Post-Infarct Left Ventricular Free Wall Rupture—Not Always a Lethal Complication of Acute Myocardial Infarction

Post-Infarct Left Ventricular Free Wall Rupture—Not Always a Lethal Complication of Acute Myocardial Infarction

ORIGINAL ARTICLE Original Article Post-Infarct Left Ventricular Free Wall Rupture— Not Always a Lethal Complication of Acute Myocardial Infarction S...

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ORIGINAL ARTICLE

Original Article

Post-Infarct Left Ventricular Free Wall Rupture— Not Always a Lethal Complication of Acute Myocardial Infarction Sylvia S.M. Chen, MBBS, a,∗ Permyos Ruengsakulrach, MD, PhD, FRCST, b Ronald J.L. Dick, MBBS, FRACPa and Brian F. Buxton, MBBS, FRACSc a

Department of Cardiology, Epworth Hospital, Melbourne, Vic., Australia Heart Institute, Saint Louis Hospital and Foundation, Bangkok, Thailand Department of Cardiac Surgery, Austin & Repatriation Medical Centre, The University of Melbourne, Melbourne, Vic., Australia b

c

Post-myocardial infarction cardiac rupture is an important complication and cause of death in the period following myocardial infarction. It is rarely diagnosed before death. However, early diagnosis is crucial as successful treatment is possible with surgery. A successful outcome is sometimes compromised by difficult anatomy or an extensive infarct. Presentation, diagnosis and treatment of cardiac rupture is reviewed in this article, and is illustrated by five cases of cardiac rupture. (Heart Lung and Circulation 2004;13:26–30) © 2004 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved. Keywords. Heart rupture; Myocardial infarction; Pericardial effusion; Thoracic surgery; Coronary arteriosclerosis

Introduction

Case Histories

P

Case 1

ost-infarct cardiac rupture (PICR) occurs as a mechanical complication of acute myocardial infarction. In addition to cardiac failure and arrhythmia, it is another important cause of death following myocardial infarction.1–4 Pre-mortem diagnosis of rupture is made in approximately 15% of in-hospital deaths from acute myocardial infarction in a coronary care unit era.2,5–8 However, up to 31% in an autopsy series had cardiac rupture.5 Therefore, relatively few are diagnosed before death, which highlights the importance of expedient diagnosis as many ruptures can be successfully managed with surgery. With the advent of newer and better surgical techniques, the prognosis after cardiac rupture repair has improved. In this report, we review our experiences with five patients with PICR over the period 1978–2000 from the records of 23 000 patients who underwent cardiac surgery at both the Epworth and the Austin Hospitals.

The data for this work was collected from both the Epworth Hospital and the Austin & Repatriation Medical Centre, Victoria. The work was written at the Epworth Hospital. ∗ Corresponding author. Present address: Flat 85, No. 49 Hallam Street, London W1W 6JP, UK. Tel.: +44-78-67-97-4280; fax: +44-207-3809-469. E-mail address: [email protected] (S.S.M. Chen).

A 48-year-old man was admitted for an elective coronary angiogram in 1984. He had a myocardial infarct 2 months previously, following an exercise test which was ceased at 4 min due to dyspnoea. Coronary angiography revealed severe triple vessel disease. During left ventriculography, he developed chest pain and became hypotensive and unconscious. He was resuscitated with adrenalin, intraaortic balloon pump insertion, closed cardiac massage, and then open cardiac massage. An extensive haemorrhagic anteroapical infarct with rupture was found at surgery. Triple vessel coronary artery bypass grafting (CABG) was performed. The rupture was repaired with Teflon sutures, but it was not possible to wean the patient from cardiopulmonary bypass, and he died.

Case 2 A 67-year-old man was admitted following a collapse in 1991. There was a preceding history of 7 days of intermittent chest discomfort. He was haemodynamically unstable, peripherally vasoconstricted and had pulmonary oedema on the chest X-ray. A transesophageal echocardiogram revealed a large haemorrhagic pericardial effusion with tamponade. At surgery, there was a rupture in the anterolateral wall, which was repaired with Teflon sutures. Coronary artery bypass grafting was not performed. Post-operative coronary angiography revealed an 80% stenosis of the left anterior descending

© 2004 Australasian Society of Cardiac and Thoracic Surgeons and the Cardiac Society of Australia and New Zealand. Published by Elsevier Inc. All rights reserved.

1443-9506/04/$30.00 doi:10.1016/j.hlc.2004.01.006

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artery, a 70% stenosis in the distal circumflex artery, and minor distal disease in the right coronary artery. He was managed medically because there was non-reversible ischaemia in the anterior wall on a myocardial perfusion study. Seven years later, he developed recurrent angina. Repeat angiography revealed progressive severe triple vessel disease, and he underwent triple vessel CABG. He is still alive and well 2 years afterwards.

Case 3 A 72-year-old man presented with an 8-day history of left shoulder pain and subsequent collapse in 1998. A transthoracic echocardiogram revealed a pericardial effusion with tamponade. Right ventricular free wall rupture with acute inferior right and left ventricular infarction were identified at surgery. The rupture was repaired with a bovine pericardial patch. Coronary artery bypass grafting was not performed. Post-operative coronary angiography showed triple vessel disease with occlusion of the right coronary artery. He was managed medically as he was asymptomatic. He is still alive 3 years after repair, but remains dyspneic with exertion due to chronic airways disease, heart failure and atrial fibrillation.

Case 4 A 56-year-old man was admitted with a non-Q wave infarct in 2000. Coronary angiography revealed a 95% stenosis in the first obtuse marginal artery. On Day 5 post-myocardial infarction, he collapsed and became unconscious. He was severely hypotensive. A pericardial effusion (Fig. 1) with tamponade was seen on urgent transthoracic echocardiography. Attempted pericardiocentesis was unsuccessful. At surgery, a small rupture was identified on the lateral wall, which was repaired with a bovine pericardial patch. He is alive and doing well 1 year post-repair.

Case 5 A 79-year-old woman was admitted with a late presentation non-Q wave infarct (approximately 2 days old) in 2000. She had electro-mechanical dissociation a few hours later. There was marked anterior ST elevation on the electrocardiogram. She was resuscitated with adrenalin, however, remained hypotensive. Urgent coronary angiography showed severe triple vessel disease, with a proximal left anterior descending artery stenosis of 80%. An intra-aortic balloon pump was inserted for haemodynamic support. Right heart catheterisation suggested pericardial tamponade. Urgent transthoracic echocardiography confirmed a large tamponading effusion. At surgery, a rupture in the anterolateral wall was identified. It was adjacent to the origin of the left anterior descending artery. Coronary artery bypass grafting was performed. The major vessels were grafted using an internal mammary artery and saphenous vein grafts. A pericardial patch was applied, but suture reinforcement was difficult because of the proximity of the origin of the left anterior descending artery and the adjacent subepicardial fat. Subsequently, 3 days postoperatively, she had a cardiac arrest electro-mechanical dissociation from which she was unsuccessfully resus-

Figure 1. Transthoracic echocardiogram: subcostal view of both right and left ventricles with an overlying haematoma in the pericardial space. RV, right ventricle; LV, left ventricle.

citated. Post-mortem examination revealed a defect at the previous rupture site with tamponade and partial dehiscence of the pericardial patch.

Discussion Ventricular free wall rupture occurs up to ten times more frequently than septal or papillary muscle rupture.9 Right ventricular free wall rupture is very rare. The incidence of right ventricular free wall rupture in a series of autopsies was 0.44%.10 In our series, three of the ruptures occurred in the anterior wall of the left ventricle, one in the lateral wall, and another in the right ventricular wall. Significant disease was found in all culprit vessels (left anterior descending artery, the first obtuse marginal artery and the right coronary artery). Severe disease of the other two major vessels was also present in four patients. Risk factors for rupture include hypertension, the elderly, female gender, first infarct, left anterior descending artery infarction, and large transmural infarction of at least 20%.4–6,9,11–14 Most ruptures occur within the first week after infarction, with approximately 50% within the first 4 days.4,15 The remainder present later, sometimes with a pseudoaneurysm.16,17 Three of our patients ruptured within the first 5 days. None of the patients had received thrombolytic therapy. Late thrombolysis (given after 6 h) appears to accelerate but not increase the number of ruptures.4 Rupture occurs through an area of necrosis. Contributory factors include shearing forces of muscular contraction against

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the necrotic area, decreased perfusion from either poor collateralisation of a totally occluded artery4 or marked necrosis at the terminal end of the blood supply and disruption of the myocardial microstructure. Presentation is usually dramatic, and is acute or subacute.3,6 The acute presentation is one of sudden chest pain with dramatic haemodynamic collapse, with rapid deterioration into asystole or electro-mechanical dissociation as in Case 1. Subacute rupture may present with syncope and hypotension or it may present over a few days with malaise and persistent vomiting.4,6 Early diagnosis is imperative as many ventricular ruptures can be surgically corrected, with a good long-term outcome. The key to diagnosis is the finding of a pericardial effusion, which is usually but not always haemorrhagic, on transthoracic echocardiography.3,4,18 The definitive diagnosis is made at surgery. Pericardiocentesis prior to surgery, which confirms a haemorrhagic effusion, further supports the diagnosis.3 The use of right heart cathetherisation has been superseded by transthoracic echocardiography. The standard treatment for cardiac rupture is surgical repair.4,6,19–25 Pericardiocentesis can be performed preoperatively for the relief of tamponade in a desperate situation. Intra-aortic balloon counter-pulsation may also be used for haemodynamic stabilisation prior to immediate surgery. Cardiopulmonary bypass can be established by femoro-femoral bypass under local anesthesia in order to re-establish circulation. This technique can be used percutaneously before transport to the operating theater.26–28 It is also useful as a bridge to urgent surgery in cases of subacute cardiac rupture.29–31 A median sternotomy is then performed and the pericardium opened. Repair is performed under cardiopulmonary bypass. The surgical technique, and the type of repair depends on the age of rupture, the viability of the myocardium, the type of defect32 and the clinical status of the patient. For instance, acute ruptures are probably best repaired with a patch reinforced with sutures. In subacute rupture, sutureless repair may be with a patch applied with glue.32,33 Surgical repair can be performed with a direct suture following excision of necrotic tissue, or infarctectomy and a closure buttressed with polytetrafluoroethylene (PTFE) surgical felt strips, an overlay patch or by using muscle flap closure. In the past repair was achieved using a monofilament suture in a horizontal mattress fashion over the PTFE felt strips (Cases 1 and 2). More recently, however, repair procedures have employed a pericardial patch (Fig. 2), with or without infarctectomy (Cases 3–5). The material used is either an autologous graft or a xenograft. The patch is glued on with BioGlue Surgical Adhesive® (CryoLife International® Inc., Georgia, USA) and then sutured to the epimyocardium. Bovine pericardial patches (Baxter International Inc., CA, USA) were used in Cases 3 and 4, and Case 5 utilised an autologous pericardial patch. However, regardless of the type of patch employed, the most important step is to define the extent of the cardiac rupture defect and to approximate viable myocardium. In some cases, the repair can be performed using pericardium or Teflon patch and glue without sutures and cardiopulmonary bypass.34–39 If the patient cannot be

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Figure 2. Opened pericardium at surgery: view of pericardial patch over the site of rupture. IMA, internal mammary artery; RA, radial artery; LV, left ventricle; RV, right ventricle.

weaned off cardiopulmonary bypass, percutaneous extracorporeal life support or left ventricular assist device may be used to obtain left ventricular decompression, salvage the damaged myocardium and allow suture repair of the friable myocardium.40–44 The timing of coronary angiography is controversial, and will be directly influenced by the urgency for repair, stability or otherwise of the patient as available time. Coronary artery bypass grafting as a staged procedure can be performed later. The result of this condition is not always lethal. A small number of patients with subacute cardiac rupture have survived without emergency surgery and had good long term survival.45 Operative mortality (up to 90 days postoperative) ranges up to 33%, but, in those who survive, the long-term outcome (up to 7 years post-operative) is good.3,24,33,38,46 The mortality rate was significantly higher in acute cardiac rupture. An important determinant of survival is the pre-operative haemodynamic status.16 The overall hospital mortality in patients with and without surgery was 60.7%.6 Up to 14.3% of patients died while waiting for surgery.3 Rapid diagnosis of cardiac rupture is imperative as it can be successfully treated with surgical repair. However, as illustrated by Case 5, the anatomic location or the extensive nature of the infarct may still complicate the surgical repair and preclude a successful outcome. Thanks to Elizabeth Croce and David Dupuche for their help with the figures.

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