Ann Thorac Surg 1999;68:2152-2157
© 1999 The Society of Thoracic Surgeons
Original Articles: Cardiovascular
Surgical repair of postinfarction structural failure of the posterobasal part of the heart
René Prêtre, MDa,
Nicole Stalder, MDa,
Qing Ye, MDa,
Jurg Grünenfelder, MDa,
Rolf Jenni, MDb,
Marko I. Turina, MDa
a Departments of Department of Cardiovascular Surgery, Zürich, Switzerland
b Department of Cardiology, University Hospital, Zürich, Switzerland
Address reprint requests to Dr Prêtre, Klinik für Herzgefässchirurgie, Universitätsspital, 100 Rämistrasse, 8091 Zürich, Switzerland
e-mail: rene.pretre{at}chi.usz.ch
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Abstract
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Background. This study is an analysis of our results with endoventricular repair of postinfarction structural defects of the posterobasal part of the heart.
Methods. Thirty-four patients who underwent endoventricular repair of a postinfarction structural defect of the posterobasal heart were reviewed. Patients with rupture of the ventricular septum (18 patients) or free wall (1 patient) were operated on acutely and patients with ventricular aneurysm (15 patients) electively. Restitution of the ventricular geometry was achieved by evertion (11 patients), resection (4 patients), or augmentation of the ventriculotomy (4 patients) in patients with ventricular rupture, and by resection of the aneurysm in the others. Coronary artery bypass was performed in 24 patients.
Results. Six patients died postoperatively (five due to rupture and one from aneurysm) and nine patients (six due to rupture and three from aneurysm) during follow-up. Survival rate at 5 years (including operative mortality) was 43% for patients with rupture and 61% for patients with aneurysm. The majority of the survivors were in New York Heart Association functional class I or II after a median follow-up of 5 years.
Conclusions. Endocardial repair, ventricular remodeling, and selective myocardial revascularization provided overall good results in the treatment of this difficult cardiac area.
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Introduction
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The posterobasal part of the heart represents the zone of insertion of the ventricles on the atrioventricular groove and the heart skeleton. The terminal branches of the circumflex and right coronary arteries perfuse this part. A transmural infarction in this area may lead to a structural failure of the ventricular wall. In the worst cases, the wall ruptures and leads to a usually fatal pericardial tamponade. In more favorable cases, the rupture remains temporarily contained by a local hematoma or more permanently by adhesions and leads to a chronic pseudoaneurysm [1, 2], or else the rupture occurs in the ventricular septum and leads to a left-to-right shunt [3–5]. Finally, the transmural infarction may not lead to a ventricular rupture but to a fibrotic scar that expands with time in a chronic aneurysm [6–9]. Most cases of structural failure require surgical correction [6, 10, 11]. The surgical approach to the posterobasal part of the heart is difficult, because it lies posteriorly, fixes the ventricles to the heart skeleton, and is surrounded by important structures. These include, on the inside of the left ventricle, the posterior mitral annulus and leaflet and the papillary muscles; on the outside, the posterior descending artery, the posterolateral branches of the right coronary or circumflex artery, and the coronary sinus. Finally, the technical difficulties are enhanced when the operation is performed emergently on friable, freshly necrotic tissues. Our approach to this area of the heart was reviewed and our strategy of repair discussed.
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Patients and methods
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All the patients who underwent a left ventriculotomy to correct a structural failure (rupture of the septum, rupture of the ventricular wall, and ventricular aneurysm) of the posterobasal myocardium after infarction were reviewed. Patients with avulsion of an ischemic papillary muscle, with small aneurysms that were treated by a plicature and with epicardial repair of a ventricular rupture were not included. During this experience, no patient was excluded from operation. From 1984 and 1997, there were 34 patients, 26 men and 8 women with ages ranging from 45 to 77 years (median, 65 years), who fulfilled the inclusion criteria.
The diagnosis of septal or ventricular rupture, or aneurysm was established by transthoracic or transesophageal echocardiography, or both. A coronarography was obtained in all patients after occurrence of the rupture or aneurysm. The myocardial infarction was attributable to an occlusion of the right coronary artery in 23 patients, the circumflex artery in 8, and both vessels in 2 patients. One patient with left ventricle aneurysm had no significant coronary artery disease. Additional coronary artery disease was found in 9 of 19 patients with ventricular rupture, and in 11 of 15 patients with ventricular aneurysm. The median delay between myocardial infarction and septal or ventricular rupture was 5 days. The delay between infarction and the occurrence of a ventricular aneurysm could not be determined precisely. The diagnosis of the aneurysm was established between 3 and 36 months after myocardial infarction. Because of the enhanced difficulties brought by handling freshly necrotic myocardial tissue in comparison to fibrotic ones, two groups of patients were distinguished. Group 1 comprised patients with septal or ventricular rupture who were operated on emergently (in the course of a fresh myocardial infarction) and group 2, patients with ventricular aneurysm who were operated on electively. Group 1 consisted in 19 patients, 18 with a septal rupture and 1 with free wall rupture. Ten patients were in shock (defined as a systolic pressure < 80 mm Hg and inadequate peripheral perfusion) before operation and 2 patients required reanimation with cardiac massage. An intra-aortic balloon pump was inserted in 8 patients before going to the radiology suite for coronarography or to the operating room. The morphology of the ventricular rupture (determined in 15 patients) was simple (ie, a direct defect) in 4 patients and complex (ie, with multiple tracts) in 11 patients. Two patients (including the patient with free wall rupture) had associated mitral regurgitation due to avulsion of the posteromedial papillary muscle. Group 2 consisted in 15 patients, all in stable condition. The aneurysm appeared as an dyskinetic area (with typical paradoxical motion) in 11 patients and as an akinetic area in 4 patients. One patient had an associated mitral regurgitation due to dysfunction of the posteromedial papillary muscle and dilatation of the mitral annulus. The main indication for surgical correction used in both groups are summarized in Table 1 and in Figures 1 and 2 . The type of ventricular repair were patch closure (15 group 1 patients), infarct–exclusion (4 group 1 and 2 group 2 patients), resection–suture (8 group 2 patients), and subendocardial resection and patch closure (5 group 2 patients).
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Fig 1. Decision flow chart in patients with posterobasal structural defect. (CABG = coronary artery bypass grafting.)
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Fig 2. Endocardial patch repair of structural failure of the posterobasal area of the left ventricle performed in 26 patients. Patch closure of a ventricular septal rupture (15 patients) (top left), infarct–exclusion of a septal rupture (3 patients) or aneurysm (2 patients) (top right), infarct–exclusion of a free wall rupture (1 patient) (bottom left), and subendocardial resection and patch closure of ventricular aneurysm (5 patients) (bottom right). Patch augmentation of the ventriculotomy closure as performed in 4 patients is illustrated (top left). Gray area depicts the extent of myocardial infarction.
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Operative technique and choice of ventricular repair
Fresh ventricular rupture
The septal or ventricular rupture was repaired in normothermia with a perfused heart in 13 patients when the aortic valve was competent and in moderate hypothermia with cardioplegic arrest of the heart in 6 patients when it was not. The incision in patients with septal rupture was started in the left ventricle parallel to and a few millimeters away from the posterior descending artery, high toward the base of the heart (between the papillary muscle insertion and the mitral annulus) to avoid injury to the posteromedial papillary muscle, which may lie close to the septum. The patient with free wall rupture had multiple hemorrhagic tracts between both papillary muscles. The incision was performed at the middle of the hemorrhagic area. Upon entering the left ventricle, the position of the papillary muscles was identified before extending the incision. A patch of Gore-Tex (W.L. Gore & Assoc, Flagstaff, AZ) or pericardium was used to cover the ventricular defect (Fig 2). The insertion of the patch started on the annulus of the mitral valve and was pursued as much as possible on macroscopically viable endocardium. This was possible on the septum, but usually not on the inferior wall of the left ventricle because of the insertion of the posteromedial papillary muscle. In 15 patients with a septal rupture, therefore, the patch was sutured inferiorly on the ventriculotomy border, and the ventriculotomy closed with Teflon-reinforced sutures. A more extensive exclusion of the infarct area was performed in 3 patients with septal rupture and in the patient with free wall rupture. The patch was further inserted on the endocardium of the inferior wall of the left ventricle to bridge the ventriculotomy, which was closed underneath [11, 12]. Remodeling of the left ventricle was attempted in all patients and tailored to the degree of ventricular dilatation. In 4 patients with significant infarct expansion, the size of the left ventricle was reduced by resection of a stripe of myocardium. In 11 patients with mild infarct expansion, the size of the left ventricle was reduced by simple evertion of the ventriculotomy borders. In 4 patients without ventricular dilatation, the size of the left ventricle and the position of the papillary muscle were maintained by the interposition of a shallow stripe of Gore-Tex between the ventriculotomy borders. Two patients had a concomitant avulsion of the posteromedial papillary muscle at the time of ventricular rupture. The muscle was reimplanted in 1 patient with free wall rupture, and the mitral valve replaced by a mechanical prosthesis in the other patient. Coronary artery bypass was performed on 11 patients who received between one and five distal anastomoses (mean, two anastomoses). The bypass was performed during a period of aortic cross-clamping and hypothermic cardioplegic arrest of the heart in 8 patients, and on an unloaded, beating heart in 3 patients. Because they become entrapped in the suture line of the ventriculotomy, the posterior descending artery and last posterolateral branch were not bypassed. Bypass to the right coronary artery was performed if it could improve blood supply to an obtuse marginal artery, as it occurred in 6 patients.
Chronic ventricular aneurysm
Ventricular aneurysms were repaired and coronary artery bypass grafting performed in moderate hypothermia with cardioplegic arrest of the heart. The incision on the left ventricle did not present the same risk of injury to the posteromedial papillary muscle, because expansion of the infarct area had occurred. A vent was inserted through the right superior pulmonary vein in the left ventricle to induce collapse of the aneurysm. The incision on the left ventricle was started on the center of the depressed area. The choice of repair was made depending on two criteria: the presence of a thrombogenic surface (history of systemic emboli or presence of thrombotic material in the aneurysm) and the presence of an arrhythmic focus (history of clinical or inducible ventricular arrhythmia). When none of these two criteria was present, the excess of fibrotic tissue was resected and the ventriculotomy closed directly. This simple repair was also selected when the thrombogenic surface could be entirely resected. In the other patients, an endocardial exclusion of the aneurysm was performed with a pericardial or Gore-Tex patch (Fig 1). The patch was tailored to reduce the size of the enlarged ventricle and was inserted on the borders of the infarct. External scar tissues were then folded to reinforce the suture line. Cryotherapy of the infarct borders was performed in patients with ventricular arrhythmia. Coronary artery bypass grafting was performed in 13 patients. Two patients did not receive a bypass because they had no significant coronary artery stenosis beside the infarct artery, whose branches became included in the suture line. The number of distal anastomoses ranged from one to five (mean, 2.5 anastomoses). One patient underwent concomitant replacement of the mitral valve because of severe regurgitation.
Assessment of repair, follow-up, and statistical analysis
Upon discharge, the patients were treated with Coumadin for life (and a targeted international normalized ratio from 2.0 to 2.5), and low-dose aspirin. Follow-up was established by telephone contact with the patient’s physician or cardiologist between February and April 1998, and was complete in all but 1 patient. Follow-up ranged from 4 months to 13.8 years. Postoperative transthoracic echocardiography was performed 3 months after operation and was chosen for comparison with preoperative findings. Pre- and postoperative mean values of the left ventricle ejection fraction were compared by the Wilcoxon signed rank test. Preoperative shock and age more than 70 years were tested for their significance in predicting operative mortality in group 1 by the Fisher’s exact test. Cumulative survival curves after ventricular septal rupture and ventricular aneurysm repair were calculated by the Kaplan-Meier method.
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Results
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Five patients in group 1 and 1 patient in group 2 died postoperatively. The cause of death is given in Table 2. In group 1 patients, preoperative shock (p = 0.14) and age more than 70 years (p = 0.14) showed a weak trend for an increased mortality. Significant morbidity occurred in 10 of the 13 survivors of group 1, and in 2 of the 14 survivors in group 2 (Table 2). Postoperative echocardiography revealed a residual septal defect in 3 patients, who presented a complex morphology of the septal rupture. Elective reoperation to close the defect was performed in 2 patients (at 3 and 8 months) because of a pulmonary shunt of more than 50% (Qp/Qs > 2) and signs of congestive heart failure. In the other patient, with a Qp/Qs of 1.5, reoperation is yet not considered.
Late death occurred in 6 patients of group 1 and in 3 patients of group 2, the cause of which is listed in Table 2. The survival rate, including operative mortality, at 5 years was 43% and 61% for group 1 and 2, respectively (Fig 3). The evolution of left ventricular ejection fraction before and 3 months after operation in group 2 patients is depicted in Figure 4. The mean ejection fraction increased from 40% to 44%. The improvement did not reached statistical significance (p = 0.18). Among 7 patients of group 1 available for follow-up, 4 were in New York Heart Association functional class II, 2 in class III, and 1 in class IV after a median follow-up of 5 years. Among the 10 patients of group 2 available for follow-up, 8 were in functional class I or II and 2 in class III after a median follow-up of 4 years.
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Fig 3. Survival curves after repair of posterobasal structural defects. Kaplan-Meier survival curves (including operative mortality). Group 1 = repair of posterobasal ventricular rupture; group 2 = repair of posterobasal ventricular aneurysm.
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Fig 4. Evolution of left ventricle ejection fraction (LVEF). (pre-op = preoperative; post-op = 3 months after repair of ventricular aneurysm.) One patient who underwent mitral valve replacement for preoperative severe regurgitation is not represented.
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Comment
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Transmural infarction may deteriorate in structural failure of the ventricular wall and impose surgical correction. Although the approach to the difficult posterobasal part of the heart and the technique used for ventricular repair are crucial for successful outcome, few reports exist in the literature on this subject, and none presents a rational and detailed management to this area. The approach to the ventricular defect is made through the infarct area of the left ventricle, and presents special consideration if performed in the acute or in the chronic phase of infarction.
Approach to acute structural failure
Rupture of the left ventricle occurs a few days after myocardial infarction and provokes a rapidly progressing cardiac failure [11, 13–16]. Operative risk is increased during this phase due to the heart vulnerability to operative insult and to difficulties in handling freshly infarcted myocardium. We operated on 19 such patients. To reduce operative damage, we closed the septal or ventricular rupture (and lately also performed coronary artery bypass grafting) on a perfused and unloaded heart. Ruptures in the posterobasal myocardium bear specific characteristics that make repair difficult [4, 15–18]. They usually present a complex morphology with many serpiginous and hemorrhagic tracts away from the primary laceration. This contrasts with ruptures in the anteroapical myocardium, which often present a simple morphology with a more direct rent. Edwards and associates [19], in an autopsy series, demonstrated that 69% of posterior ruptures had a complex morphology in contrast to only 21% of anterior ruptures. The complex morphology enhances the difficulty to obtain complete closure of the defect. Obliterating all the tracts and securing a patch on a endocardium with ill-demarcated border of viability is more challenging and may explain the higher rate of residual defects reported after repair of posterior septal ruptures [16–18]. Residual defects occur with an insufficient coverage of the defective area or with the tearing of friable myocardium from the suture line. A large coverage of the infarcted area with insertion of the patch on viable myocardium, as advocated by David [11] and Komeda [12] and their colleagues, reduces the occurrence of residual leaks. We found that starting to anchor the patch on the annulus of the mitral valve was useful. This provided a solid insertion of the patch and allowed traction to better expose the posterobasal septum and the limits between viable and necrotic myocardium. Inferiorly (at the level of the ventriculotomy), the patch was either brought through the incision or was used to bridge the ventriculotomy and further cover the infarcted inferior wall of the left ventricle.
Closure of the ventriculotomy demands consideration regarding the size of the left ventricle and position of the posteromedial papillary muscle [14, 20]. The degree of expansion of the infarcted area and the displacement of the posteromedial papillary muscle away from the septum depends on the amount of shunted blood through a septal defect and on the time that lapsed from rupture to operation. Resection or evertion of the ventriculotomy borders may restore a normal geometry in patients with large infarct expansion. Direct closure of the ventriculotomy is appropriate when the posteromedial muscle has only been slightly displaced laterally. Infarct expansion of the ventricle, however, may not have occurred significantly in some patients, especially those operated on within hours of the rupture. Direct closure of the ventriculotomy may displace the posteromedial papillary muscle against the septum and induce a mitral valve insufficiency. To prevent this complication and preserve a normal geometry of the left ventricle, we inserted a 10-mm-wide patch to close the ventriculotomy. This repair, initially advocated by Daggett [14], may become more often necessary than before because of the earlier referral and surgical treatment of patients with septal rupture. Skillington and associates [16] reported a similar experience. To prevent tension on the ventriculotomy, they used a similar patch augmentation of a small left ventricle in 4 of 44 patients with posterior ventricular rupture.
The literature contains only a few case reports of usually successful repair of posterobasal ventricular rupture. More data are available regarding the outcome of patients with a rupture of the posterobasal ventricular septum. Cox [13] and Skillington [16] and their colleagues reported, in two of the largest series, overall early mortality rates of 34% and 32%, respectively. Both groups acknowledged a substantial decrease in mortality in recent years, in part attributable to patients being referred earlier for treatment, before occurrence of organ dysfunction. Mortality rates around 15% to 20% are now regularly achieved [11, 16].
Approach to chronic structural failure
The repair of chronic defects of the posterobasal part of the left ventricle is technically less demanding, and the heart, no longer in the acute phase of infarction, is less vulnerable to ischemic and reperfusion injuries. The posteromedial papillary muscle has been progressively displaced away from the septum and is not jeopardized during ventricular opening [6, 21]. The incision is performed in the middle of the aneurysm leaving two borders of fibrotic tissue for a safe and strong closure. Two types of aneurysm repair were elected based on preoperative and operative findings. One repair, simple, consisted in the resection of excessive fibrotic tissues and direct closure of the ventriculotomy. The other repair, more complex, consisted in the exclusion of the infarct area from the left ventricle by a patch of Gore-Tex or pericardium. The resection–suture repair, because of its simplicity, was favored in patients with uncomplicated aneurysms (those without ventricular arrhythmia or embolization). When ventricular arrhythmia was present, a subendocardial resection of the aneurysm and cryotherapy of the borders were performed, and a patch was used to close the neck of the aneurysm [10]. When a history of systemic embolization was present or a thrombus or thrombogenic area found, an exclusion of the infarct area with an endoventricular patch was preferred.
The improvement in left ventricular ejection fraction after repair of the aneurysm was modest in our series and inferior to the values usually reported in the literature [7, 22, 23]. Di Donato and associates [7] reported an improvement of 36% to 50% in 245 patients after endoventricular patch plasty repair. Improvement was most impressive after resection of large and dyskinetic aneurysms [6–9, 23]. These aneurysms are typically located on the anterolateral part of the left ventricle, and heart failure is the usual indication for repair [7, 9, 23]. Aneurysms found on the posterobasal part of the heart are smaller and many show only an akinetic area, as was the case in 25% of our patients [6]. The indication for operation in our patients was mostly angina pectoris (from associated coronary artery disease) and ventricular arrhythmia. Although resection of an akinetic or a relatively small dyskinetic area has a limited impact on ventricular function [8, 9], we believe it still to be indicated if it can be performed without increased mortality, when complications of aneurysm are likely.
In conclusion, the posterobasal part of the heart, because of its deep location and close relation to important structures, brings special difficulties when surgical repair of a ventricular wall failure is necessary. Defects, like septal or ventricular rupture, appear a few days after transmural infarction and impose early correction to reverse a progressing shock. Techniques that avoid ischemia–reperfusion injuries on the heart are advantageous. Large coverage of the infarct area with a patch provides good results and seems especially indicated when the defect has a complex morphology. Defects, like aneurysms and pseudoaneurysms, appear later after myocardial infarction and can usually be repaired electively. Myocardial protection is less critical and adequately achieved by regular blood cardioplegia. The ventricular defect can be repaired by a simple resection–suture technique or, when complications or potential complications of the aneurysm exist, by an infarct–exclusion technique with good immediate and long-term results.
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Accepted for publication May 6, 1999.
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Abstract
Introduction
