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Interact CardioVasc Thorac Surg 2009;8:619-623. doi:10.1510/icvts.2008.200535
© 2009 European Association of Cardio-Thoracic Surgery

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Institutional report - Cardiac general

Short-term and mid-term follow-up of sutureless surgery for postinfarction subacute free wall rupture

Manuel Carnero-Alcázara,*, Ali Alswiesa, Lepoldo Pérez-Islab, Jacobo A. Silva-Guisasolaa, Juan J. González-Ferrerb, Fernando Reguillo-Lacruza, José Luis Zamoranob and Enrique Rodríguez-Hernándeza

a Cardiac Surgery Department, Hospital Clinico San Carlos, Martin Lagos St, 28040, Madrid, Spain
b Cardiology Department, Hospital Clinico San Carlos, Martin Lagos St, 28040, Madrid, Spain

Received 9 December 2008; received in revised form 10 March 2009; accepted 10 March 2009

*Corresponding author. Secretaria del Servicio de Cirugía Cardiaca, Hospital Clínico San Carlos, Calle Martín Lagos, s/n, 28040, Madrid. Tel.: +34 615238104/+34 913303691.

E-mail address: manuelcarneroalcazar{at}hotmail.es (M. Carnero-Alcázar).


    Abstract
 Top
 Abstract
 1. Introduction
 2. Patients, materials and...
 3. Results
 4. Discussion
 5. Conclusions and limitations
 References
 
We report our short-term and mid-term results with sutureless repair of postinfarction subacute left ventricular free wall rupture (LVFWR). For this purpose, we evaluated the short-term and mid-term postoperative results assessed by clinical examination and echocardiography of all patients who underwent surgery for subacute LVFWR between January 2004 and January 2009. Twenty-one patients were operated. Direct suture repair of LVFWR was carried out in only one patient. In all other cases we used a pericardial patch with biological glue. Early mortality was 19% (n=4). The median duration of follow-up was 17.3 months (interquartile range, 5–38.7), with a 13-month survival of 76%. Follow-up echocardiography showed no constriction associated with the rupture zone in any patient. According to our early experience, sutureless LVFWR repair is safe, effective and reproducible, and offers acceptable morbidity and mortality during follow-up.

Key Words: Free wall rupture


    1. Introduction
 Top
 Abstract
 1. Introduction
 2. Patients, materials and...
 3. Results
 4. Discussion
 5. Conclusions and limitations
 References
 
Left ventricular free wall rupture (LVFWR) is a serious and often fatal complication of acute myocardial infarction (AMI) [1]. It is estimated that 14–26% of all deaths due to AMI are a consequence of this complication [2], although the incidence of LVFWR secondary to AMI does not exceed 1% [3].

In 90% of all cases, LVFWR occurs in the first two weeks after infarction. Two well-differentiated clinicopathological patterns are distinguished [4, 5]: acute rupture, comprising acute, early, extensive, and deep myocardial rupture which usually proves fatal; and subacute rupture, which is characterized by late-onset myocardial hemorrhagic suffusion and involves a more benign prognosis.

Conservative management of subacute LVFWR using sutureless techniques (involving pericardial or other patches and biological glue) has gained popularity in the past decade, with quite promising results [6, 7]. However, the existing literature on the subject is still limited; as a result, much remains to be known of the safety and efficacy of such techniques.

We report our short-term and mid-term results with the surgical repair of subacute LVFWR secondary to AMI.


    2. Patients, materials and methods
 Top
 Abstract
 1. Introduction
 2. Patients, materials and...
 3. Results
 4. Discussion
 5. Conclusions and limitations
 References
 
A retrospective evaluation was made of all patients operated upon in our institution for post-AMI LVFWR between January 2004 and February 2009. Clinical, anatomical and anthropometric data were collected before, during, and after the surgery. Likewise, the patients were subjected to follow-up with clinical and echocardiographic evaluation. This study was approved by the Institutional Review Board of Hospital Clínico San Carlos.

2.1. Surgical technique

A midline sternotomy was performed in all cases. In those patients where LVFWR was the only mechanical complication of AMI, direct repair was carried out, without cardiopulmonary bypass (CPB) support. The rupture zone was identified (Fig. 1). A heterologous bovine pericardial patch [PERIGUARD® (Synovis©)] was cut to adequate size to cover the zone, and 2-octylcyanoacrylate biological glue [DERMABOND® (Ethicon©)] (Fig. 2) was applied to one of the surfaces of the patch, which was then applied to the rupture zone (Fig. 3). In more complicated cases involving severe post-AMI acute mitral valve regurgitation or ventricular septal defect, ECC-supported surgery with systemic heparinization proved necessary. In such situations, we preferred suture closure of the LVFWR zone, due to the high risk of bleeding. When allowed by the hemodynamic condition of the patient, and after identifying coronary lesions amenable to surgical revascularization, the pertinent coronary anastomoses were made.


Figure 1
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Fig. 1. Identification of the left ventricular free wall rupture (LVFWR) zone. LVFWR in the medial-apical segment of the anterior wall.

 

Figure 2
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Fig. 2. Impregnation of the pericardial patch with biological glue.

 

Figure 3
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Fig. 3. Pericardial patch applied to the left ventricular free wall rupture zone.

 
2.2. Follow-up

We evaluated the incidence of major adverse events during the postoperative period (during the hospital stay or 30 days after the operation). For follow-up, patients were contacted by telephone and underwent clinical and echocardiographic evaluation.

2.3. Adverse events

Cardiac and non-cardiac mortality was assessed during the postoperative period, along with the incidence of repeat free wall rupture and bleeding complications. We also recorded other complications, such as myocardial infarction, cerebrovascular accidents, mediastinitis, renal failure (with hemofiltration or hemodialysis), etc. During follow-up, we recorded the occurrence of new LVFWR and patient survival. In addition, follow-up echocardiography evaluated left ventricle contractility and the occurrence of pericardial constrictions and aneurysms or pseudoaneurysms in the patch implantation zone.

2.4. Statistical analysis

Qualitative variables were reported as absolute (n) and relative (%) frequencies. Quantitative variables in turn were expressed as the median and interquartile range (IQR). The survival curves were plotted using the Kaplan–Meier method. The SPSS® version 15.0 statistical package for Microsoft Windows® was used.


    3. Results
 Top
 Abstract
 1. Introduction
 2. Patients, materials and...
 3. Results
 4. Discussion
 5. Conclusions and limitations
 References
 
3.1. Sample

In the period between January 2004 and January 2009, we diagnosed 27 cases of post-AMI LVFWR. Six patients died shortly after admission. The remaining 21 patients underwent surgery. Cardiovascular risk factors and other relevant history of these patients are shown in Table 1.


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Table 1 Patient history

 
The median time elapsed from AMI to the diagnosis of LVFWR was two days (IQR, 1–4). Once the diagnosis was established, patients were stabilized in the intensive care unit and then underwent surgery. The time elapsed from the diagnosis to the operation was 2.5 h (IQR 1–4). The median troponin I peak was 51 ng/ml (IQR, 43–70). In all cases the diagnosis was established on the basis of the clinical condition, physical examination, and echocardiography. Fourteen patients were in critical condition (according to EuroSCORE criteria [8]) at the time of the diagnosis: 3 (14.3%) required advanced cardiopulmonary resuscitation maneuvers shortly before surgery, 9 (42.9%) were in a state of cardiogenic shock at the time of the operation, and 2 (10.5%) presented acute heart failure. The rest (n=7; 33.3%) were hemodynamically stable.

Based on the electrocardiographic and echocardiographic findings, anterior infarction was identified in 10 cases (47.6%), inferior infarction in 5 (23.8%), lateral infarction in 3 (14.3%), and multiple infarction in the rest. Thirteen patients (61.9%) presented left ventricular dysfunction, with an estimated ejection fraction below 40%. Additionally, 2 (9.5%) had severe pulmonary hypertension (pulmonary arterial systolic pressure ≥60 mmHg). In 11 of the 21 patients, coronary angiography had been performed prior to the diagnosis. Four patients (19%) presented triple-vessel disease, 2 (9.5%) had two diseased arteries, 2 (9.5) presented single-vessel disease, and another three patients (14.3%) showed no coronary lesions in any major coronary vessels. Six of these patients had undergone rescue percutaneous revascularization between one and seven days before the LFWR.

3.2. Surgical treatment

The median mortality rate estimated by logistic regression according to the EuroSCORE risk scale [8] was 25.1 (IQR, 19.5–29.9).

Twenty of the 21 patients (95.2%) were operated without ECC support. In all these patients, we treated the rupture zone with a heterologous pericardial patch and biological glue. Patients hemodynamically unstable were stabilized with inotropic drugs support (n=20), intraaortic balloon pump counterpulsation (n=3), coronary artery bypass grafting (n=1) or percutaneous coronary artery angioplasty shortly after surgery (n=3). The two patients that had received cardiopulmonary resuscitation maneuvers shortly before surgery did so because of cardiac tamponade. They underwent a pericardiocentesis before surgery and were stabilized in the intensive care unit before the moment of the operation. None of these patients, therefore, was assisted with cardiopulmonary bypass during surgery.

The remaining case corresponded to a patient with ventricular septal defect and LVFWR, both secondary to AMI. In this case, we used an exclusion technique with a ventriculotomy through the ventricular free wall rupture. The rupture area was subsequently closed with polypropylene sutures supported on autologous pericardium. One patient was also treated with a complete surgical revascularization.

3.3. Postoperative period

Postoperative outcomes are shown in Table 2. Four patients (19%) died in the immediate postoperative period. In two cases (9.5%), death resulted from an acute transmural cardiac rupture with incoercible bleeding in areas of myocardium close to those that had been repeated. The other two deaths (9.5%) were due to intractable cardiogenic shock.


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Table 2 Immediate postoperative period. Morbidity and mortality

 
As regards the major postoperative complications, three patients (14.3%) required prolonged orotracheal intubation for >24 h (two required a tracheotomy). Two patients experienced renal failure that was treated with continuous veno-venous hemofiltration. One patient presented mediastinitis requiring reintervention. Two patients had severe congestive heart failure that was medically treated. Three of the 17 survivors underwent elective coronary angioplasty in the postoperative period.

The median duration of the postoperative stay in the Intensive Care Unit was 3 days (IQR, 2.5–5). The median postoperative hospital stay was 12 days (IQR, 5.5–16.5).

3.4. Follow-up

Sixteen of the 17 survivors were contacted during follow-up. Patients who had not received a coronary angiography during the peri-operative period (n=4) did so early after discharge. Two patients underwent percutaneous revascularization in the follow-up. The other two didnot have amenable vessels for coronary angioplasty.

The median follow-up for the survivors was 17.3 months (IQR, 5–38.7). Two patients (11.8%) died during follow-up. One of them (5.9%) died of complicated out-of-hospital pneumonia, while the other died of AMI. Survival after 30 months was 76%. There were no new cases of LVFWR during follow-up (Fig. 4).


Figure 4
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Fig. 4. Follow-up and survival.

 
In eight of the 17 survivors during follow-up, we were able to conduct follow-up echocardiography to evaluate the presence of left ventricle aneurysms or pseudoaneurysms, pericardial constriction in the patch implantation zone, and left ventricle ejection fraction. Three patients had developed an aneurysm in the LVFWR zone (37.5%). No pseudoaneurysms were observed. Likewise, none of the patients showed evidence of pericardial constriction (Table 3). The median left ventricular ejection fraction of these patients was 45% (IQR, 42–54.5).


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Table 3 Diastolic and systolic ventricular and auricular function evaluation in the follow-up

 

    4. Discussion
 Top
 Abstract
 1. Introduction
 2. Patients, materials and...
 3. Results
 4. Discussion
 5. Conclusions and limitations
 References
 
LVFWR is one of the most common (1%) and serious mechanical complications of AMI [2, 3]. Its acute presentation is usually fatal, whereas subacute LVFWR often allows surgical management [5].

Different surgical techniques have been developed over the years for the management of LVFWR.

Infarctectomy with direct closure using a sutured patch, or direct closure with ECC [9], has fallen into disuse as a result of the generalized adoption of biological glues. Such techniques are more complicated; suturing must be made over friable myocardial tissue, and heparinization associated with ECC increases the risk of postoperative bleeding. These procedures are possibly now limited to the management of acute massive ruptures [7].

Padro et al. [10] reported excellent LVFWR closure results using non-sutured Teflon® patches with biological glue. Many alternatives have been described in the literature, involving Dacron® or autologous pericardial patches [11, 12], and using different biological glues [7]. These less invasive techniques have yielded excellent results, with acceptable morbidity and mortality. However, the patient series found in the literature are still small. We have reported our short-term and mid-term clinical and echocardiographic results in 21 patients consecutively operated for subacute LVFWR secondary to AMI.

In all but one of our cases, we used a sutureless technique with the application of a heterologous pericardial patch [PERIGUARD® (Synovis©)] and biological glue (2-octylcyanoacrylate) [DERMABOND® (Ethicon©)]. The patch was cut to adequate size to cover the LVFWR zone, impregnating one of its surfaces with the biological glue. The affected myocardial area was then covered with the patch. The remaining case corresponded to a patient with ventricular septal defect and LVFWR secondary to AMI. In this case, we repaired both defects with direct polypropylene suturing and bovine pericardium.

Our short-term results are similar to those reported in other series [6, 7, 10]. Early mortality (n=4, 19%) was essentially due to repeat free wall rupture (n=2, 9.5%) or cardiogenic shock secondary to the initial AMI (n=2, 9.5%). None of the survivors required early reintervention due to bleeding complications.

Mid-term follow-up also yielded acceptable results, with morbidity and mortality that were not attributable to the surgical technique employed, and which was probably conditioned by the age of the patients, and by concomitant disorders other than post-AMI LVFWR. Follow-up echocardiography also yielded interesting data, such as the absence of pericardial constrictions in the repaired LVFWR zone, or the preservation of left ventricular ejection fraction. To date, only Canovas et al. [6] have reported echocardiographic data over follow-up.

The appearance of pseudoaneurysms in the pericardial patch-covered zone was one of our concerns during the follow-up of these patients. Such complications were feasible, since the patch could contain a transmural myocardial rupture subsequently evolving towards a pseudoaneurysm, with consequent surgical intervention. None of our patients presented this complication, however. To date, we have found no other studies on this subject in the literature.


    5. Conclusions and limitations
 Top
 Abstract
 1. Introduction
 2. Patients, materials and...
 3. Results
 4. Discussion
 5. Conclusions and limitations
 References
 
Sutureless subacute LVFWR repair using a patch and biological glue (2-octylcyanoacrylate) is reproducible, effective, and safe. Our short-term and mid-term results seem to corroborate those of other series published in the literature.

In the same way as in earlier publications, the limitations of our study are those inherent to small sample sizes. It is therefore essential to increase the number and size of the patient series. The long-term results of the technique also require evaluation in order to establish scientifically sound indications for the surgical management of this pathology.


    References
 Top
 Abstract
 1. Introduction
 2. Patients, materials and...
 3. Results
 4. Discussion
 5. Conclusions and limitations
 References
 

  1. Reeder GS. Identification and treatment of complications of myocardial infarction. Mayo Clin Proc 1995;70:880–884.[Abstract]
  2. Stevenson WG, Linssen GC, Havenith MG, Brugada P, Wellens HJ. The spectrum of death after myocardial infarction: a necropsy study. Am Heart J 1989;118:1182–1188.[CrossRef][Medline]
  3. Patel MR, Meine TJ, Lindblad L, Griffin J, Granger CB, Becker RC, van de Werf F, White H, Califf RM, Harrington RA. Cardiac tamponade in the fibrinolytic era: analysis of >100,000 patients with ST-segment elevation myocardial infarction. Am Heart J 2006;151:316–322.[CrossRef][Medline]
  4. Purcaro A, Costantini C, Ciampani N, Silenzi C, Gili A, Belardinelli R, Astolfi D. Diagnostic criteria and management of subacute ventricular free wall rupture complicating acute myocardial infarction. Am J Cardiol 1997;80:397–405.[CrossRef][Medline]
  5. Nakatsuchi Y, Minamino T, Fujii K, Negoro S. Clinicopathological characterization of cardiac free wall rupture in patients with acute myocardial infarction: difference between early and late phase rupture. Int J Cardiol 1994;47:S33–S38.[CrossRef][Medline]
  6. Canovas SJ, Lim E, Dalmau MJ, Bueno M, Buendia J, Hornero F, Gil O, García R, Paya R, Pérez J, Echanove I, Montero J. Midterm clinical and echocardiographic results with patch glue repair of left ventricular free wall rupture. Circulation 2003;108(suppl_1):II237–II240.[Medline]
  7. Sakaguchi G, Komiya T, Tamura N, Kobayashi T. Surgical treatment for postinfarction left ventricular free wall rupture. Ann Thorac Surg 2008;85:1344–1347.[Abstract/Free Full Text]
  8. Roques F, Nashef SA, Michel P, Gauducheau E, de Vincentiis C, Baudet E, Cortina J, David M, Faichney A, Gabrielle F, Gams E, Harjula A, Jones MT, Pintor PP, Salamon R, Thulin L. Risk factors and outcome in European cardiac surgery: analysis of the EuroSCORE multinational database of 19030 patients. Eur J Cardiothorac Surg 1999;15:816–822.[Abstract/Free Full Text]
  9. Anagnostopoulos E, Beutler S, Levett JM, Lawrence JM, Lin CY, Replogle RL. Myocardial rupture. Major left ventricular rupture treated by infartectomy. J Am Med Assoc 1997;238:2715–2716.[CrossRef]
  10. Padro JM, Mesa JM, Silvestre J, Larrea JL, Caralps JM, Cerron F, Aris A. Subacute cardiac rupture: repair with a sutureless technique. Ann Thorac Surg 1993;55:20–23.[Abstract]
  11. Iemura J, Oku H, Otaki M, Kitayama H, Inoue T, Kaneda T. Surgical strategy for left ventricular free wall rupture after acute myocardial infarction. Ann Thorac Surg 2001;71:201–204.[Abstract/Free Full Text]
  12. Pretre R, Benedikt P, Turina MI. Experience with postinfarction left ventricular free wall rupture. Ann Thorac Surg 2000;69:1342–1345.[Abstract/Free Full Text]




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