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Ann Thorac Surg 2000;69:1342-1345
© 2000 The Society of Thoracic Surgeons

Original articles: Cardiovascular

Experience with postinfarction left ventricular free wall rupture

René Prêtre, MDa, Peter Benedikt, MDa, Marko I. Turina, MDa

a Cardiovascular Surgery, 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


   Abstract
Top
 Abstract
Introduction
 Patients and methods
 Results
 Comment
 References
 
Background. Postinfarction rupture of the left ventricle is a rare event in which approach is not clearly standardised and outcome after repair is unknown. Our experience with this pathology was reviewed to analyze methods of repair and assess outcome beyond the patient’s hospitalisation.

Methods. Five patients underwent surgical repair of a postinfarction ventricular rupture between 1990 and 1998. Electromechanical dissociation (3 patients) and sudden hypotension and bradycardia (2 patients) were clinical indicators of rupture. Four patients underwent repair with cardiopulmonary bypass and 1 patient without. Repair consisted of epicardial patching (2 patients), direct suture (1 patient), infarct-exclusion (1 patient), and debridement and patch closure (1 patient) of the rupture. Myocardial revascularization was performed in 3 patients and mitral valve repair in 1 patient.

Results. A satisfactory hemodynamic state was restored and bleeding was controlled in all patients. Two patients died postoperatively and another patient died 4 months after hospital discharge as a result of cardiac failure and/or sepsis. The other 2 patients are alive and in excellent condition 6 and 30 months respectively after repair.

Conclusions. Postinfarction rupture of the left ventricle bears a high mortality, but survival with an excellent quality of life is possible after surgical repair.


   Introduction
Top
 Abstract
 Introduction
Patients and methods
 Results
 Comment
 References
 
Rupture of the left ventricle after myocardial infarction occurs more commonly than appreciated [1–6]. With increasing awareness of this complication in the face of suggestive clinical features and availability of echocardiography to establish the diagnosis, more patients are now referred for surgical repair [7, 8]. The best method of repair has not yet been clearly established and, because the literature contains only case reports of usually successful outcome, the results of surgical repair remain essentially unknown. This report presents our results in five consecutive patients with a post-infarction ventricular rupture and proposes a rational approach to this challenging complication.


   Patients and methods
Top
 Abstract
 Introduction
 Patients and methods
Results
 Comment
 References
 
Five consecutive patients treated in our clinic for a rupture of the left ventricle after transmural infarct from 1990 to 1998 were reviewed. The clinical characteristics of these patients are presented in Table 1. All but one patient presented typical symptoms or signs of an acute myocardial infarction, which allowed precise timing of the myocardial events. A coronarography had been performed in 3 patients before the rupture occurred and was performed in 2 patients (who remained extremely stable after reanimation) after the rupture occurred. The rupture was preceded by persistent precordial pain (4 patients) or restlessness and retching (3 patients), and was heralded by an acute hemodynamic decompensation in all patients. Three patients presented an electromechanical dissociation that required mechanical massage, and 2 patients presented severe hypotension and bradycardia that could be corrected with medication. The diagnosis was established by echocardiography which showed a pericardial effusion with signs of cardiac tamponade. One patient had concomitant mitral valve regurgitation due to avulsion of one head of a two-head posteromedial papillary muscle. Transfer of the patient to the operating room was organized immediately after establishment of the diagnosis. An intraaortic balloon pump was inserted in 3 patients before and in 2 patients during operation. One patient required subxyphoidal decompression of the pericardial tamponade before preparation for operation.


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  		Table 1. Clinical Characteristics of Patients With Post-Infarct Ventricular Rupture

 
The patients were approached through a standard median sternotomy. The rupture was located inferiorly on the left ventricle in 2 patients, laterally in 2, and anteriorly in 1 patient (Table 1). In 3 patients, the rupture appeared as multiple tracts emerging from necrotic myocardial which was heavily infiltrated with blood. In 2 patients, the rupture appeared as a more direct tear through the myocardium which was partially sealed by loose pericardial adhesions. Repair of the rupture (Fig 1) necessitated cardiopulmonary bypass in 4 patients and could be performed without circulatory support in 1 patient with anterior rupture. In this patient, it was possible to expose the infarcted area without excessively compromising circulation. This was achieved by lifting up the left edge of the sternum with a mammary retractor and inserting a lap-pad underneath the heart. The bleeding could be controlled with two fingers while a patch of xenopericard was sutured on the epicardium and covered a large area around the bleeding site (Fig 2). Fibrin glue was injected underneath the patch at the time of tying. Repair was performed with the aid of cardiopulmonary bypass in the other patients primarily because they required mobilization of the heart to expose the rupture. In 1 patient, the rupture appeared as a relatively direct tear. It was closed with mattress stitches pledgeted with Teflon felts (Bard-Medica, Oberrieder, Zurich, Switzerland). In the other 3 patients, it appeared as multiple tracts emerging from an infiltrated myocardium. The area was covered with a patch of pericardium sutured on the pericardium in 1 patient, debrided and closed with patch of Gore-Tex in another patient, and excluded by a patch of pericardium sutured on the endocardium in the last patient. The latter patient also had mitral valve regurgitation due to avulsion of a papillary muscle. Therefore, the left ventricle was entered through the hemorrhagic area, the avulsed papillary muscle reimplanted and the area of infarction (including the rupture) excluded by a patch of pericardium. The patch was anchored on the mitral annulus, then sutured on macroscopically viable endocardium, thus excluding as much as possible the infarct area [9, 10]. The edges of the ventriculotomy were simply re-approximated over the patch. In 3 patients, aorto-coronary bypass using segments of saphenous veins were performed on a beating and unloaded heart in 2 patients and during a period of cardioplegic arrest in 1 patient.



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  		Fig 1. Repair of the ventricular rupture included epicardial patching (2 patients - top left), direct suture (1 patient - top right), debridement and patch closure (1 patient - bottom left) and infarct-exclusion (1 patient - bottom right). Grey area indicates extent of infarction.

 


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  		Fig 2. Epicardial patching of a rupture of the anterior part of the left ventricle. Exposure of the heart was achieved by retracting the left edge of the sternum with a mammary artery retractor and by inserting a lap-pad underneath the left ventricle.

 

   Results
Top
 Abstract
 Introduction
 Patients and methods
 Results
Comment
 References
 
A satisfactory hemodynamic state could be maintained in the patient operated on without cardiopulmonary bypass. The other 4 patients could be weaned from cardiopulmonary bypass. Bleeding was controlled in all patients. Perioperative transesophageal echocardiography revealed a left ventricular function ranging from 25% to 60% (Table 2). The mitral valve was competent in the patient whose papillary muscle was reimplanted. Two patients died of multiple organ failure 16 days and 63 days respectively after operation. The origin of the failure was a persistent low cardiac output in the first patient and a sepsis in the second. The postoperative course was also difficult for a third patient who presented a septic state and required prolonged intubation and hemofiltration. He eventually could be discharged, but died four months later of cardiac failure. The other two patients had a relatively uneventful postoperative course, resumed a normal life and are in a New York Heart Association (NYHA) functional class I and II, respectively.


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  		Table 2. Surgical Technique and Outcome

 

   Comment
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
References
 
Clinical presentation
Rupture of the ventricular free wall accounts for 12 to 20 percent of deaths due to myocardial infarction [1, 4–6, 8, 11]. The complication is almost always fatal. The diagnosis is rarely established before the patient’s death, and extremely few clinical series have been reported in the literature. Circulatory arrest and death rapidly follow rupture if blood is freely ejected into the pericardial cavity. Survival is possible only if an obstruction to the egress of blood exists. An adherent thrombus or pericardial adhesions may seal a ventricular rupture, and some ruptures are not direct through and through communications but rather multiple tracts emerging from an infiltrated necrotic area. Pathologists have established that rupture of the ventricles occurs in stages and progress from endocardium to epicardium [4–6, 11].

In clinical practice, many ruptures actually appear as a two-stage process, where a protracted course after myocardial infarction suddenly deteriorates [1, 12]. Infarction leading to rupture frequently presents persistent or progressive elevation of ST segment on ECG, and rupture is often preceded by positional pleuritic chest pain, repetitive and unprovoked emesis, and restlessness and agitation [1, 11]. The ECG changes reflect the slowly outward advancing intramyocardial hemorrhage, while the pleuritic pain and emesis are caused by the distension and irritation of the epicardium. Sudden hypotension and bradycardia, often with cyanosis and loss of consciousness, is a frequent indicator of impending rupture. It is provoked by the entry of blood in the pericardial cavity and is often transient because the resultant small hemopericardium acts as a tampon to prevent further egress of blood [1]. Hypotension and bradycardia should be considered a "forme frustre" of electromechanical dissociation and prompt aggressive diagnostic and therapeutic actions.

Reanimation
Restoration of a satisfactory hemodynamic state may require inotropic support, intraaortic counterpulsation, pericardial drainage or mechanical massage [7, 8, 13]. Subxyphoidal drainage of the pericardium may improve circulation although correct drainage is not always easy to obtain. Pericardiocenthesis has been reported to adequately decompress the pericardium and has even been proposed as a definitive treatment in perforations of the right ventricle. The dismal fate of untreated fresh pseudoaneurysms of the left ventricle warns, however, against this exclusively conservative approach in perforations of the left ventricle [14]. Decompression of the pericardium may also be obtained expeditiously by a classic sternotomy. The theoretic concern that profuse hemorrhage might ensue after opening of the pericardium has almost never been confirmed in practice and would certainly be more easily controlled through a sternotomy than through a subxyphoidal incision [7, 8].

Transfer of the patient to the operating room should be immediately organized. Many reports advise against any further investigation [7, 8]. Although we were aware of these recommendations, we performed, without untoward effect, a coronarography in two patients who were extremely stable after initial reanimation and insertion of an intraaortic balloon counterpulsation.

Surgical management
The goal of surgery is to control the life thread by relieving the tamponade and closing the ventricular rupture. The fact that the operation must be performed a few days after an acute myocardial infarction and frequently after a period of circulatory arrest and low cardiac output greatly increases the surgical risk. Simple procedures, especially when cardiopulmonary bypass can be avoided, seem preferable to complex repair. Epicardial patching of the bleeding area is easy to perform, does not require unloading of the heart and effectively controls the bleeding. Padro and coworkers [15] reported excellent results with an even simpler technique where a large patch of Teflon was glued on the pericardium. These approaches, especially if cardiopulmonary bypass can be avoided, are definitely preferable to more aggressive repairs involving debridement of necrotic myocardium or opening of the left ventricle. Anterior and inferoapical ruptures are easily accessed through a sternotomy, while lateral and inferobasal ruptures require mobilization of the heart and, often, unloading of the heart. The ease with which bleeding can be controlled on a beating and working heart with epicardial patching makes us wonder if the principle of avoiding cardiopulmonary bypass should not be extended to lateral and posterior rupture by directly approaching them through a left thoracotomy, especially in patients with reduced ventricular function. Simple repair techniques such as sutureless patch gluing, epicardial patching, or direct closure are, however, not suitable for all types of ventricular rupture [7, 8]. Opening of the left ventricle may be indicated when an intraventricular defect like a septal rupture co-exists. In such a case, endocardial patching of the whole defective infarcted area is a logical choice of technique [9, 10]. The patch, anchored on macroscopically viable myocardium, bridges the necrotic area that includes the site of ruptures, and the ventricular incision. We also used an endoventricular repair in a patient with concomitant avulsion of a papillary muscle. Epicardial patching of the ventricular rupture and repair of the mitral valve through a left atriotomy would have been another, less aggressive and possibly preferable, option.

The benefit of grating diseased coronary arteries, although unequivocal on long-term survival, may be only marginal on short-term survival and certainly does not justify establishment of cardiopulmonary bypass for the sole purpose of myocardial revascularization. The right coronary and the left anterior descending artery can be grafted without cardiopulmonary bypass. If cardiopulmonary bypass is necessary for ventricular repair, it then seems appropriate to more extensively revascularize the myocardium [7, 8]. Target revascularization, if a coronarography was performed, or blind revascularization to major coronary arteries that show arteriosclerosis on palpation may be achieved with minimal additional morbidity if performed on a continuously perfused heart.

Bleeding was controlled and appropriate revascularization performed in all our patients. Three, however, died within 6 months of operation. The cause of death was not directly related to the surgical intervention but to the extent of initial infarction and the preoperative reanimation. In this context, the least aggressive approach to the heart should be preferred. Epicardial patching and myocardial revascularisation without cardio-pulmonary bypass appears as the most attractive option.


   References
Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

  1. Oliva P.B., Hammill S.C., Edwards W.D. Cardiac rupture, a clinically predictable complication of acute myocardial infarction. J Am Coll Cardiol 1993;22:720-726.[Abstract]
  2. Becker R.C., Gore J.M., Lambrew C., Weaver W.D., Rubison R.M., French W.J., et al. A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction. J Am Coll Cardiol 1996;27:1321-1326.[Abstract]
  3. Becker R.C., Charlesworth A., Wilcox R.G., et al. Cardiac rupture associated with thrombolytic therapy. J Am Coll Cardiol 1995;25:1063-1068.[Abstract]
  4. Perdigao C., Andrade A., Ribeiro C. Cardiac rupture in acute myocardial infarction. Various clinico-anatomical types in 42 recent cases observed over a period of 30 months. Arch Mal Coeur 1987;80:336-344.
  5. Stevenson W.G., Linssen G.C., Havenith M.G., Brugada P., Wellens H.J. The spectrum of death after myocardial infarction. Am Heart J 1989;118:1182-1188.[Medline]
  6. Reddy S.G., Roberts W.C. Frequency of rupture of the left ventricular free wall or ventricular septum among necropsy cases of fatal acute myocardial infarction since introduction of coronary care units. Am J Cardiol 1989;63:906-911.[Medline]
  7. Sutherland F.W., Guell F.J., Pathi V.L., Naik S.K. Postinfarction ventricular free wall rupture. Ann Thorac Surg 1996;61:1281-1285.[Abstract/Free Full Text]
  8. Reardon M.J., Carr C.L., Diamond A., Letsou G.V., Safi H.J., Espada R., et al. Ischemic left ventricular free wall rupture. Ann Thorac Surg 1997;64:1509-1513.[Abstract/Free Full Text]
  9. Komeda M, David TE, Fremes SE. Surgical repair of postinfarction ventricular septal defect. Circulation 1990;82(Suppl):IV:243–7.
  10. David T.E., Dale L., Sun Z. Postinfarction ventricular septal rupture. J Thorac Cardiovasc Surg 1995;110:1315-1322.[Abstract/Free Full Text]
  11. Lopez-Sendon J., Gonzalez A., Lopez de Sa E., et al. Diagnosis of subacute ventricular wall rupture after acute myocardial infarction. J Am Coll Cardiol 1992;19:1145-1153.[Abstract]
  12. Figueras J., Cortadellas J., Calvo F., Soler Soler J. Relevance of delayed hospital admission on development of cardiac rupture during acute myocardial infarction. J Am Coll Cardiol 1998;32:135-139.[Abstract/Free Full Text]
  13. Hvass U., Chatel D., Frikha I., Pansard Y., Depoix J.P., Julliard J.M. Left ventricular free wall rupture. Long-term results with a pericardial patch and fibrin glue repair. Eur J Cardiothorac Surg 1995;9:75-76.[Medline]
  14. Frances C., Romero A., Grady D. Left ventricular pseudoaneurysm. J Am Coll Cardiol 1998;32:557.[Abstract/Free Full Text]
  15. Padro J.M., Mesa J.M., Silvestre J., et al. Subacute cardiac rupture. Ann Thorac Surg 1993;55:20-24.[Abstract]
Accepted for publication September 22, 1999.




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