Asian Cardiovasc Thorac Ann 1998;6:108-114
© 1998 Asia Publishing EXchange Pte Ltd
Surgical Approach to Myocardial Rupture After Acute Myocardial Infarction
Chukwumere E Nwogu, MD,
John M Moran, MD,
Richard M Becker, MD1,
A Thomas Pezzella, MD1
Divisions of Cardiac Surgery
1 Division of Cardiology Saint Vincent Hospital and University of Massachusetts Medical School Worcester, MA, USA
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For reprint information contact: A Thomas Pezzella, MD Division of Cardiothoracic Surgery University of Massachusetts Medical Center 55 Lake Avenue North Worcester, MA 01655-0304, USA Tel: 1 508 856 6529 Fax: 1 508 856 3740 Email: thomas.pezzella{at}banyan.ummed.edu
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ABSTRACT
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Rupture of the ventricular wall is a highly lethal complication of acute myocardial infarction that is diagnosed more frequently with the increased use of two-dimensional echocardiography. External patching techniques were used to treat 4 patients with ventricular rupture, thus avoiding resection of necrotic myocardium. Three of the patients survived. One patient developed a large left ventricular pseudoaneurysm requiring reoperation. The other 2 patients had intact repairs on follow-up echocardiogram obtained after 5 weeks and 3 years, respectively. With prompt recognition and treatment, patient survival and excellent short-term results can be achieved.
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INTRODUCTION
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Cardiac rupture after acute myocardial infarction is not a rare event. The reported incidence ranges from 4% to 24% of patients dying from an acute myocardial infarction.1–3 The incidence of free-wall rupture in cases of fatal acute myocardial infarction is about 10 times that of septal or papillary muscle rupture, well-known mechanical complications of acute myocardial infarction for which surgical treatment is widely and successfully applied.2 The ventricular free-wall is the most common site of rupture in the human cardiovascular system.4 Prompt diagnosis is facilitated by two-dimensional echocardiography. Swan-Ganz catheter findings may be indicative of pericardial tamponade. The usefulness of coronary angiography is controversial and the appropriate acute management is surgical. Several options for repair are available. Four illustrative cases are presented with emphasis on early repair utilizing less radical surgical techniques.
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PATIENTS AND METHODS
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From April 1995 to June 1996, four patients underwent repair of postmyocardial infarction ventricular rupture at St. Vincent Hospital.
PATIENT 1
A 79-year-old male with a history of hypertension, paroxysmal atrial fibrillation, and recent myocardial infarction failed a low-level stress test and two-dimensional echocardiography showed inferior hypokinesis with an ejection fraction of 40%. Cardiac catheterization revealed occlusion of the right coronary artery in its mid-portion and diffuse disease in the left anterior descending artery. Attempted right coronary artery percutaneous transluminal angioplasty was unsuccessful and urgent surgery was recommended. Left ventriculography was not performed. On opening the pericardium, 200 mL of old blood under tension was released. Triple coronary artery bypass grafting with left internal mammary artery-to-left anterior descending artery and reversed saphenous vein grafts to its second and third diagonal branches was performed. The inferior wall of the left ventricle was very ecchymotic due to recent infarction and a sealed rupture was found halfway down the posterior wall just to the left of the interventricular septum. The rupture was repaired using a glutaraldehyde-fixed autologous pericardial patch with abundant resorcinol formaldehyde glue applied to the ventricular side of the patch. Circumferential sutures were used to fix the patch to the surrounding normal myocardium, thus keeping the edges sealed. The patient's postoperative course was uncomplicated and he was transferred to a rehabilitation facility on the 5th postoperative day. Three years after his surgery, he is asymptomatic with an echocardiogram showing an intact posterior wall repair and a normal ejection fraction of 50%.
PATIENT 2
A 72-year-old male smoker was admitted with chest and back pain associated with a brief syncopal episode. His electrocardiogram showed an infarction in the inferior myocardial wall. Transthoracic and transesophageal echocardiography revealed inferior-wall hypokinesis but no evidence of thoracic aortic dissection. A small amount of pericardial fluid was noted. A tract in the inferior myocardial wall extending from the left ventricular cavity towards the epicardial surface was demonstrated and free-wall rupture was suspected. Cardiac catheterization showed occlusion of the proximal right coronary artery and significant stenoses of the left anterior descending and ramus intermedius arteries. An intra-aortic balloon pump was inserted and emergency surgery was undertaken. A large hemopericardium and extensive right and left inferior wall infarction were noted, with a contained rupture of the right ventricle. Coronary artery bypass grafting with reversed saphenous vein grafts to the left anterior descending and ramus intermedius arteries was performed. A bovine pericardial patch was applied over the entire infarcted area using resorcinol formaldehyde glue applied to the ventricular surface of the patch. The edges were somewhat loose so a larger Teflon felt patch was applied over the area with the same glue. Deep muscular sutures were placed through the patches circumferentially around the sealed right ventricular rupture site to further isolate it. A pulmonary artery balloon pump was inserted to treat severe right ventricular failure and enable weaning from cardiopulmonary bypass. The sternum was left open. The patient gradually improved over the next 48 hours when the pulmonary artery balloon ruptured and was removed. He subsequently developed coagulopathy and renal failure. His hemodynamics gradually deteriorated in spite of inotropic support and he died 4 days after the operation. An autopsy was not performed.
PATIENT 3
A 73-year-old hypertensive female was undergoing a cerebral arteriogram to evaluate a large recurrent right anterior cerebral artery aneurysm when she developed atypical chest pain. An electrocardiogram showed evidence of an acute anterior myocardial infarction. Two-dimensional echocardiography revealed an ejection fraction of 40% and a small pericardial effusion. A coronary arteriogram showed an occluded left anterior descending artery that was opened by balloon angioplasty and stented. There was no aortic dissection. She became hypotensive several hours later and a repeat echocardiogram confirmed cardiac tamponade. Pericardiocentesis yielded 400 mL of bloody fluid and a catheter was left in place. Cardiac catheterization revealed no evidence of iatrogenic perforation during the earlier procedure. However, a left ventriculogram showed apical akinesis and a small nipple at the apex compatible with a sealed perforation. An intra-aortic balloon pump was inserted and emergency surgery was undertaken. A transmural anteroapical infarct and a sealed left ventricular apical perforation were noted. On cardiopulmonary bypass, the perforation was closed with 3/0 polypropylene stitches over Teflon felt bolsters. The entire infarcted area was reinforced with a Teflon felt patch using resorcinol formaldehyde glue. Epicardial mattress sutures were then placed circumferentially through the edges of the patch into healthy myocardium. Attempts to close the sternum after weaning the patient from cardiopulmonary bypass resulted in poor hemodynamics so the chest was left open for 2 days. Her postoperative course was complicated by right femoral artery bleeding after intra-aortic balloon pump removal, which required operative control. Persistent pulmonary problems resulted in a protracted hospital stay. After tracheostomy and percutaneous endoscopic gastrostomy, she was transferred to a chronic respiratory care unit on the 42nd postoperative day. Echocardiography prior to discharge showed that the repair was intact. She expired 5 months postoperatively from aspiration pneumonia.
PATIENT 4
A 68-year-old hypertensive and diabetic male had progressively increasing angina over 3 weeks. He then presented to another hospital with an acute inferior wall myocardial infarction. He received thrombolytic therapy with tissue plasminogen activator and was transferred to our institution for cardiac catheterization. This showed an ejection fraction of 35% to 40% with severe triple-vessel coronary artery disease. There was inferior-wall hypokinesis with a ventricular pseudoaneurysm (Figure 1
). An echocardiogram showed a moderate sized pericardial effusion with compromise of right ventricular filling. On surgical exploration, he had a large pericardial effusion consisting of some old defibrinated blood, and fibrinous pericarditis was noted. No discrete perforation was found but an ecchymotic edematous area of recent infarction of the left ventricular inferior wall was clearly the source of hemorrhage and impending rupture. Triple coronary artery bypass grafting to the left anterior descending, first obtuse marginal, and right coronary arteries was performed. A bovine pericardial patch was applied to the weakened infarcted left ventricular inferior wall using resorcinol formaldehyde glue. It was sewn circumferentially to the healing myocardium using 4/0 polypropylene suture. An intra-aortic balloon pump was inserted for 2 days. His postoperative course was complicated by atrial flutter that was treated with digoxin and procainamide, and by a pulmonary embolism for which he was anticoagulated with intravenous heparin and then oral warfarin. He was discharged on the 13th postoperative day. An elective ventriculogram 5 months later showed an enlarged left ventricular pseudoaneurysm (Figure 2). On reoperation, the left ventricular inferior wall had a discrete rupture that was contained by the bovine pericardium. The fibrous defect was closed using pledgetted sutures reinforced with the adjacent bovine pericardium and the patient's pericardium. His recovery was uneventful and he was discharged on the 4th postoperative day. He was asymptomatic and doing well one year after his second operation.
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Figure 2. Left ventriculogram with arrow showing contrast flow into a pseudoaneurysm encompassed by a pericardial patch.
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DISCUSSION
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Ventricular rupture remains one of the major causes of death after acute myocardial infarction. The diagnosis is currently made more frequently because of a higher index of suspicion and the increased use of echocardiography. Patients may present with severe persistent chest pain or features of cardiac tamponade, sometimes culminating in electromechanical dissociation. Differential diagnosis includes global left ventricular failure and postinfarction septal or papillary muscle rupture. Predisposing factors include increasing age, female sex, absence of previous myocardial infarction, lack of coronary collaterals, and preexisting hypertension.5
In the setting of an acute transmural infarction, extensive necrosis and granulocyte infiltration occur. With the occurrence of a small endocardial tear, blood may pass through the myocardium to the epicardium, either directly or circuitously. It is this pathway through the myocardium that largely determines the clinical presentation. Four patterns of rupture have been described.5 Type I exhibits an almost direct trajectory through the myocardium with little dissection or bloody infiltration of the myocardium. Type II has a multi-canalicular trajectory with extensive myocardial dissection and bloody infiltration. In type III, the orifice is protected either by thrombus on the ventricular side or by pericardial symphysis. Type IV rupture is incomplete and the trajectory does not extend through all layers. Rupture usually results when blood under pressure dissects through the wall at the periphery of the infarct, at the junction of infarcted and intact muscle.6 A direct route with blowout of the epicardium results in acute hemopericardium, tamponade, and hemodynamic collapse. The circuitous route with dissection of blood through the myocardium results in a slower clinical or subacute course. This influences the mode of management of the individual patient.
Hemodynamic collapse characterized by shock or electromechanical dissociation in the setting of acute myocardial infarction should arouse the suspicion of cardiac rupture. Echocardiography can demonstrate pericardial fluid and clots, wall motion abnormalities, and intramyocardial hematomas. Transthoracic echocardiography can be obtained more readily than a transesophageal study but the latter provides better delineation of myocardial structures, especially the ventricular wall.7 Pericardiocentesis is both diagnostic and therapeutic and may be lifesaving. Continuous drainage with a pigtail catheter can be useful but drainage is often transient due to thrombus formation over the rupture site. Fluid resuscitation, afterload reduction, and inotropes are temporary therapeutic modalities.
The use of coronary angiography is controversial. Several authors report the frequent finding of single-vessel occlusion involving only the territory of transmural infarction which does not need revascularization.1,2,7,8 In this setting, coronary angiography is not worthwhile since its risks seem to outweigh its benefits. Others have demonstrated multiple-vessel disease requiring bypass at the time of ventricular rupture repair.9 In one postmortem study, more than 80% of patients were found to have multiple-vessel disease.10 Faced with these two different approaches to management, the patient's clinical status is the best guide to decision-making. After pericardiocentesis and resuscitation, if the patient is hemodynamically stable, the coronary anatomy may be studied. However, this may lead to undue delay in surgical therapy. Ventriculography is a very insensitive modality for the diagnosis of subacute free-wall rupture.11 Intra-aortic balloon counterpulsation may be used to reduce afterload, thus reducing transmyocardial tension and the likelihood of frank rupture. This may also reduce stress at the site of repair postoperatively.
The location of the rupture is most commonly the anterior or lateral walls and most occur within the first week after infarction.5 Definitive therapy for ventricular rupture is surgical. The goals of surgery are relief of tamponade, cardiac resuscitation, and repair or containment of the defect. Concomitant myocardial revascularization is controversial as discussed earlier. Our approach is to repair the defect and bypass major obstructed arteries. Several repair techniques have been utilized. Mattress sutures buttressed with felt have been used to close tears in the myocardium. However, these sutures pass through necrotic tissue and thus may come apart. The addition of a peri-infarct pursestring stitch to partially approximate the margins of the affected area has been described.12 Classic repair involves infarctectomy and linear repair with prosthetic material utilizing cardiopulmonary bypass.5
The approach used in our 4 patients has been reported by others and has been quite successful.1,2 This involves the application of a Teflon or pericardial patch to the epicardial surface of the myocardial tear using biologic glue such as fibrin or resorcinol formaldehyde glue. The use of cyanoacrylate glue has also been reported.1 It does not require an activating substance because it polymerizes rapidly when in contact with water or tissue moisture. It has a much stronger adhesive capacity than biologic or biocompatible glues. Its use in the cardiovascular system is becoming commonplace and appears safe. It will probably emerge as the adhesive of choice in combination with Teflon felt for patch repair of ventricular rupture. With an anteriorly or laterally located rupture, repair can be performed without cardiopulmonary bypass. However, with inferior ruptures, bypass is usually required in order to obtain adequate exposure for proper repair of the defect. Postoperative use of intra-aortic balloon counterpulsation or a left ventricular assist device can minimize stress on the area of the repair during early healing. The need for these devices will be dictated by the patient's clinical condition.
A review of the literature illustrates the various surgical approaches applied to this problem (Table 1). Coletti and colleagues2 reported 5 patients who had suture and patch repair of ruptured left ventricle after myocardial infarction. There was one intraoperative death. Echocardiograms performed on the surviving patients between 2 weeks and 4 months postoperatively showed good repairs in all but one who had an inferoposterior aneurysm. Padro and colleagues1 reported 13 patients who underwent sutureless left ventricular patch repairs with a follow-up extending to 5 years (mean 26 months). There were no deaths, 11 patients were asymptomatic, and 2 had mild exertional angina. Five patients had echocardiograms performed between 3 and 7 months after the repair, 3 had dyskinesis of the wall affected by the rupture and 2 had good ventricular function. There was no pseudoaneurysm detected.
The appeal of the external patch technique lies in its simplicity and expediency. Long-term follow-up of these patients with echocardiography is indicated in order to assess the durability of this surgical treatment for postinfarction ventricular free-wall rupture.
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ABSTRACT
INTRODUCTION
