ECMO support for the treatment of cardiogenic shock due to left ventricular free wall rupture
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《血管的通路杂志》
a Cardiac Surgery Clinic, Department of Surgical Science and Intensive Care, University of Milan-Bicocca, San Gerardo Hospital, Via G.Donizetti 106, 20052 Monza (MI), Italy
b Cardiac Anaesthesia Service, Department of Surgical Science and Intensive Care, University of Milan-Bicocca, San Gerardo Hospital, Monza, Italy
Abstract
Left ventricular free wall rupture (LVFWR) is still an uncommon catastrophic complication after acute myocardial infarction (MI), and it is one of the most frequent causes of sudden cardiac death. Immediate surgical repair is the treatment of choice. When LVFWR presents acutely with tamponade and cardiogenic shock in emergency department, salvage with a good outcome is still possible by timely pericardiocentesis and extracorporeal membrane oxygenation (ECMO) support. We report a case of cardiac rupture with tamponade and cardiogenic shock in which cardiopulmonary support with portable ECMO was used to rescue the patient before the operation.
Key Words: Left ventricular wall rupture; Myocardial infarction; Extracorporeal membrane oxygenation; Cardiogenic shock
1. Introduction
Perioperative management of left ventricular free wall rupture (LVFWR) is not clearly standardized and surgical repair is the only therapeutic option. When cardiogenic shock (CS) occurs in emergency department (ED), the option to stabilize the patient with percutaneous ECMO should be taken into consideration.
2. Case description
A 51-years-old man with a history of coronary artery disease and a previous myocardial infarction (MI) was admitted to ED in collapse. The 12-leads ECG showed an inferior ST sopraelevation. Because of a strong suspicion of acute MI, a trans-oesophageal echocardiogram (TEE) was done. It showed pericardial effusion around the heart and consequently the LVFWR was diagnosed. Emergent pericardiocentesis was performed without improvement of haemodynamic. Due to haemodynamic instability, an ECMO was inserted percutaneously via the right femoral vessels to salvage the patient. A 17 F percutaneous cannula (Medtronic, Minneapolis, MN, USA) was inserted in the right femoral artery and a 25 F percutaneous cannula (Medtronic, Minneapolis, MN, USA) in right femoral vein. The ECMO circuit was based on a centrifugal pump (Rota Flow RF-32, Jostra Medizintechnik AG, Hirrlingen, Germany), and a hollow-fibre membrane oxigenator (Quadrox D, Jostra Medizintechnik AG, Hirrlingen, Germany). All circuit components were heparin surface coated.
Heparin was administered; the activated clotting time (ACT) target was 180–200 s. The pump flow was maintained at 2.5 l/min/m2 obtaining a mean systemic pressure of 60 mmHg. Therefore, coronary perfusion improved and cardiac workload reduced. Under more stable conditions, the patient underwent coronary angiography before the operation.
The coronary angiography showed a three-vessel disease with proximal occlusion of LAD and of RCA. An emergency operation was planned and the patient reached the operating room supported with full flow ECMO, and with moderate dose of inotropic drugs. The duration of support before surgery was 3 h and 25 min.
ECMO was converted in standard cardiopulmonary bypass (CPB) through ascending aorta and right atrium. The criteria to convert ECMO into CPB was as follows: easier management of operation with a venous reservoir, easier left heart venting and the opportunity to return the blood from the opened heart. During CPB, the ECMO circuit was flowing through a shunt between arterial and vein lines to use it again to support the patient in the intensive care unit (ICU).
The aorta was cross-clamped and a cold blood cardioplegia solution with warm induction was delivered via antero-retrograde route. The LVFWR was localized in the inferior wall along the course of the posterior descending artery. The length was about 4–5 cm. Infartectomy was performed and the site of rupture was directly sutured between felt strips plus resorcin-formolo glue (Gluetiss, Berlin Heart, Berlin, Germany). Then, LAD artery was grafted with left internal thoracic artery, and RCA and obtuse marginal were grafted with two single vein grafts.
CPB was weaned off and the ECMO flow was resumed. An IABP was inserted through the left femoral artery to keep a low afterload after ECMO was removed and therefore reducing greatly the risk of re-rupture.
The ECMO flow was adjusted to achieve mixed venous oxygen saturation (SvO2) of 70%. Oxygen flow (FiO2) ranged between 40 and 60 ml to maintain a postoxygenator partial oxygen pressure of approximately 300 mmHg. Carbon dioxide was kept between 35 and 45 mmHg.
Intravenous heparin was administered continuously and varied according to ACT with a target of 160–180 s. The hematocrit was maintained between 30 and 35%. Red packet cells and fresh frozen plasma were transfused as required.
Exploration for bleeding was necessary in the first operative day.
Sedation by infusion of midazolam and fentanyl was obtained. During ECMO, ventilation set at 10 breaths per minute, tidal volume of 7 ml/kg, positive end expiratory pressure of 5 cm H2O. Inotropic support with dobutamine was maintained throughout the ECMO and after.
The criteria for ECMO weaning included SvO270%, stable haemodynamic and inotropic support, echocardiographic absence of tamponade and of left heart distension, and a left ventricle EF0.35. These criteria are also used in all prior ECMO cases treated. The ECMO flow was reduced gradually and at the same time, the cardiac function was continuously monitored with TEE.
Then the flow was maintained at 0.5 l/min/m2 for 2 h, and the patients was decannulated at the bedside once the heart did not show any impaired function.
The ECMO duration after surgery was 36 hs. The patient had a good recovery in ICU. He was extubated on the fifth postoperative day, and discharged on 20th operative day. The pre-dimission TEE showed a mild reduction of EF (=0.45) without mitral regurgitation.
At 5 months follow-up, the patient was in NYHA I-II, the EF was 0.45 and the left ventricle had normal dimension.
3. Discussion
Cardiac rupture during AMI is one of the most frequent causes of sudden cardiac death. LVFWR occurred with an incidence between 0.96 and 3.5% [1,2] and 30-day mortality rate between 17.6 and 83.3% [1–3]. The suggested risk factors of LVFWR are advanced age (>65 years), female gender, lower body mass index (<1.66), first MI, re-infarction, anterior MI, hypertension, increased sympathetic tone [1,4]. Use of IABP is described as support, [1,5,6] nevertheless, it is not always useful to avoid further complications in critical patients and when death of patient is imminent. In this latter case, the role of portable ECMO, implanted in ED, could be useful to stabilize the haemodynamic status, improving the postoperative course and reducing the mortality rate.
Use of ECMO for emergency resuscitation is not recent. In 1937, John Gibbon proposed this concept to treat severe pulmonary tromboembolism. Nowadays, portable CPB systems allow to act rapidly, and to stabilize the patient's condition in such circumstances in which an operation cannot be performed in a very short period.
Indications for going on ECMO are now clarified as follows: cardiac arrest, failure to wean off CPB, acute deterioration, CS with anatomically problems, bridge to transplantation [7].
Most frequently described complications are bleeding, sepsis, ARDS, renal failure, ischemia of lower limbs, stroke, and oxygenator failure [7,8]. The main causes of in-hospital death are myocardial failure, multiorgan failure, cerebral infarction or bleeding, sepsis, disseminated intravascular coagulation, and leg ischemia [8,9].
Since 1999 in our Department, we are regularly using the Jostra Rota Flow (RF-32) as pump head and the Quadrox D as oxigenator. Some advantages about RF-32 have been described: no traumatism, compact prime volume (32 ml), high biocompatibility and no thrombus formation [9].
The high preoperative mortality of cardiac rupture [10], and the short interval time from onset of acute MI and cardiac rupture (below 72 h in most of cases), are the limiting factors to establish a timely surgical strategy. Often, the LVFWR occurs out of the hospital or in the clinical department where obtaining a diagnosis of cardiac rupture in time is sometimes difficult. Moreover, apart from ED or intensive care unit, ECMO preparation is difficult, or even impossible, in other hospital areas.
In conclusion, to go on ECMO in ED to treat cardiogenic shock due to LVFWR is a valid rescue mean when death is imminent. The current portable ECMO systems allow a relatively rapid haemodynamic stabilization of the patient, so that any other diagnostic procedure could be arranged before operation.
Appendix A. ICVTS on-line discussion
Author: S. Ibrahim Sersar (Department of Cardiothoracic Surgery, Mansoura, 123 Egypt)
eComment: William Harvery was the first to describe LV rupture in 1647. Morgagni reported 11 cases of myocardial rupture at autopsy and he himself died of myocardial rupture [1]. Pericardiocentesis is both a diagnostic and therapeutic option. Aspiration of unclotted blood is considered the most reliable diagnostic tool in subacute LV rupture. Aspiration of a clear serous fluid excludes LV rupture. Pericardiocentesis provides a short term improvement of the hemodynamics [2]. Some studies suggest an association of VFWR with single vessle disease and with first infarction. Both conditions might be related to poorly development collateral circulation. Different opinions have been published about the opportunity to perform coronary angiograms or avoiding this investigation in order to save time and to perform "blind" coronary artery bypass. A coronary angiogram should be promptly performed as soon as pericardial effusion is noted in MI patients, before they deteriorate. Proper revascularization has a positive impact on survival and freedom from angina and our policy is to bypass major vessels with significant stenoses supplying non-infarcted areas. Two specific advantages of knowing the coronary status are seen in the covering technique. The coronary arteries known to be healthy can be covered with minimal risk of needing a CABG in the future; the knowledge of coronary status is of great help in deciding where and how to place the semicontinuous sutures. Our aim is to put a large number of shallow stitches along the whole patch margin [3]. With the advent of tissue adhesives many authors advocate a completely sutureless technique 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. 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, gelatinresorcin formaldehyde is cytotoxic owing to the release of formaldehyde during degration, raising concerns regarding potential long-term complications. 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 oozing. 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. 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. 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. 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 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 catherterization, and only 1 patient was palced on cardiopulmonary bypass because of a posterior tear. Most patients appeared to have sealed the rupture by the time the operation was performed. The five-year follow-up also demonstrated excellent functional status with 100% survival [4]. Biologic glues may be very useful, but there is no free lunch in this world. We should be alert for any patterns of late complications that would suggest that the use of biologic glue has some downsides.
Pseudoaneurysms in patients treated with a glue may arise for many reasons including:
I. Local cell death from toxic products in the glue that lead to tissue breakdown over time.
II. The aortic glue may have stopped bleeding in an area that would have been better served over the long term with a suture than by glue closure (analogous to duct taping an area that should have been bloted together).
III. Patients who would not have survived surgery due to bleeding from coagulopathy and local tissue compromise are now surviving. They may be at more risk for late complications than patients who did not need the glue to get out of the operating room [5].
References
1 Willius FA and Dry TJ. A history of the heart and circulation 1948;Philadelphia: WB Saunder
2 Coma Canella I, Lopez Sendon J, Gonzalez A. Hemodynamic effect of Dobutamine, Dextran and pericardiocentesis in cardiac tamponade following acute myocardial infarction. Am Heart J 1987;114:78
3 Mantovani V, Vanoli D, Chelazzi P, Lepore V, Ferrarese S, Sala A. Post-infarction cardiac rupture: surgical treatment. Eur J Cardiothorac Surg 2002;22:777–80
4 Lachapelle K, deVarennes B, Ergina PL, Cecere R. Sutureless Patch Technique for postinfarction Left Ventricular Rupture. Ann Thorac Surg 2002;74:96–101
5 Downing SW. What are the risks of using biologic glues. Ann Thorac Surg 2003;75:1063–4
Acknowledgments
We are grateful to our perfusionist Mr Teresio Ravasi for his useful technical support.
Footnotes
Poster Session presentation at the 53rd International Congress of the European Society for Cardiovascular Surgery. June 2–5, 2004, Ljubljana, Slovenia.
References
Ikeda N, Yasu T, Kubo N, Hirohara T, Sugowara Y, Kobayashi N, Hashimoto S, Tsuruya Y, Fujii M, Saito M. Effect of reperfusion therapy on cardiac rupture after myocardial infarction in Japanese. Circ J 2004;68:422–6.
Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, Chen MC. Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era. Chest 2003;124:565–71.
Mantovani V, Vanoli D, Chelazzi P, Lepore V, Ferrarese S, Sala A. Post-infarction cardiac rupture: surgical treatment. E J Cardiothorac Surg 2002;22:777–80.
Tanaka K, Sato N, Yasutaka M, Takada S, Takano T, Ochi M, Tanaka S, Tamura K. Clinicopathological characteristics of 10 patients with rupture of both ventricular free wall and septum (double rupture) after myocardial infarction. J Nippon Med SCH 2003;70:21–7.
Baillot R, Pelletier C, Trivino-Marin J, Castonguay Y. Postinfarction ventricular septal defect: delayed closure with prolonged mechanical circulatory support. Ann Thorac Surg 1983;35:138–42.
Birnbaum Y, Chamoun AJ, Anzuini A, Lick SD, Ahmad M, Uretsky BF. Ventricular free wall rupture following acute myocardial infarction. Coron Artery Dis 2003;14:463–70.
von Segesser LK. Cardiopulmonary support and extracorporeal membrane oxygenator for cardiac assist. Ann Thorac Surg 1999;68:672–7.
Doll N, Kiaii B, Borger M, Bucerius J, Kramer K, Schmitt DV, Walther T, Mohr FW. Five-year results of 219 consecutive patients treated with extracorporeal membrane oxygenation for refractory postoperative cardiogenic shock. Ann Thorac Surg 2004;77:151–7.
Smith C, Bellomo R, Raman JS, Matalanis G, Rosalin A, Buckmaster J, Hart G, Silvester W, Gutteridge GA, Smith B, Doolan L, Buxton BF. An extracorporeal membrane oxygenator-based approach to cardiogenic shock in an older population. Ann Thorac Surg 2001;71:1421–7.
Fujimoto K, Kawahito K, Yamaguchi A, Sakuragawa H, Tsuboi J, Yuri K, Tanaka M, Endo H, Adachi H, Ino T. Percutaneous extracorporeal life support for treatment of fatal mechanical complications associated with acute myocardial infarction. Artif Organs 2001;25:1000–3.(Francesco Formica, Fabriz)
b Cardiac Anaesthesia Service, Department of Surgical Science and Intensive Care, University of Milan-Bicocca, San Gerardo Hospital, Monza, Italy
Abstract
Left ventricular free wall rupture (LVFWR) is still an uncommon catastrophic complication after acute myocardial infarction (MI), and it is one of the most frequent causes of sudden cardiac death. Immediate surgical repair is the treatment of choice. When LVFWR presents acutely with tamponade and cardiogenic shock in emergency department, salvage with a good outcome is still possible by timely pericardiocentesis and extracorporeal membrane oxygenation (ECMO) support. We report a case of cardiac rupture with tamponade and cardiogenic shock in which cardiopulmonary support with portable ECMO was used to rescue the patient before the operation.
Key Words: Left ventricular wall rupture; Myocardial infarction; Extracorporeal membrane oxygenation; Cardiogenic shock
1. Introduction
Perioperative management of left ventricular free wall rupture (LVFWR) is not clearly standardized and surgical repair is the only therapeutic option. When cardiogenic shock (CS) occurs in emergency department (ED), the option to stabilize the patient with percutaneous ECMO should be taken into consideration.
2. Case description
A 51-years-old man with a history of coronary artery disease and a previous myocardial infarction (MI) was admitted to ED in collapse. The 12-leads ECG showed an inferior ST sopraelevation. Because of a strong suspicion of acute MI, a trans-oesophageal echocardiogram (TEE) was done. It showed pericardial effusion around the heart and consequently the LVFWR was diagnosed. Emergent pericardiocentesis was performed without improvement of haemodynamic. Due to haemodynamic instability, an ECMO was inserted percutaneously via the right femoral vessels to salvage the patient. A 17 F percutaneous cannula (Medtronic, Minneapolis, MN, USA) was inserted in the right femoral artery and a 25 F percutaneous cannula (Medtronic, Minneapolis, MN, USA) in right femoral vein. The ECMO circuit was based on a centrifugal pump (Rota Flow RF-32, Jostra Medizintechnik AG, Hirrlingen, Germany), and a hollow-fibre membrane oxigenator (Quadrox D, Jostra Medizintechnik AG, Hirrlingen, Germany). All circuit components were heparin surface coated.
Heparin was administered; the activated clotting time (ACT) target was 180–200 s. The pump flow was maintained at 2.5 l/min/m2 obtaining a mean systemic pressure of 60 mmHg. Therefore, coronary perfusion improved and cardiac workload reduced. Under more stable conditions, the patient underwent coronary angiography before the operation.
The coronary angiography showed a three-vessel disease with proximal occlusion of LAD and of RCA. An emergency operation was planned and the patient reached the operating room supported with full flow ECMO, and with moderate dose of inotropic drugs. The duration of support before surgery was 3 h and 25 min.
ECMO was converted in standard cardiopulmonary bypass (CPB) through ascending aorta and right atrium. The criteria to convert ECMO into CPB was as follows: easier management of operation with a venous reservoir, easier left heart venting and the opportunity to return the blood from the opened heart. During CPB, the ECMO circuit was flowing through a shunt between arterial and vein lines to use it again to support the patient in the intensive care unit (ICU).
The aorta was cross-clamped and a cold blood cardioplegia solution with warm induction was delivered via antero-retrograde route. The LVFWR was localized in the inferior wall along the course of the posterior descending artery. The length was about 4–5 cm. Infartectomy was performed and the site of rupture was directly sutured between felt strips plus resorcin-formolo glue (Gluetiss, Berlin Heart, Berlin, Germany). Then, LAD artery was grafted with left internal thoracic artery, and RCA and obtuse marginal were grafted with two single vein grafts.
CPB was weaned off and the ECMO flow was resumed. An IABP was inserted through the left femoral artery to keep a low afterload after ECMO was removed and therefore reducing greatly the risk of re-rupture.
The ECMO flow was adjusted to achieve mixed venous oxygen saturation (SvO2) of 70%. Oxygen flow (FiO2) ranged between 40 and 60 ml to maintain a postoxygenator partial oxygen pressure of approximately 300 mmHg. Carbon dioxide was kept between 35 and 45 mmHg.
Intravenous heparin was administered continuously and varied according to ACT with a target of 160–180 s. The hematocrit was maintained between 30 and 35%. Red packet cells and fresh frozen plasma were transfused as required.
Exploration for bleeding was necessary in the first operative day.
Sedation by infusion of midazolam and fentanyl was obtained. During ECMO, ventilation set at 10 breaths per minute, tidal volume of 7 ml/kg, positive end expiratory pressure of 5 cm H2O. Inotropic support with dobutamine was maintained throughout the ECMO and after.
The criteria for ECMO weaning included SvO270%, stable haemodynamic and inotropic support, echocardiographic absence of tamponade and of left heart distension, and a left ventricle EF0.35. These criteria are also used in all prior ECMO cases treated. The ECMO flow was reduced gradually and at the same time, the cardiac function was continuously monitored with TEE.
Then the flow was maintained at 0.5 l/min/m2 for 2 h, and the patients was decannulated at the bedside once the heart did not show any impaired function.
The ECMO duration after surgery was 36 hs. The patient had a good recovery in ICU. He was extubated on the fifth postoperative day, and discharged on 20th operative day. The pre-dimission TEE showed a mild reduction of EF (=0.45) without mitral regurgitation.
At 5 months follow-up, the patient was in NYHA I-II, the EF was 0.45 and the left ventricle had normal dimension.
3. Discussion
Cardiac rupture during AMI is one of the most frequent causes of sudden cardiac death. LVFWR occurred with an incidence between 0.96 and 3.5% [1,2] and 30-day mortality rate between 17.6 and 83.3% [1–3]. The suggested risk factors of LVFWR are advanced age (>65 years), female gender, lower body mass index (<1.66), first MI, re-infarction, anterior MI, hypertension, increased sympathetic tone [1,4]. Use of IABP is described as support, [1,5,6] nevertheless, it is not always useful to avoid further complications in critical patients and when death of patient is imminent. In this latter case, the role of portable ECMO, implanted in ED, could be useful to stabilize the haemodynamic status, improving the postoperative course and reducing the mortality rate.
Use of ECMO for emergency resuscitation is not recent. In 1937, John Gibbon proposed this concept to treat severe pulmonary tromboembolism. Nowadays, portable CPB systems allow to act rapidly, and to stabilize the patient's condition in such circumstances in which an operation cannot be performed in a very short period.
Indications for going on ECMO are now clarified as follows: cardiac arrest, failure to wean off CPB, acute deterioration, CS with anatomically problems, bridge to transplantation [7].
Most frequently described complications are bleeding, sepsis, ARDS, renal failure, ischemia of lower limbs, stroke, and oxygenator failure [7,8]. The main causes of in-hospital death are myocardial failure, multiorgan failure, cerebral infarction or bleeding, sepsis, disseminated intravascular coagulation, and leg ischemia [8,9].
Since 1999 in our Department, we are regularly using the Jostra Rota Flow (RF-32) as pump head and the Quadrox D as oxigenator. Some advantages about RF-32 have been described: no traumatism, compact prime volume (32 ml), high biocompatibility and no thrombus formation [9].
The high preoperative mortality of cardiac rupture [10], and the short interval time from onset of acute MI and cardiac rupture (below 72 h in most of cases), are the limiting factors to establish a timely surgical strategy. Often, the LVFWR occurs out of the hospital or in the clinical department where obtaining a diagnosis of cardiac rupture in time is sometimes difficult. Moreover, apart from ED or intensive care unit, ECMO preparation is difficult, or even impossible, in other hospital areas.
In conclusion, to go on ECMO in ED to treat cardiogenic shock due to LVFWR is a valid rescue mean when death is imminent. The current portable ECMO systems allow a relatively rapid haemodynamic stabilization of the patient, so that any other diagnostic procedure could be arranged before operation.
Appendix A. ICVTS on-line discussion
Author: S. Ibrahim Sersar (Department of Cardiothoracic Surgery, Mansoura, 123 Egypt)
eComment: William Harvery was the first to describe LV rupture in 1647. Morgagni reported 11 cases of myocardial rupture at autopsy and he himself died of myocardial rupture [1]. Pericardiocentesis is both a diagnostic and therapeutic option. Aspiration of unclotted blood is considered the most reliable diagnostic tool in subacute LV rupture. Aspiration of a clear serous fluid excludes LV rupture. Pericardiocentesis provides a short term improvement of the hemodynamics [2]. Some studies suggest an association of VFWR with single vessle disease and with first infarction. Both conditions might be related to poorly development collateral circulation. Different opinions have been published about the opportunity to perform coronary angiograms or avoiding this investigation in order to save time and to perform "blind" coronary artery bypass. A coronary angiogram should be promptly performed as soon as pericardial effusion is noted in MI patients, before they deteriorate. Proper revascularization has a positive impact on survival and freedom from angina and our policy is to bypass major vessels with significant stenoses supplying non-infarcted areas. Two specific advantages of knowing the coronary status are seen in the covering technique. The coronary arteries known to be healthy can be covered with minimal risk of needing a CABG in the future; the knowledge of coronary status is of great help in deciding where and how to place the semicontinuous sutures. Our aim is to put a large number of shallow stitches along the whole patch margin [3]. With the advent of tissue adhesives many authors advocate a completely sutureless technique 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. 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, gelatinresorcin formaldehyde is cytotoxic owing to the release of formaldehyde during degration, raising concerns regarding potential long-term complications. 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 oozing. 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. 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. 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. 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 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 catherterization, and only 1 patient was palced on cardiopulmonary bypass because of a posterior tear. Most patients appeared to have sealed the rupture by the time the operation was performed. The five-year follow-up also demonstrated excellent functional status with 100% survival [4]. Biologic glues may be very useful, but there is no free lunch in this world. We should be alert for any patterns of late complications that would suggest that the use of biologic glue has some downsides.
Pseudoaneurysms in patients treated with a glue may arise for many reasons including:
I. Local cell death from toxic products in the glue that lead to tissue breakdown over time.
II. The aortic glue may have stopped bleeding in an area that would have been better served over the long term with a suture than by glue closure (analogous to duct taping an area that should have been bloted together).
III. Patients who would not have survived surgery due to bleeding from coagulopathy and local tissue compromise are now surviving. They may be at more risk for late complications than patients who did not need the glue to get out of the operating room [5].
References
1 Willius FA and Dry TJ. A history of the heart and circulation 1948;Philadelphia: WB Saunder
2 Coma Canella I, Lopez Sendon J, Gonzalez A. Hemodynamic effect of Dobutamine, Dextran and pericardiocentesis in cardiac tamponade following acute myocardial infarction. Am Heart J 1987;114:78
3 Mantovani V, Vanoli D, Chelazzi P, Lepore V, Ferrarese S, Sala A. Post-infarction cardiac rupture: surgical treatment. Eur J Cardiothorac Surg 2002;22:777–80
4 Lachapelle K, deVarennes B, Ergina PL, Cecere R. Sutureless Patch Technique for postinfarction Left Ventricular Rupture. Ann Thorac Surg 2002;74:96–101
5 Downing SW. What are the risks of using biologic glues. Ann Thorac Surg 2003;75:1063–4
Acknowledgments
We are grateful to our perfusionist Mr Teresio Ravasi for his useful technical support.
Footnotes
Poster Session presentation at the 53rd International Congress of the European Society for Cardiovascular Surgery. June 2–5, 2004, Ljubljana, Slovenia.
References
Ikeda N, Yasu T, Kubo N, Hirohara T, Sugowara Y, Kobayashi N, Hashimoto S, Tsuruya Y, Fujii M, Saito M. Effect of reperfusion therapy on cardiac rupture after myocardial infarction in Japanese. Circ J 2004;68:422–6.
Yip HK, Wu CJ, Chang HW, Wang CP, Cheng CI, Chua S, Chen MC. Cardiac rupture complicating acute myocardial infarction in the direct percutaneous coronary intervention reperfusion era. Chest 2003;124:565–71.
Mantovani V, Vanoli D, Chelazzi P, Lepore V, Ferrarese S, Sala A. Post-infarction cardiac rupture: surgical treatment. E J Cardiothorac Surg 2002;22:777–80.
Tanaka K, Sato N, Yasutaka M, Takada S, Takano T, Ochi M, Tanaka S, Tamura K. Clinicopathological characteristics of 10 patients with rupture of both ventricular free wall and septum (double rupture) after myocardial infarction. J Nippon Med SCH 2003;70:21–7.
Baillot R, Pelletier C, Trivino-Marin J, Castonguay Y. Postinfarction ventricular septal defect: delayed closure with prolonged mechanical circulatory support. Ann Thorac Surg 1983;35:138–42.
Birnbaum Y, Chamoun AJ, Anzuini A, Lick SD, Ahmad M, Uretsky BF. Ventricular free wall rupture following acute myocardial infarction. Coron Artery Dis 2003;14:463–70.
von Segesser LK. Cardiopulmonary support and extracorporeal membrane oxygenator for cardiac assist. Ann Thorac Surg 1999;68:672–7.
Doll N, Kiaii B, Borger M, Bucerius J, Kramer K, Schmitt DV, Walther T, Mohr FW. Five-year results of 219 consecutive patients treated with extracorporeal membrane oxygenation for refractory postoperative cardiogenic shock. Ann Thorac Surg 2004;77:151–7.
Smith C, Bellomo R, Raman JS, Matalanis G, Rosalin A, Buckmaster J, Hart G, Silvester W, Gutteridge GA, Smith B, Doolan L, Buxton BF. An extracorporeal membrane oxygenator-based approach to cardiogenic shock in an older population. Ann Thorac Surg 2001;71:1421–7.
Fujimoto K, Kawahito K, Yamaguchi A, Sakuragawa H, Tsuboi J, Yuri K, Tanaka M, Endo H, Adachi H, Ino T. Percutaneous extracorporeal life support for treatment of fatal mechanical complications associated with acute myocardial infarction. Artif Organs 2001;25:1000–3.(Francesco Formica, Fabriz)