41. In these 6 patients, eight coronary artery bypasses were also performed. In the 9 patients with acute mitral regurgitation, mitral valve replacement was done using a Starr-Edwards ball-valve prosthesis or a Bjork-Shiley disc prosthesis. 602 THE ANNALS OF THORACIC SURGERY

6 VSD and MR Complicating Acute Myocardial Znfarction Fifteen saphenous vein bypass grafts to the coronary arteries were performed at the same time. Infarct resection was also carried out in 3 patients. All patients who survived the operation were maintained on balloon assistance for variable periods postoperatively. R eszcl ts Hemodynamic improvement occurred in all patients while they were on balloon assistance. In patients with acute mitral regurgitation the mean pulmonary capillary wedge pressure fell from an average level of 25 to 20 mm. Hg with initiation of IABPA. There was an associated rise in the average cardiac output from 3.2 to 3.7 liters per minute. Mean arterial pressure remained essentially unchanged. Cessation of balloon assistance was marked by a rise in pulmonary capillary wedge pressure and an increase in the amplitude of the V waves in the pulmonary capillary wedge tracing. In the patients who received angiotensin, at a rate of 1.25 pg. per minute, the cardiac output, pulmonary capillary wedge pressure, and regurgitant V waves all returned to the prepumping levels. Patients with VSD showed a fall from 17 to 13 mm. Hg in pulmonary capillary wedge pressure. The systemic arteriovenous oxygen difference fell from an average of 9.7 to 8.1 vol. per 100 ml., while the pulmonary arteriovenous oxygen difference remained unchanged. Thus the pulmonic-to-systemic flow ratio fell from 5.1 : 1 to 4.2 : 1 secondary to a selective increase in systemic output. There was no significant change in heart rate. Mean arterial pressure rose slightly. Cessation of balloon assistance resulted in an immediate rise in pulmonary capillary wedge pressure to the preassist levels. Angiotensin was infused during balloon assistance at a rate sufficient to elevate systolic arterial pressure to the preassist level. At that point the pulmonic-tosystemic flow ratio returned to the preassist level despite a marked rise in diastolic pressure. Despite the beneficial effects of balloon assistance, recurrent hemodynamic deterioration occurred. Maximum stabilization had been achieved by 24 hours, and all patients were dependent upon the balloon as evidenced by rising pulmonary capillary wedge pressures and decreased cardiac output whenever balloon assistance was stopped. Early in the study 2 patients with VSD and 3 with acute mitral regurgitation were continued on IABPA for periods greater than 48 hours before angiography was carried out. Recent patients have had angiographic studies performed within 24 hours of insertion of the balloon pump unit. In the patients with VSD, the coronary angiograms revealed high-grade obstruction of the proximal left anterior descending coronary artery. Five of the 7 patients showed high-grade obstruction of the right coronary artery, and 3 had triple-vessel disease. The left ventriculograms in the right anterior oblique projection showed left-to-right shunts with opacification of the right ventricle. All patients with acute mitral regurgitation had high-grade ob- VOL. 16, NO. 6, DECEMBER,

7 BUCK.LEY ET AL. struction of the proximal left anterior descending and right coronary arteries. Three had triple-vessel disease. Mitral regurgitation was moderately severe in 5 patients with papillary dysfunction and was severe in 4 with papillary muscle rupture. Studies were carried out even in the presence of severe systolic hypotension while balloon assistance was maintained. There were no significant complications related to the catheterization. Two of the 3 patients with anterior VSDs survived surgical correction. These patients had a limited infarct resection of the anterior and apical segment of the left ventricle together with direct closure of the VSD. The 2 surviving patients had occlusion of the left anterior descending coronary artery at or just beyond the level of the first diagonal branch with sparing of the first septal perforator. Right coronary artery bypass grafting was carried out in 1 of these patients for associated coronary artery stenosis. The third patient in this group had extensive infarction of the entire septum with occlusion of his left anterior descending coronary artery at its origin. There was also high-grade stenosis of the right coronary artery so that there was marked infarction of the posterior septum as well. Four patients had inferior VSDs. Total occlusion of the right coronary artery and severe stenosis of the left anterior descending coronary artery were present. Three of these patients were operated upon. At operation 1 patient had marked destruction of the entire posterior and superior septum with involvement of the posteromedial papillary muscle and posterior ventricular wall. Direct closure of this defect could not be maintained, and the patient died in the operating room. The other 2 surgically treated patients died two and twenty-one days postoperatively, respectively, from complications of their low-output state. The fourth patient, who had an inferior VSD, had extensive posterior infarction with septal perforation and evidence of extensive poor contraction on ventriculogram, not only of the posterior and septal areas of the left ventricle but also of the apical and lateral ventricular walls. The patient had three-vessel disease and was thought not to be a candidate for corrective operation. He died in persistent cardiac failure one week after the initiation of IABPA. Postmortem examination confirmed extensive infarction. The 4 patients with rupture of a papillary muscle are long-term survivors. At the time of mitral valve replacement 3 of these patients had concomitant vein bypasses of their right coronary and left anterior descending coronary arteries, while the other had bypass only of his left anterior descending coronary artery. In these patients the extent of the associated myocardial infarct was not marked, and the predominant lesion was free rupture of all or part of one papillary muscle and marked mitral regurgitation with decreased ventricular contraction in association with myocardial ischemia. Five patients had severe mitral regurgitation secondary to papillary muscle dysfunction and extensive inferior wall and lateral wall infarction in most cases. In 3 of 604 THE ANNALS OF THORACIC SURGERY

8 VSL) ctnd MR Complicating Acute Myocardial Infarction these patients infarct resection was carried out at the time of mitral valve replacement. Four of these patients had extensive coronary disease involving their left anterior descending and right coronary arteries. Both vessels were bypassed at the time of operation. The fifth patient had left anterior descending and circumflex marginal disease with coronary artery occlusion and required valve replacement with infarctectomy alone. Long-term survival of three and six months has been obtained in 2 patients, respectively. In those patients who died, postmortem examination showed extensive myocardial infarction with involvement of both the left and right posterior ventricular wall and septum as well as the apex of the ventricle.,411 patients who survived operation were maintained on balloon assistance for an average of four days postoperatively. Conzmen t Early diagnosis of the mechanical complications of mitral regurgitation or ruptured interventricular septum subsequent to acute myocardial infarction has become easier to confirm with use of the flow-directed Swan-Ganz catheter [S]. The correlation of pressure measurements and oxygen saturation samples readily determines the presence of severe mitral regurgitation or VSD. It is evident that the patients who can survive the acute onset of these lesions have an excellent prognosis with repair at a later date [7]. Many patients, however, despite intensive medical therapy, receive little if any benefit and rapidly deteriorate. Pressor agents, when needed, may greatly increase left ventricular work with associated extension of ischemia. In this study, intraaortic balloon assistance demonstrated a beneficial effect upon left ventricular function by reducing afterload and increasing aortic diastolic root pressure. Such benefit was partly related to reduced afterload as evidenced by the reversal of its effect with the infusion of angiotensin. Because of the extensive prior injury to the myocardium [5], however, these beneficial effects were short-term and were not able to maintain the heart in a state of prolonged compensation sufficient to allow a prolonged period for recovery and possible surgical correction later. Since the beneficial effect of intraaortic balloon pumping was only temporary, it was evident that very early cardiac catheterization with angiography should be done and, when possible, surgical intervention should be attempted. In the latter part of the series these studies were carried out within the first 24 hours after initiation of IABPA and operations were performed within the first 36 hours. In patients with anterior ventricular septa1 rupture, a greater survival was obtained if the superior and posterior septum had been preserved. Despite the presence of significant associated lesions in the right coronary artery, marked decrease in perfusion of the posterior septum with resultant infarction had not occurred in these patients. In contrast, however, patients VOL. 16, NO. 6, DECEMBER,

9 BUCKLEY ET AL. with high inferior VSDs had extensive infarction of the posterior wall of the left and right ventricles related to total proximal occlusion of their right coronary artery. The anterior septum in most cases was also ischemic because of significant stenosis of the left anterior descending coronary artery. This led to a massive lesion of the left ventricle, with not only rupture of the interventricular septum and inferior wall infarction, but also ischemic changes in the posteromedial papiiiary muscle. At the present time such lesions are so extensive that unless surgical intervention occurs very early after infarction, successful surgical repair by revascularization and reconstruction is extremely difficult and is attended by a high mortality. When extensive poor contraction of the ventricle and mitral regurgitation are observed at the time of angiography, operation has been withheld in recent cases. In patients with acute mitral regurgitation, similar findings are evident. Patients with discrete rupture of a papillary muscle and only moderate involvement of the left ventricular wall were able to survive surgical correction by valve replacement and revascularization. However, those patients who had extensive ventricular wall damage in association with papillary muscle infarction and dysfunction were able to survive surgical intervention only if it was applied early and the ventricular wall dyskinesis was reparable. More coronary artery bypass grafts and more extensive infarct resection were required. From this experience with these complications of acute myocardial infarction, it is evident that surgical intervention may be beneficial to these patients. Our experience has shown us, however, that because of the ongoing process of muscular ischemia and destruction associated with the shock state of these patients, intervention should not be delayed. The ischemic state may be stabilized with the use of IABPA and the hemodynamic defect corrected with surgical intervention. The patients selected for this surgical intervention must still have some viable muscle remaining in the ventricle, and the chances of having muscle in a viable state are greatest with early intervention. Thus, patients who appear to have a systolic murmur during the course of acute myocardial infarction would benefit from IABPA; and if their hemodynamic measurements show a significant mechanical defect, coronary angiography and ventriculography should be carried out and an operation performed when indicated. References 1. Austen, W. G., Sokol, D. M., DeSanctis, R. W., and Sanders, C. A. Surgical treatment of papillary muscle rupture complicating myocardial infarction. N..Engl. J. Med. 278:1137, Buckley, M. J., Leinbach, R. C., Kastor, J. A., Laird, J. D., Kantrowitz, A. R., Madras, P. N., Sanders, C. A., and Austen, W. G. Hemodynamic evaluation of intra-aortic balloon pumping in man. Circulation 41 (Suppl. 11): , THE ANNALS OF THORACIC SURGERY

10 VSL) and MR Complicating Acute Myocardial Infarction Buckley, hi. J., Mundth, E. D., Daggett, W. M., DeSanctis, R. W., Sanders, C. A., and Austen, W. G. Surgical therapy for early complications of myocardial infarction. Surgery 70:814, Daggett, W. hi., Burwell, L. R., Lawson, D. W., and Austen, W. G. Resection of acute ventricular aneurysm and ruptured interventricular septum after myocardial infarction. N. Engl. J. Med. 283: 1507, Gold, H. K., Leinbach, R. C., Sanders, C. A., Buckley, M. J., Mundth, E. D., and Austen, W. G. Intra-aortic balloon pumping for ventricular septa1 defect or mitral regurgitation complicating acute myocardial infarction. Circulation 47: 1191, hlaroko, P. R., Braunwald, E., Covell, J. W., and Ross, J., Jr. Factors influencing the severity of myocardial ischemia following experimental coronary occlusion. Circulation 40 (Suppl. III):III-140, Mueller, H., Ayres, S. M., Conklin, E. F., Giannelli, S., Mazzara, J. T., Grace, W. T., and Nealson, T. F. The effects of intra-aortic counterpulsation on cardiac performance and metabolism in shock associated with acute myocardial infarction. J. Clin. Invest. 50: 1885, Mundth, E. D., Buckley, M. J., Daggett, W. M., Sanders, C. A., and Austen, W. G. Surgery for complications of acute myocardial infarction. Circulation 45: 1279, Page, D. L., Caulfield, J. B., Kastor, J. A., DeSanctis, R. W., and Sanders, C. A. Myocardial changes associated with cardiogenic shock. N. Engl. J. Med. 285:145, Selzer, A., Gerbode, F., and Kerth, W. J. Clinical, hemodynamic, and surgical considerations of rupture of the ventricular septum after myocardial infarction. Am. Heart J. 78:598, DR. ROBERT J. FLEMMA (Milwaukee, Wis.): Dr. Buckley and his associates have convincingly added another dimension to the repertoire of the balloonassisted device by its use in these devastating complications of myocardial infarction. In Milwaukee we have treated 6 patients with postinfarction VSD, of whom 3 with chronic infarction were long-term survivors at more than two and three years. In the acute group there were no survivors, however, and 1 of the patients died upon induction of anesthesia. In retrospect, use of the balloon assist device might well have helped get the operation under way and at least given us a chance to save the patient. We have not had any experience with acute mitral rupture as described by Dr. Buckley. Chronic mitral dysfunction due to coronary disease, however, presents a real problem in delineating appropriate therapy. We believe you must have both disease of the papillary muscle and ventricular wall fibrosis to produce mitral insufficiency necessitating valve replacement. If there is just ischemia of the ventricular wall, we think this can be treated with revascularization and not valve replacement. The case of a 2-year-old child who had anomalous origin of the left coronary from the pulmonary artery and severe mitral regurgitation is somewhat interesting. The ventriculogram showed marked mitral regurgitation. At the time of operation we carried out a saphenous vein bypass graft, ligated the anomalous artery, and then examined the posterior myocardium, which was viable and contracted well. We did not think valve replacement should be carried out because this was viable muscle. We believe, and would like to emphasize along with Dr. Buckley, that myocardial revascularization should be utilized when one is treating these two com- VOL. 16, NO. 6, DECEMBER,

11 BUCKLEY ET AL. plications in order to concomitantly revascularize any other lesion and guarantee long-term success. DR. ALBERT B. IBEN (Davis, Calif.): At the 1969 meeting of the Society, my colleagues and I had the opportunity of presenting a paper wherein was described a double-layer patching technique for repair of postinfarction VSD. Its use eliminates disruption of friable septa1 and mural cardiac muscle by sutures. Postoperative VSD recurrence is not seen, and success is dependent on left ventricular reserve. In patients in whom the left ventricle is not involved by infarction, the repair is done through the right ventricle. The most salient feature was to urge surgical repair of the postinfarction VSD as soon as it becomes evident that cardiac failure cannot be controlled medically. We have experience with 13 patients. There were 4 survivors among the initial 8 patients operated upon at varying intervals following perforation. Subsequently, 5 more patients have been treated for this problem. One patient was treated medically for ten days and underwent successful repair but died of pulmonary and renal causes on the fifteenth postoperative day. One patient in this group had the unusual experience of undergoing elective repair. Three patients were operated upon in the period immediately following perforation. The first of these 3 experienced a posterior perforation which was successfully closed using a right ventriculotomy approach. Two patients underwent surgical repair within eighteen hours of VSD formation. Both required administration of significant amounts of norepinephrine and had barely palpable pulses at the beginning of their operations. Repair required infarctectomy of the left ventricular apex, debridement of the lower third of the septum, and double-layer Teflon-felt replacement of the lower septum. The left ventricle was closed against the double-layer patch utilizing bolstered mattress sutures. Both patients required doses of isoproterenoll for approximately 24 hours, and both are alive two and four months postoperatively, respectively. Eight of the 13 patients are alive. It continues to be our belief that the treatment of postinfarction VSD is surgica.1 repair at the earliest possible time. The experience with several patients shows this technique to be successful. DR. WATTS R. WEBB (Syracuse, N.Y.): I wish to commend Dr. Buckley and his associates on this excellent presentation and endorse their concepts of preoperative and postoperative support for the heart that fails primarily because of acute rnechanical problems. We believe it is much more rewarding to use IABPA and proceed with an immediate operation than to undertake revascularization of the patient who is in coronary shock. More important than assistance to the heart at this particular time is improvement of the peripheral circulation. Any patient in failure this severe should be studied immediately, utilizing IABPA, and then should undergo operation without delay. We have not been able to get any of them off the assist device without immediate operation. We have had 6 similar patients, 4 with acute mitral regurgitation and 2 with overwhelming failure from rapidly developing aneurysm, 1 of whom had a large VSD. An overwhelming aneurysm three weeks after myocardial infarction when the patient was in intractable failure was due mainly to its rapid enlargement. The patient was studied with the intraaortic balloon in place and was immediately taken to the operating room, where the aneurysm was resected. He required IABPA for four days and was discharged in two weeks. Six weeks later his heart was normal in size. In addition to these 6 patients, 4 of whom lived, 10 other patients have required postoperative support after a variety of other cardiac procedures. Postoperative support continued for as long as twelve days, with 9 of the patients successfully weaned from the pump. 608 THE ANNALS OF THORACIC SURGERY

12 VSD and MR Complicating Acute Myocardial Infarction We think this is by far the best method for relief of the low-output syndrome. Instead of having to walk the tightrope between overinfusion and underinfusion, trying to reduce the afterload with peripheral dilators, and administering cardiotonic drugs, we prefer the use of balloon assistance. This truly constitutes an invaluable and essential addition to the armamentarium of any cardiovascular surgeon. DR. JACOB ROSENSWEIG (Hartford, Conn.): I think Dr. Buckley and his group have made a very important clinical observation, i.e., that balloon counterpulsation can be effectively used to increase patient salvage. We have had similar experience. I rise, however, to point out that unfortunately one cannot always depend on being able to utilize balloon counterpulsation. We recently encountered 2 patients in whom, because of tortuous aorta and iliac arteries, the balloon catheter could not be inserted, and we have subsequently learned of 11 other cases. In 1 of our patients the catheter became kinked in its iliac course, resulting in obstruction of the catheter lumen and inability to inflate the balloon. Kinking developed repeatedly during passage of three different catheters from bilateral femoral arteriotomy sites, at times even when the catheter tip was still in the abdominal aorta. DR. ROBERT L. BERGER (Boston, Mass.): I will comment on Dr. Buckley s presentation by saying that we have used the balloon for supporting patients with complications of infarction such as rupture of the ventricular septum. One of the additional advantages is that you can take a patient about eight or ten days after infarction whose muscle is still friable for suturing, keep him on the balloon for seven to ten additional days, and then go ahead with the surgical procedure. By that time there is significant fibroplasia, the sutures hold much better, and probably the long-term results will be improved. DR. BUCKLEY: I wish to thank the discussants for their remarks. Certainly our feelings are similar to Dr. Flemma s in that mitral regurgitation should be regarded as a dynamic defect unless there is frank mechanical rupture of the papillary muscle in both the acute and chronic states. Attempts should be made to evaluate whether functional regurgitation can be reversed by revascularization before going ahead with valve replacement. Dr. Iben s series certainly is a remarkable one, and we have not had similar success with the right ventricular approach. We have been reluctant recently to make right ventricular incisions because we think this may interrupt separate collateral coronary artery pathways, and we have been concerned that this might lead to more ventricular wall destruction. Dr. Webb, we certainly agree with you and appreciate your feelings about the intraaortic balloon. At this time we look upon it entirely as a support system for patients who are severely ill, a system to give us more time to organize definitive therapy. Dr. Rosensweig, we also have had problems inserting balloons. I am afraid we haven t been able to tie them into such delicate knots as yours. We have been unable to insert the balloon in only 6 of more than 135 patients. All 6 of these patients died. There has been dissection of aortic plaques in 3 patients, and in 1 patient a total dissection of the aorta was discovered at postmortem examination. There was no rupture or massive bleeding from the aorta related to this, however, nor was any hemodynamic defect produced. I think the balloon is an agent which can be used to support critically ill patients while we evaluate them for corrective procedures. As with any surgical adjunct, it does have its limitations. VOL. 16, NO. 6, DECEMBER,