Ventricular septal defect after acute myocardial infarction

J

THoRAc CARDIOVASC SURG

80:61-67, 1980

Ventricular septal defect after acute myocardial infarction Early repair Thirty-eight patients have been operated upon early after acute myocardial infarction with rupture of the ventricular septum. Preoperative management included bedside hemodynamic evaluation. mechanical left heart support. and pharmacologic agents. The results of the surgical repair refiected both the effectiveness and the duration of preoperative treatment. Operation was performed in 14 patients with refractory cardiogenic shock. 10 of whom died (71 %). Hemodynamic and clinical stability was achieved in 24 patients. Early operation (average 46 hours of medical management) in 17 patients permitted accurate repair. even with friable tissues; four of these patients died (23%). Delayed operation (average 12 days of nonoperative treatment) was performed in seven patients and resulted in a higher mortality rate. three patients dying (43%). The location of the ventricular septal defect (VSD) also influenced the operative risks. the prognosis for posterior defects being worse than that for anterior defects. Optimal myocardial preservation during the entire procedure is of crucial importance to the success of the operation.

D. Y. Loisance, M.D., J. P. Cachera, M.D., H. Poulain, M.D., Ph. Aubry, M.D., A. M. Juvin, M.D., and J. J. Galey, M.D., Creteil, France

Accepted for publication Nov. 7, 1979.

years (range 49 to 72 years). Eight patients were over 70 years of age. These patients were the survivors of a group of 57 patients with the same diagnosis, treated in various medical intensive care units (lCU), for whom surgical therapy was considered. Despite aggressive treatment with the intra-aortic balloon pump* (lABP) in 37 cases and pharmacologic support with vasodilator therapy, 19 patients died, 11 during IABP support before an operation could be attempted. The presenting episode for this admission was the first clinical manifestation of coronary artery disease in most cases. A previous myocardial infarction could be documented in only four patients. A presenting infarction was anterior or apical in 26 patients and posterior or posterolateral in 12 patients. The VSD was diagnosed an average of 3.7 days (range 0 to 6 days) after the onset of symptoms of myocardial infarction. The patients were admitted to our medical coronary care unit an average of 44 hours (6 hours to 8 days) after VSD diagnosis. Twenty-seven of the 38 patients were in cardiogenic shock with pulmonary edema and

Address for reprints: D. Y. Loisance, M.D., Service de Chirurgie Cardiaque, C.H.U. HENRI MONDOR, 94000 Creteil, France.

*Datascope Corp., Paramus, N. J.

Rupture of the ventricular septum after acute myocardial infarction is infrequent but often catastrophic. Its surgical management has benefited from progress achieved within the last ten years in the preoperative treatment of high-risk patients and in surgical techniques. Recent reports'r" illustrate that with improvement in the early and late results of an aggressive surgical approach, a fifty percent survival rate may be expected.:' We present our total surgical experience with this problem, 38 cases.

Patients Between October, 1972, and July, 1979,38 patients have undergone operation for ventricular septal defect (VSD) complicating acute myocardial infarction. There were 32 men and six women, with a mean age of 66 From the Department of Cardiothoracic Surgery and the "Centre de Recherches Chirurgicales" C.H.U. HENRI MONDOR, 94000 Creteil, France. Received for publication Oct. 9, 1979.

0022-5223/80/070061 +07$00.70/0 © 1980 The C. V. Mosby Co.

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62 Loisance et al.

Surgery

Fig. 1. Technique of septal reinforcement with two Teflon felt strips. The strip on the right side is placed through the defect itself. oliguria, and the remaining II were in compensated left ventricular failure. Treatment included IABP in 26 patients . In one patient, venoarterial extracorporeal circulation with membrane oxygenation and extracorporeal renal dialysis was begun in the ICU to reverse cardiogenic shock unresponsive to IABP . The other 12 patients were treated pharmacologically with inotropic agents (digitalis or dobutamine) and vasodilators. The coronary and ventricular anatomy were studied preoperatively by angiography in 22 case s.

Selection for operation The 38 patients were divided in two groups on the basis of the results of medical treatment. Group I consisted of 14 patient s in whom cardiogen ic shock was refractory to treatment and surgical repair appeared to be the only chance for survival. In this group , the mean age was 68 years (range 62 to 72 years ). The VSD was anterior in eight patients and posterior in six and was diagno sed 4 .6 days (range I to 6 day s) after the onset of symptoms. Preoperative treatment was maintained for 26.6 hours (range 16 to 32 hours) . Eight patients had IABP support; in six, the balloon could not be inserted for technical reason s. The operation was performed as an emergency a mean of 6 days (range 2 to 8 days) after myocardial infarction . Group II comprised the 24 patients in whom the clinical and hemodynamic condition was dramatically im-

proved by treatment and pulmonary edema was controlled as diuresis resumed . These patient s were further subdivided into two groups: those for whom efforts were made to postpone the operation as long as possible (Group IIa) and those who underwent operation as soon as the maximum benefit of medical treatment was obtained and an operating room was available (Group lib). Group IIa consisted of seven patients, six of whom were treated during the first 2 years of our experience . The mean age was 64 years (range 46 to 72 years). The VSD was diagnosed an average of 24 hours (range 2 to 36 hours) after infarction and was topographically anterior in five patients and posterior in two. IABP was used in every case and was maintained for 12.0 days (range 8 to 15 days) after myocardial infarction. The operation was performed an average of 16.5 days (7 to 19 days) after myocardial infarction . Group lIb consisted of 17 patients treated since 1974. Their mean age was 64 years (range 55 to 72 years ) . The VSD was diagnosed 2.6 days (range I to 4 days) after infarction and was anterior in 13 patients and posterior in four. The preoperative treatment was IABP support in II patients and pharmacologic support in six . An emergency operation was performed an average of 5.3 days (range 2 to 6 days) after infarction.

Operative technique The operation was performed after neuroleptic analgesia and tracheal intubation with local anesthesia. " Extracorporeal circulation was instituted with ascending aortic and caval cannulation in every case but one (the patient treated by venoarterial extracorporeal circulation) . The circuit was equipped with a bubble oxygenator early in the series and a membrane oxygenator since 1974 . The perfusion was performed with the patient fully vasodilated, with hemodilution and hypothermia (21 C). The pump flow was adjusted to the venou s return with no regard to the mean aortic pressure. The left ventricle was drained by an atrial cannula. Myocardial preservation was achieved with cold card ioplegia during the period of aortic cross-clamping required for surgical repair. The general principles of the surgical technique were as follows : ( 1) recognition of the anterior or posterior location of the VSD; (2) extensive infarctectomy, permitting exposure of the VSD through the infarcted area; (3) excision of the most friable border of the ruptured septum; (4) septal reinforcement with two Teflon felt strips; (5) closure of the VSD by insertion of a single or double Teflon-patch on the reinforced septum; and (6) treatment of the associated lesions, such as 0

Volume 80 Number 1 July, 1980

papillary muscle damage and significant coronary artery stenosis. The repair was easily achieved in the cases of anteriorand apical VSDs. A left ventricular approach was used for the 24 anterior lesions and permitted a rapid repair. Two Teflon felt strips, I em wide, were attached on each side of the septum with interrupted mattress sutures (Fig. I). The untied mattress sutures were placed through a large piece of Teflon patch, which was inserted on the reinforced left side of the septum. Each suture was placed far from the border of the rupture, as close as possible to the border between the friable myocardium and normal tissues. Excision of the most friable tissues permitted good exposure and proper positioning of the Teflon felt strip on the right side of the septum through the VSD. The septal patch on the left side was included anteriorly in the closure of the anterior left ventriculotomy (Fig. 2). Interrupted Teflon felt-reinforced mattress sutures were used for the ventriculotomy closure. Two apical ruptures were repaired in nearly the same way. After similar reconstruction of the septum, the right and left ventricles were closed by interrupted teflon feltreinforced mattress sutures passed through the free wall of each ventricle and the septal patch. Twelve posteroinferior VSDs were difficult to repair for three reasons. First, exposure of the defect was always awkward. The heart was dislocated anteriorly out of the pericardium, and the ventriculotomy was made in the middle of the parietal infarction, parallel to the posterior descending artery, either on its right side (nine patients) or its left side (three patients). Although this approach exposed the defect, proper evaluation was still difficult. Second, the anatomic features of the posterior septal ruptures (Fig. 3) were more complex than those of anterior ruptures. These features were the same in all cases studied. Openings on the left side of the septum were much more anterior than openings on the right, being almost in the middle of the septum. Furthermore, the involvement of the right side of the septum was more extensive than that of the left, for the entire posterior insertion of the septum was involved from the atrioventricular anulus posteriorly to the apex anteriorly. The resulting Z configuration of the VSD led to difficulty in assessing its limits. Furthermore, intraseptal necrosis led to a sagittal dissociation of the septum, which resulted in two septal flaps and made difficult the proper localization of the posterior insertion of the septum into the free wall. The transseptal mattress sutures on the Teflon felt strips placed on each side of the septum were positioned from the atrioven-

VSD after acute myocardial infarction

63

Fig. 2. Schematic representation of the closure of an anteriorly located ventricular septal defect through an anterior left ventriculotomy.

Fig. 3. Sagittal viewof the intraseptal dissection by the hematoma, as observed in a topographically posterior ventricular septal defect. The hematoma is close to the auriculoventricular anulus. tricular anulus posteriorly to the apical limit of the rupture. Two Teflon patches were positioned on the untied sutures on each side of the septum in order to obliterate the intra septal cavity from both sides. The posterior free border of the patches was fixed to the unopened ventricle by transparietal sutures, and to the opened ventricle by incorporation in the closure of the ventriculotomy (Figs. 4 and 5). The third special feature of the posterior VSD was the proximity of the posteromedial mitral papillary muscle and septal tricuspid papillary muscle. The three

The Journal of Thoracic and Cardiovascular Surgery

64 Loisance et al.

Fig. 4. Repair of a posterior ventricular septal defect through a right-sided approach. The septal patch on the left side is placed through the ventricular septal defect.

Fig. 5. Repair of a posterior ventricular septal defect through a left-sided approach. Papillary muscle necrosis may necessitate mitral valve replacement. The septalTeflon felt stripsand the Teflon patch are attached to the valve prosthesis. patients with extension of the infarction to the left posterior wall had left ventriculotomy. Mitral valve replacement was required in all three because of papillary muscle necrosis. This was performed through the left ventriculotomy. The eight patients with extension of the infarction to the right ventricle had a right ventriculotomy. The tricuspid valve was replaced in two, a tricuspid valvuloplasty was performed in one, and the septal papillary muscle was reimplanted in one. In

every case, the proximity of the tricuspid valve and choradae tendineae made difficult the correct placement of the transseptal sutures. Aorta-coronary bypass was performed in only two patients. Angiographic indications for bypass were present in six additional patients, but bypass was not performed because of long aortic cross-clamp time and the technical difficulties of dissecting coronary arteries in the presence of epicardial hematoma. After release of the aortic cross-clamp, the left ventricle was kept completely decompressed by the left atrial cannula for a minimum of 30 minutes. The left ventricle was then kept ejecting for 15 minutes and the filling pressure was increased progressively. During this period, the IABP was activated, initially in an asynchronous mode and then synchronously. The IABP was withdrawn at the end of the procedure in 17 cases, after 24 hours in three, and after 48 hours in five.

Results Mortality rates correlated closely with the preoperative condition and were influenced by the location of the VSD. In Group I, 10 of 14 patients died in the ICU. Death was related to refractory cardiogenic shock in three patients, extension of myocardial necrosis in two, refractory pulmonary edema and anuria in four, and intractable ventricular fibrillation in one. The difficulties of surgical repair were comparable in the two subgroups in Group II: The friability of the necrotic tissues did not seem reduced after a 2 week delay. The mortality rate, however, differed in the two subgroups: Three of seven patients (43%) died in the group operated upon as late as possible (Group lIa), and four of 17 patients (23%) died in the group operated upon as soon as possible (Group lIb). The causes of death in Group lIa were sepsis (one case), neurologic complications (one case), and ventricular fibrillation (one case). In Group lIb, death was due to ventricular fibrillation (two cases) and refractory pulmonary insufficiency (two cases), related in one case to preexisting asthma. Three cases of postoperative left-to-right shunt were observed. In each of these cases, reinforcement of the septum was not complete, and the leakage occurred in the vicinity of the unreinforced septum. In one case, the shunt was diagnosed in the sixth postoperative hour and was responsible for intractable cardiac insufficiency and cardiogenic shock. In the other two cases, the shunt was diagnosed after the second postoperative week and reoperation was performed during the third week. Complete septal reinforcement and repair were achieved. The postoperative course was uneventful in

Volume 80

VSD after acute myo cardial infarction

Number 1

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one case but was complicated by progressive neurologic deterioration in the other. The nece ssity for valve replacement increased the postoperative death rate. Every patient who required mitral (three cases) or tricuspid (two cases) valve replacement died within 15 days . The two patients who underwent conservative procedures on the tricuspid valve were discharged from the hospital. The location of the VSD influenced the immediate postoperative course . Death related to a cardiac problem-left ventricular failure (nine cases) and right ventricular failure (four cases)-was more common in patients with posterior VSDs (seven of twelve patients, 58%) than in those with anterior VSDs (six of 26 patients , 23%). The occurrence of four noncardiac deaths (sepsis , neurologic complications, or general deterioration) in the group of patients with anterior VSDs reduces the differences between the groups in the final outcome (10 deaths in 26 patients , 38 %) . Twenty-one patients were discharged from the hospital. One died suddenly 3 weeks later from an unknown cause . Twenty patients are long-term survivors . The average follow-up is 33 months (range , 4 months to 5 years). Seven patients underwent operation more than 3 years ago. Each of the 20 has been restored to normal social and professional activitie s and is free of angina pectoris and symptoms of left ventricular failure . One of them was hospitalized recently for a pleural epithelioma (Fig . 6). Discussion Since the first reports of successful repair of VSD following acute myocardial infarction by Proudfit and

associates" in the United States and Faivre and colleagues' in France , sporadic reports of success and reports of larger surgical series have indicated that a survival rate near 50 % may be expected . I. 3 . 8- 12 However, major problems such as optimal preoperative management , the be st timing for repair, and the best surgical technique remain unsolved. There seems to be general agreement that operation should be deferred until 3 week s after infarction;' This delay allows a technically easier operation in scarred myocardial tissues and , consequently , a low rate of postoperative septal leakage . Cardiac support with IABP permits prolongation of preoperative management and safer preoperative definition of coronary and ventricular anatomy. The high operative mortality rate in patients operated upon before 3 weeks (52%), compared with the low postoperative risk in patients in whom operation could be deferred longer than 3 weeks (7%) , seems to justify such an attitude .' However, our clinical experience shows that such an approach may not produce maximal survival. Despite the use of the IABP and vigorous pharmacologic treatment, 19 of 57 patients with a diagnosed VSD died before surgical intervention . A more aggressive attitude toward operation might have saved some of those patients. Furthermore , IABP reversed cardiogenic shock in only 15 patients . Rapid deterioration was observed following dramatic improvement in two patients. In the current state of mechanical support of a failing heart, no other technique is likely to reduce this preoperative death rate . Although venoarterial perfusion is conceptually quite interesting, it remains clinically difficult to use routinely." A second cause of failure of the preopera-

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66 Loisance et at.

tive treatment must be considered in the discussion of the optimal timing for operation. It is related to the higher risk of non-cardiac related complications as the preoperative period is lengthened. The risk of prolonged invasive hemodynamic monotoring and IABP at the bedside, mainly a risk of sepsis, is now well recognized. Furthermore, the risks of general and neurologic deterioration and renal insufficiency are increased in prolonged intensive treatment of elderly patients. Operation has been performed for VSD within the first 2 weeks after myocardial infarction in a few reported series. A mortality rate of 58% was observed in 33 collected cases. 4 Our results compare favorably with these series, since a 23% mortality rate was achieved in 17 consecutive patients operated upon within a few days of myocardial infarction. The latter mortality rate appears much lower than that of patients operated upon as late as possible, when the myocardial infarction is presumed healed. The only significant difference between these two groups is our increasing experience. As a matter of fact, anesthesia, myocardial protection, and surgical procedure were identical in the two groups. The surgical techniques developed by others- 9. 14 and in our department permit early surgical repair, despite the friability of the infarcted tissues. The main technical advance may be the use of Teflon felt strips for buttressing the friable, necrotic myocardial tissues. This technique permits secure reconstruction of the septum, with no risk of leakage, if it is applied properly. However, some technical comments must be made. Whereas repair of the anterior apical defect is associated with steadily improving results, repair of the posterior defect remains difficult. Observations of anatomic disease of operation as well as at autopsy have permitted better understanding of the structure of the posterior VSD, the resulting surgical difficulties, and the consequence of inappropriate repair. The posterior VSD is characterized by nonconcentric openings on the right and left sides, a much larger opening on the right than on the left, a large intraseptal cavity extending from the atrioventricular annulus to the apex, and frequent involvement of papillary muscles. The extensiveness of necrosis and hematoma make correct interpretation of the lesion difficult at operation. These observations strongly support the posterior approach to the defect, as suggested by Shumacker" and advocated by Dagget and associates. 1 They also permit understanding of technical errors which may be responsible for early postoperative death. When exposure is through the right ventricle, using only a rightsided septal patch in the repair will allow the develop-

Thoracic and Cardiovascular Surgery

ment of aneurysm within the septum, Furthermore, this may reduce excessively the volume of the right ventricle and may explain the lethal right ventricular failure observed in three of our cases. Therefore, we emphasize the necessity of a double patch closure of the posterior VSD. Another complicating feature of posterior VSD is tricuspid insufficiency. The correct placement of the right-sided septal patch positions it very close to the septal leaflet of the tricuspid valve. This leaflet may adhere to the patch itself, and the presence of a Teflon felt strip immediately below the tricuspid anulus may increase the chance of such a complication. In such cases, tricuspid annuloplasty is probably more effective than valve replacement. Prosthetic replacement of a segment of ventricular free wall, as suggested by Iben," Dagger;' and their associates, is an elegant additional technique in the repair of posterior VSD. The successful result obtained in one case 1 emphasizes the benefit of a method that avoids volume reduction of the ventricular cavities. We have not used this recently proposed technique. The necessity for concomitant coronary bypass grafting is unsettled. The Boston group': 4. 10 strongly advocates repair of associated coronary disease, despite the lack of a clearly beneficial effect on hospital survival rate, because one late death occurred in their group of patients with nonbypassed lesions. Williamson and associates'" could not demonstrate any benefit of concurrent myocardial revascularization. Only two of our patients underwent coronary grafting: Six bypassable coronary lesions were not operated upon because of the duration of aortic cross-clamping and the technical difficulties of coronary artery dissection. In only one case was the early postoperative period complicated by lethal myocardial necrosis. All 20 long-term survivors who did not have coronary operations are free of angina. The technique of myocardial preservation used in our series of patients deserves some comment. The myocardium was protected before, during, and after aortic cross-clamping. Neuroleptic analgesia" produces vasodilatation, avoiding hypertension and tachycardia before bypass and reducing left ventricular afterload. Myocardial preservation during aortic cross-clamping is obtained by the effects of combined systemic cooling to 21 C and topical hypothermia by intermittent cardiac immersion in 0 C saline. Extensive experimental evaluation of this method has clearly shown that the deleterious effect on the myocardium of 2 hours of nonperfusion is minimal. 17 Myocardial reperfusion is continued for at least 30 minutes, the left ventricle is kept beating but nonwork0

0

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VSD after acute myocardial infarction

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ing, and aortic pressure is kept below 60 mm Hg. The improvement in the width of the QRS complex, reduction of ST-segment abnormalities, and the infrequency of left ventricular irritability as filling pressure is increased permit a slow, progressive discontinuation of the external perfusion. The potentially deleterious effects of increased perfusion time engendered by this technique have been reduced by the use of membrane oxygenators and nonocclusive pumps; minimal use of intracardiac suction; and neuroleptanalgesia, which permits homogeneous tissue perfusion and reduction in myocardial energy demands. We 18 have shown that these methods permit safe long-term extracorporeal circulation. The deleterious effects in the postoperative period of inotropic agents in patients with a recent myocardial infarction and of IABP in elderly patients are now widely recognized. The need for such pharmacologic or mechanical support has been drastically reduced by the methods of myocardial protection and the intraoperative circulatory support that we have advocated. We thank Robert M. Sade, M.D., for assistance in preparation of the manuscript. REFERENCES Daggett WM, Guyton RA, Mundth ED, Buckley MJ, McEnanay MT, Gold HK, Leinbach RC, Austen WG: Surgery for post myocardial infarct ventricular septal defect. Ann Surg 186:260-271, 1977 2 Hill JD, Lary D, Kerth WJ, Gerbode F: Acquired ventricular septal defects. Evolution of an operation, surgical technique, and results. J THORAC CARDIOVASC SURG 70:440-450, 1975 3 Kitamura S, Mendez A, Kidy JM: Ventricular septal defect following myocardial infarction. Experience with surgical repair through a left ventriculotomy and review of literature. J THORAC CARDIOVASC SURG 61: 186-199, 1971 4 Mundth ED: Surgical treatment of cardiogenic shock and of acute mechanical complications following myocardial infarction, Coronary Bypass Surgery, SH Rahimtoola, ed, Philadelphia, 1977, F. A. Davis Company, pp 241263 5 O'Byrne P, Huguenard P, Romano PL, Decant E, Loisance D: Neuroplegie et circulation extra-corporelle. Ann Anesth Franc 17:1405-1409, 1976 6 Proudfit WL, Tapia FA, McCormack LJ, Effler DB: Rup-

ture of the ventricular myocardium and perforation of the interventricular septum, complicating acute myocardial infarction. Circulation 20: 128-134, 1959 7 Faivre G, Chalnot P, Gilgenkfrantz JM, Grosdidier J, Frisch R, Cherrier F: Un cas d'infarctus septal perfore. Succes de l'intervention reparatrice , Arch Mal Coeur 57:212-223, 1964 8 Cooley DA, Belmonte BA, Zeis LB, Schnur S: Surgical repair of ruptured interventricular septum following acute myocardial infarction. Surgery 41:930-937, 1957 9 Freeny PC, Schattenberg TT, Danielson GK, McGoon DC, Greenberg BH: Ventricular septal defect and ventricular aneurysm secondary to acute myocardial infarction. Report of four cases with successful surgical treatment. Circulation 43:360-364, 1971 IO Gold HK, Leinbach RC, Sanders CA, Buckley MJ, Mundth ED, Austen WG: Intra-aortic balloon pumping for ventricular septal defect or mitral regurgitation complicating acute myocardial infarction. Circulation 47: 1191-1196, 1973 11 Slama R, Piwnica A, Masquet Ch, Beaufils Ph, Bouvrain Y: Traitement d 'urgence des complications mecaniques de I 'infarctus du myocarde. Arch Mal Coeur 70:557-564, 1977 12 Stinson EB, Becker J, Shumway NE: Successful repair of postinfarction ventricular septal defect and biventricular aneurysm. J THORAC CARDIOVASC SURG 58:20-24, 1969 13 Loisance D, Bouillot M, Lellouche D, Teisseire B, Richome Cl, Cachera JP: Apport de la derivation veinoarterielle au cours du choc cardiogenique par rupture septale refractaire ala contre pulsion diastolique. Coeur Med Int 1 4:435-437, 1975 14 Iben AB, Pupello DF, Stinson EB, Shumway NE: Surgical treatment of postinfarction ventricular septal defects. Ann Thorac Surg 8:252-262, 1969 15 Shumacker HB Jr: Suggestion concerning operative management of postinfarction septal defects. J THORAC CARDIOVASC SURG 64:452-459, 1972 16 Williamson MD, Smith MC, Giuliani ER, Lie rr, Maloney JD, Pluth JR: Pronostic factors in postmyocardial infarction ventricular septal defects (abstr). Circulation 56:Suppl 3:59, 1977 17 Caehera JP, Loisance D, Tricot IF, Laurent F, Fournial IF, Bloch G, Galey JP: Protectin hypothermique du myocarde dans la chirurgie des cardiopathies valvulaires. Coeur 9:309-318, 1978 18 Loisance D, Le Douarin B, O'Byrne P, Lautier A, Laurent D, Cachera IP: Microporous membrane oxygenation and routine cardiac surgery. Eur Soc Artif Organs 2:105-108, 1975