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Ann Thorac Surg 2002;74:96-101
© 2002 The Society of Thoracic Surgeons


Original article: cardiovascular

Sutureless patch technique for postinfarction left ventricular rupture

Kevin Lachapelle, MD*a, Benoit deVarennes, MDa, Patrick L. Ergina, MDa, Renzo Cecere, MDa

a Division of Cardiac Surgery, McGill University Health Centre, Montreal, Quebec, Canada

Accepted for publication March 1, 2002.

* Address reprint requests to Dr Lachapelle, Royal Victoria Hospital, Suite S8.30, 687 Pine Ave West, Montreal, Quebec H3A 1A1, Canada
e-mail: kevin.lachapelle{at}mcgill.ca


    Abstract
 Top
 Footnotes
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
Background. Left ventricular free wall rupture is an uncommon but catastrophic event after myocardial infarction and is associated with a high mortality. After prompt diagnosis some patients may be salvaged with immediate surgical intervention. Surgical techniques used to seal the rupture vary, as few surgeons have experience with this pathologic process. We report our experience using a sutureless patch technique to treat this entity.

Methods. A review of 6 consecutive patients during an 8-year period who were referred to one cardiac unit with postinfarction left ventricular rupture was conducted.

Results. There were 3 men and 3 women with an average age of 71.8 years. All were hemodynamically unstable, and 4 were in electromechanical dissociation. Echocardiography confirmed the diagnosis in 5 patients, and cardiac catheterization had been performed in 4 before rupture. All patients were treated promptly with fluid, inotropic agents, and, if needed, cardiopulmonary resuscitation and pericardiocentesis. Resuscitation was continued in the operating room, and the myocardial tear was sealed with a generous patch of unsupported felt secured to the heart with cyanoacrylate glue. Coronary artery bypass grafting was performed in 3 patients if the anatomy was known. All patients survived to the intensive care unit. One death occurred as a result of severe neurologic injury. Five patients were discharged from the hospital, and all were alive 2 months to 7.5 years after operation.

Conclusions. A sutureless patch technique for the treatment of postinfarction rupture is simple, effective, and associated with a favorable outcome.


    Introduction
 Top
 Footnotes
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
Left ventricular (LV) free wall rupture occurs in 1% to 4% of patients after myocardial infarction [1, 2]. Despite the overall reduction in postinfarction mortality during the last 20 years, the rate of LV rupture has not changed over time and may account for up to 20% of all deaths from infarction [14]. Most patients die shortly after rupture, and mortality after surgical repair has traditionally been high [4]. It may be possible to identify patients at risk for ventricular rupture [5], and with the availability of echocardiography, prompt premortem diagnosis is feasible. Consequently, there are increasing reports in the literature of successful surgical repair [614]; yet, the most appropriate surgical management remains controversial because each surgeon’s experience treating this entity is low [15]. Padro and colleagues [16, 17] described a sutureless technique for the treatment of cardiac rupture using a patch of polytetrafluoroethylene (Teflon) secured to the heart with cyanoacrylate glue with no mortality in 13 patients. We have adopted a similar sutureless technique to treat postinfarction LV free wall rupture and report on our experience and follow-up.


    Patients and methods
 Top
 Footnotes
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
Six consecutive patients were referred to one cardiac center between January 1993 and June 2001 with postinfarction LV free wall rupture. The clinical characteristics of the patients are outlined in Table 1. The average age was 71.8 years, with 3 men and 3 women. No patient had a prior history of coronary artery disease. All but 1 (no. 2) had been treated with thrombolytic agents for a recent myocardial infarction, and all patients had a baseline echocardiogram performed after admission to the hospital. Cardiac catheterization was performed before rupture in 4 patients owing to persistent anginal symptoms. The diagnosis of ventricular rupture was confirmed with echocardiography in 5 patients after an acute episode of hemodynamic decompensation. In 1 patient, rupture was identified during the LV angiogram injection at the time of catheterization. A diagnostic angiogram was not performed nor attempted in the 2 patients with unknown coronary anatomy once the diagnosis of rupture was made. At the time of diagnosis, all patients were unstable and were treated with immediate fluid infusion, inotropic agents (epinephrine, norepinephrine), vasoconstrictors (phenylephrine), and, if needed, pericardiocentesis and cardiopulmonary resuscitation. Four patients eventually exhibited electromechanical dissociation during the course of the resuscitation or during transfer to the operating room.


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Table 1. Preoperative Characteristics of Patients With Left Ventricular Free Wall Rupture

 
Table 2 summarizes the surgical course. A rapid sternotomy was performed in all patients, and the pericardium was evacuated of clots and blood. Cardiopulmonary bypass was instituted in 4 patients because of exsanguination, hemodynamic collapse, or the location of the tear. Three patients had massive bleeding on opening the pericardium (nos. 1, 3, and 5), two of which could not be controlled without cardiopulmonary bypass. After intraoperative resuscitation the tear was visualized in all but 1 patient (no. 4). All had an obvious area of necrosis with an epicardial hematoma in the area of infarction (Fig 1). There was active bleeding in 3 patients, 1 having only minor oozing, and 2 who appeared to have sealed. In all cases, an elliptical patch of unsupported polytetrafluoroethylene felt (Teflon; PTFE felt, Boston Scientific, Meadox Medical Inc, Oakland, NJ) is fashioned in such a manner as to be larger than the area of hematoma and muscle necrosis such that the whole perimeter of the patch lies on healthy myocardium and the area of the infarct is covered. The size of the patch is usually between 6 x 5 cm and 6 x 7 cm. The patch is placed over the infarcted area and then soaked with biocompatible glue [18] made of a cyanoacrylate monomer (Histoacryl; B. Braun Medical AG, Melsungen, Germany). This requires 7 to 10 vials (0.5 mL/vial) of Histoacryl which are packaged sterilely and refrigerated. The glue, which is dyed blue, is directly applied to the patch, which is then held in place with cotton-tipped applicators by an assistant. Once the whole patch is colored it becomes adhesive and hot. After 2 to 3 minutes the patch is firm and hemostatic (Fig 2).


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Table 2. Surgical Procedure and Clinical Results

 


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Fig 1. Schematic drawing depicting a left ventricular free wall rupture located on the anterior surface.

 


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Fig 2. Schematic drawing depicting the use of an elliptical piece of unsupported felt applied to the ventricular rupture and the surrounding infarct followed by administration of cyanoacrylate glue.

 
Coronary artery bypass grafting was performed in 3 patients as an adjunct if the coronary anatomy was known and after the patch had been secured with the glue. Inasmuch as the patch covers the whole infarct, that territory usually cannot be bypassed. Only 1 patient (no.5) had the culprit vessel bypassed distal to patch placement. The aorta was clamped, and the heart was arrested with antegrade cold blood cardioplegia in 2 patients whereas 1 patient was grafted without cardiopulmonary bypass. Separation from cardiopulmonary bypass was uneventful in 3 patients, but required high doses of epinephrine and norepinephrine and an intraaortic balloon pump in 1 patient (no.3); 1 patient had a prophylactic insertion of an intraaortic balloon pump after the operation (no. 6). The patch was hemostatic in all patients, and the chest was closed in the usual fashion with pericardial and mediastinal tubes and a right ventricular pacing wire.


    Results
 Top
 Footnotes
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
Cardiovascular stability as well as hemostasis was achieved in all patients. There was one postoperative death (1 of 6) owing to severe neurologic injury in a patient who had prolonged cardiopulmonary resuscitation before operation (no. 5), and care was discontinued at the family’s request. Prolonged ventilator support (> 3 days) occurred in 2 patients, and 1 had a deep wound infection treated with a 2-week course of antibiotics and local debridement. All 5 remaining patients survived and were discharged from the hospital at 24, 14, 12, 8, and 10 days (nos. 1, 2, 3, 4, and 6, respectively). The 2 patients who did not have coronary grafting at the time of the procedure had no reversible myocardial ischemia as determined by a Dip-Mibi scan, which was performed before discharge. On the whole, ventricular function as determined echocardiographically appeared to be preserved after operation. At follow-up ranging from 2 months to 7.5 years, all 5 patients were alive, with 4 exhibiting New York Heart Association class I symptoms and 1 exhibiting New York Heart Association class II symptoms. This last patient had an ejection fraction of 25% before discharge from hospital.


    Comment
 Top
 Footnotes
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
We have reported our experience using a sutureless technique to repair postinfarction LV free wall rupture in 6 unselected, consecutive patients. Although no patient had a concomitant ventricular septal defect or papillary muscle rupture, the initial outcome and follow-up of this small cohort is favorable despite having 4 patients in electromechanical dissociation before operation and 3 patients actively bleeding.

Surgical treatment of ventricular rupture has varied over time and is often individualized depending on the state of the tear and the presence of concomitant lesions. Standard and accepted repair involves supporting the patient with cardiopulmonary bypass, performing an infarctectomy including the area of rupture, and reconstructing the ventricle with a patch of Teflon or polyethylene terephthalate fiber (Dacron) sutured directly to the myocardium [19]. This technique continues to be reported and advocated by some authors [9, 12, 14, 15], especially if the rupture is of the "blow-out" type [12, 14, 15] or associated with a septal defect [20], or there is acute mitral regurgitation secondary to papillary muscle rupture [12]. Others have tried to avoid removing necrotic myocardium and have treated these ruptures with an on-lay patch of Dacron, Teflon, or pericardium secured with a running Prolene suture (Ethicon, Somerville, NJ) to the epicardium or healthy myocardium [1214, 21]. When the area of necrosis has been small, simple Prolene Teflon-buttressed sutures have been used without the need for cardiopulmonary bypass support [9, 12, 14]. We do not have experience with these types of sutured repairs in the acute setting, but some authors have raised concerns regarding the difficulty with sewing into fragile myocardial tissue [14] and the potential ventricular cavity distortion that may occur, especially after infarctectomy.

With the advent of tissue adhesives many authors advocate a completely sutureless technique [11, 14, 16, 17, 22] in which a patch of pericardium, Dacron, or Teflon is glued to the infarcted myocardium, thereby avoiding issues related to myocardial friability and distortion. Another distinct advantage is the potential to perform this type of repair without cardiopulmonary bypass. Adhesives reported to be successful in the treatment of ventricular rupture have been of several types and include the biologic glues (fibrin based or gelatin hydrogels) as well as the synthetic cyanoacrylate monomers.

Fibrin glues function by reproducing the normal clotting cascade and result in a stable fibrin matrix after the degradation of exogenous fibrinogen. The main advantage is their lack of toxicity and complete biocompatibility such that healing is not affected and the material is naturally degraded [23]. Gelatin-based glues have greater bonding strength than fibrin glues owing to polymerization of the gelatin-resorcin component when in contact with formaldehyde or glutaraldehyde. Although commonly used in aortic operation, gelatin-resorcin formaldehyde is cytotoxic owing to the release of formaldehyde during degradation, raising concerns regarding potential long-term complications [24]. The major limitation of both these biologic glues is that they are only effective in the absence of bleeding. Both have been used to treat selected patients with ventricular rupture but usually if the tear is sealed or is of the oozing type [11, 14, 22]. Consequently, some authors advocate tailoring the type of repair to the status of the tear at the time of operation and favor using a sutureless technique if the tear is only oozing or has sealed but a sutured approach for actively squirting lesions, fearing that the lack of sutures may result in rerupture in actively bleeding lesions [12, 14].

Synthetic glues such as cyanoacrylate are monomers that polymerize in an exothermic reaction when in contact with fluid. Although they are cytotoxic and potentially mutagenic, acetylation has greatly reduced these concerns [18]. Histoacryl (n-butyl-2 cyanoacrylate) has been used in Europe and Canada for closure of skin lacerations and as an embolic agent for control of bleeding varices [25]. Dermabond (2-octyl cyanoacrylate; Ethicon Inc), which forms a stronger but more pliable bond, is packaged and colored in a similar fashion to Histoacryl and is approved by the US Food and Drug Administration for closure of skin lacerations. In 1993, Padro and coworkers [17] reported a 100% survival rate among 13 patients treated with a totally sutureless technique obtained by securing a patch of Teflon onto the myocardium using Histoacryl. No patient underwent a preoperative cardiac catheterization, and only 1 patient was placed on cardiopulmonary bypass because of a posterior tear. Most patients appeared to have sealed the rupture by the time the operation was performed. Five-year follow-up also demonstrated excellent functional status with 100% survival.

We have adopted this sutureless technique and have used it on all patients regardless of the location of the tear, the size of the tear, or the acuity with which the patient presented. Even patients with actively bleeding lesions can be treated using this technique provided they are supported with cardiopulmonary bypass. Technical considerations believed to be important to ensure a solid hemostatic patch using this technique include the following: (1) an appropriately large patch must be applied so that it borders on healthy myocardium; (2) the patch must be completely colored blue by the glue; and (3) the patch must held in place for 1 to 2 minutes using cotton-tip applicators until it becomes hot and adherent. The patch does become hot and may potentially cause a thermal injury if overlying a coronary artery. This artery, however, is usually the source of the infarct and in general is not bypassed. The simplicity of the technique makes it easy to master regardless of surgical experience. Although we have not yet used this technique in patients with a concomitant ventricular septal defect or papillary muscle rupture it would certainly be possible to buttress the ventricular suture line when approaching a septal defect through the infarct, or in the case of a papillary rupture, close the rupture with a patch and then replace the mitral valve using a standard approach.

In our patients, hemostasis was achieved in all, and all were transferred to the intensive care unit with cardiac stability. Postoperative echocardiograms demonstrated that ventricular function was generally preserved after operation, suggesting that emergent repair with this technique can salvage the myocardium. One patient did progress to moderate mitral regurgitation but was New York Heart Association class I at 1 year follow-up. Although 4 of 6 patients were placed on bypass, the need for bypass should be individualized and depends on the hemodynamic state of the patient, the location of the tear, and whether an additional cardiac intervention is necessary. Some groups routinely insert an intraaortic balloon pump and this may stabilize the patient further and allow one to perform the procedure without bypass. In addition, counter-pulsation will reduce afterload and may reduce the potential of recurrent rupture. We inserted only two intraaortic balloon pumps in this group but believe this probably should be standard care in these patients. As with others we perform concomitant coronary artery bypass grafting only if the coronary anatomy is known and believe strongly that rapid and expedient operation to close the rupture is the main goal of surgery [15].

We believe that this sutureless technique for the treatment of LV free wall rupture is simple, versatile, and associated with a good outcome. We will continue to use it.


    Acknowledgments
 Top
 Footnotes
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
The technical assistance of Joclyn Prince is greatly appreciated. Mr David Rolling of the Audiovisual Department of the Royal Victoria Hospital made the drawings.


    Footnotes
 Top
 Footnotes
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 
This article has been selected for the open discussion forum on the CTSNet Web site: http://www.ctsnet.org/doc/5499


    References
 Top
 Footnotes
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Becker R.C., Gore J.M., Lambrew C., 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]
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  5. Oliva P.B., Hammmil S.C., Edwards W.D. Cardiac rupture, a clinically predictable complication of acute myocardial infarction. Report of 70 cases with clinicopathologic correlations. J Am Coll Cardiol 1993;22:720-726.[Abstract]
  6. Fitzgibbon G.M., Hooper G.D., Heggtveit H.A. Successful surgical treatment of postinfarction external cardiac rupture. J Thorac Cardiovasc Surg 1972;63:622-630.[Medline]
  7. Pifarre R., Sullivan H.J., Grieco J., et al. Management of left ventricular rupture complicating infarction. J Thorac Cardiovasc Surg 1983;86:441-443.[Abstract]
  8. Anagnostopoulos E., Beutler S., Levett J.M., et al. Myocardial rupture. Major left ventricular infarct rupture treated by infarctectomy. JAMA 1977;238:215-216.
  9. Zeebregets C.J., Noyez L., Hensens A.G., et al. Surgical repair of subacute left ventricular free wall rupture. J Card Surg 1997;12:416-419.[Medline]
  10. Coleman J.E., Mansfield R.J., Simpson I.A. Myocardial infarction and sub-acute ventricular rupture: successful outcome in two cases. Int J Cardiol 2000;73:285-287.[Medline]
  11. Imagawa H., Nakano S., Akagi H., et al. Pericardial hood repair of cardiac rupture secondary to extended myocardial infarction. Ann Thorac Surg 2000;69:1959-1960.[Abstract/Free Full Text]
  12. Pretre R., Benedikt P., Turina M.I. Experience with postinfarction left ventricular free wall rupture. Ann Thorac Surg 2000;69:1342-1345.[Abstract/Free Full Text]
  13. Park W.M., Connery C.P., Hochman J.S., et al. Successful repair of myocardial free wall rupture after thrombolytic therapy for acute infarction. Ann Thorac Surg 2000;70:1345-1349.[Abstract/Free Full Text]
  14. Iemura J., Oku H., Otaki M., et al. Surgical strategy for left ventricular free wall rupture after acute myocardial infarction. Ann Thorac Surg 2001;71:201-204.[Abstract/Free Full Text]
  15. Reardon M.J., Carr C.L., Diamond A., et al. Ischemic left ventricular free wall rupture: prediction, diagnosis, and treatment. Ann Thorac Surg 1997;64:1509-1513.[Abstract/Free Full Text]
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  17. Padro J.M., Mesa J., Silvestre J., et al. Subacute cardiac rupture: repair with a sutureless technique. Ann Thorac Surg 1993;55:20-24.[Abstract/Free Full Text]
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