Post myocardial infarction left ventricular free wall rupture
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《血管的通路杂志》
a Department of Cardiothoracic Surgery, Glasgow Royal Infirmary, 16 Alexandra Parade, Glasgow G31 2ER, UK
b Department of Cardiothoracic Surgery, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, UK
Abstract
Occurrence of left ventricular free wall rupture following myocardial infarction is an unpredictable event associated with very high mortality rate. The most appropriate surgical approach remains controversial. With recent advances in portable echocardiography machines there has been a progressive rise in the number of cases of left ventricular free wall rupture diagnosed and reported. Early diagnosis and expeditious relief of tamponade followed by emergency surgery could save many lives. We present a review of six patients treated at our institute for ventricular free wall rupture over the last ten years. A literature review of the optimal management strategy follows. All patients were operated using cardiopulmonary bypass. Two patients died following surgery. Intra-aortic balloon pump was used in all patients. One patient had coronary artery bypass grafting empirically based on palpable disease in the epicardial coronary arteries. None of the surviving patients showed any evidence of neurological deficit. We advocate tailoring the type of repair to the status of the tear at the time of operation.
Key Words: Myocardial infarction; Ventricular free wall rupture
1. Introduction
In recent years major advances in the management of myocardial infarction (MI), including thrombolysis and primary percutaneous intervention, has dramatically improved the outcome [1,2]. However, mortality due to left ventricular (LV) free wall rupture as a complication of MI continues to be high [1,2]. Hence prompt diagnosis and surgical treatment of this condition has gained increasing significance. Accessibility of portable echocardiography coupled with greater awareness of the condition has allowed antemortem diagnosis and emergency operative repair in some cases.
The experience of any surgical team in dealing with this catastrophic complication is likely to be limited. We present six cases that underwent operative repair during the last ten years at our institute and review the literature on the current status of diagnosis and management.
2. Material and methods
2.1. Patients
January 1996 to December 2005 six patients underwent surgical repair of left ventricular free wall rupture post MI. There were three males and three females. Mean age was 61 years (range, 44–71 years). None of the patients had a past history of MI. Four patients had a history of hypertension. Three patients had a history of angina. Only one patient had a history of treatment with thrombolytic agents.
2.2. Clinical presentation, diagnosis and initial management
In four patients rupture developed within 24 h of MI. In one patient it developed on day two and in one patient on day three following admission with chest pain.
The clinical presentation was with cardiogenic shock in Accident and Emergency in four patients. One patient was admitted in coronary care with history and electrocardiographic findings suggestive of acute myocardial infarction. He was thrombolysed and was responding well to treatment. On day three he deteriorated suddenly and had a cardiac arrest. He was successfully resuscitated and an echocardiographic diagnosis of left ventricular free wall rupture was made. One patient was admitted to coronary care with angina and on day two developed unexplained hypotension. Echocardiography revealed fluid in the pericardial cavity with tamponade.
The diagnosis was made on echocardiography in five patients and was noticed at the time of operation in one patient (preoperative diagnosis was aortic dissection). One patient had cardiac catheterisation performed as part of assessment. It revealed severe acute aortic regurgitation and echocardiography reported a suspicious aortic root with a large expanding pericardial effusion. A computed tomography scan raised doubts of aortic dissection with pericardial effusion.
Echocardiography showed normal left ventricular (LV) function (EF50%) in one, an impaired function (EF30–49%) in three and poor (EF<29%) LV function in two patients (Table 1).
All patients were haemodynamically unstable at the time of diagnosis and were treated with fluids, ionotropes and vasoconstrictors. Two patients were treated with pericardiocentesis (one in accident and emergency within 30 min of presentation) for urgent relief of tamponade. Two patients were on IABP (intraortic balloon pump) preoperatively. In the remaining patients IABP was inserted in the operating room after the completion of the surgical procedure
2.3. Surgical procedure
All patients underwent surgery immediately after the rupture was diagnosed. The rupture was localised to anterolateral wall in three, anteroapical in one, inferolateral in one patient and posterior wall in one patient. Only one patient was found to have a blow-out type of rupture while the remaining patients had an oozing type of ventricular wall rupture.
A midline sternotomy was performed. Blood and clots were evacuated from the pericardial cavity followed by establishment of cardiopulmonary bypass (CPB). One patient had massive bleeding on opening the pericardium, which necessitated volume replacement and urgent establishment of CPB. In all but one patient the aorta was cross-clamped and antegrade cardioplegia administered. In one patient the operative repair was undertaken on beating perfused heart.
In the patient with a preoperative diagnosis of dissecting thoracic aneurysm (Type A), intraoperative findings were of a normal aorta with a large haemorrhagic inferolateral infarct. An area of epicardial haematoma surrounding the tear was found in all patients. In three patients the tear was actively oozing while in the remaining three it appeared to have been sealed by the overlying clot. Excision of the infarct and direct closure with interrupted mattress sutures reinforced with Teflon was performed in two patients. In one patient direct closure (without infarct excision) with interrupted pledgetted horizontal mattress sutures was combined with coronary artery bypass grafting to four target vessels (venous grafts). In this patient patchy disease was palpable in all major epicardial arteries and the venous grafts were performed empirically. In one patient a two-layer plication of the LV aneurysm using horizontal mattress sutures through strips of Teflon on either side was performed.
A sutureless glue repair was carried out in one patient. In one patient an autologous pericardial patch closure was performed. The patch was secured to surrounding myocardium with continuous running non-pledgetted prolene sutures. A liberal spray of Tissel glue under the patch towards the end of the procedure was performed. In both these patients compression was applied by the surgeon's fingers after spraying the glue.
3. Results
All patients were successfully weaned from bypass. Two patients died in the postoperative period in the intensive care unit (ICU). Both died within 48 h of surgery due to low output syndrome.
The longest hospital stay following surgery was 12 days (mean nine days). Most of the patients required 2–3 units of blood transfusion except one patient where 13 units of blood were transfused. This patient had prolonged ICU and longest hospital stay. Longest CPB time was 163 min and shortest was 36 min. Ischemia time ranged from 0–42 min. One patient was operated on CPB without cross clamping the aorta. IABP was used in all patients. In two patients it was inserted preoperatively to stabilise haemodynamics. In the rest of the patients IABP was inserted electively before coming off CPB. The longest duration of IABP use (110 h) was in the patient with the longest duration of ischemia time. The same patient had longest ICU and longest hospital stay. Shortest duration (24 h) of IABP use was in the patient who was operated on CPB with warm perfused heart (Table 2).
None of the patients were reopened for bleeding complications. Left ventricular pseudoaneurysms were not detected by echocardiography in any of the surviving patients. None of the surviving patients had any evidence of residual neurologic deficit.
4. Discussion
Left ventricular rupture is usually a fatal complication following MI. Several autopsy series have accurately defined this entity [1,2]. Approximately 4% of myocardial infarctions will develop ventricular free wall rupture [2,3]. It accounts for 12–21% of deaths following myocardial infarction [2,3]. Animal studies on biomechanical strength of myocardium after MI has shown that the myocardium regains its normal strength after about seven days [3,4]. It correlates with the fact that the incidence of rupture was highest in the first seven days following MI [4]. Sometimes rupture of ventricular septum or papillary muscle was associated with ventricular free wall rupture [2].
The reported incidence is increasing with wider availability of noninvasive diagnostic modalities [3]. Common sites of rupture are the anterior or lateral walls [4]. According to Batts et al. [4] a midventricular position along the apex to base axis is most frequent (66%). Four morphologic types of rupture have been described [5]. Type I has little dissection or infiltration of the myocardium. Type II has a multicanalicular trajectory with extensive myocardial dissection. Type III rupture is protected either by a thrombus sitting at the orifice on the ventricular side or by pericardial adhesion. Type IV rupture is incomplete as the trajectory does not traverse through all layers. Various other terms such as blow-out and ooze rupture have been used but these pathologic variations could be easily fitted into the above classification [3].
Usually the patients are older females with long history of hypertension [4]. In our series all but one patient were 60 years or older with no history of past MI which is consistent with the characteristic features described previously [3,4]. There was no female preponderance as described in previous series [4]. The clinical presentation could be with chest pain or with features of cardiac tamponade often with frank electromechanical dissociation [3]. A high index of clinical suspicion coupled with urgent portable echocardiography could clinch the diagnosis. Other investigations like transthoracic echocardiography, cineventriculography and technetium pyrophosphate scanning, though reported to be helpful in diagnosis were more of academic interest [3]. Patients' clinical situations do not usually allow such detailed evaluation.
The role of thrombolysis and reperfusion is controversial [6,7]. Some studies showed that thrombolysis had no impact on the incidence of rupture [6]. Nakamura et al. [7], on the other hand, found a lower incidence of rupture (1.7% vs. 2.7%) in patients receiving thrombolysis. Reperfusion therapy might also decrease the incidence of late rupture (after four days) [3,7]. In our series five patients had not received thrombolysis, which supported the findings of Nakmura et al. [7].
Emergency surgery is usually the only therapeutic option available. However, the most appropriate surgical procedure remains controversial. Successful surgical treatment of this condition was first reported in literature in 1972 [8]. Any individual surgeon will have very limited experience in managing this condition.
The surgical therapy was aimed at urgent relief of tamponade and closure of ventricular wall defect [9]. Several different techniques have been described in the literature [10,11]. These include direct closure without excision; excision of infarct segment and direct closure or closure using a prosthetic or autologous patch [10,11]. Recent reports suggest that the conventional technique of infarctectomy might be avoided and a more conservative approach can give equally good results [3,12]. Simple mattress sutures buttressed with Teflon felt can achieve haemostasis [12]. The suture line in all cases should be along the nonischemic area and deep preferably trasmural stitches are required which can lead to further deterioration in ventricular function due to damage to the nonischemic myocardium [13]. If sutures are placed in the necrotic myocardium, myocardial tearing can occur [13]. The technique described by Nunez et al. [14] was adopted in one of our patients with excellent results. In this technique the patch covering the area of infraction was anchored to normal myocardium with continuous running sutures taking shallow bites through the epicardium and through the superficial layers of myocardium [14]. Myocardial damage could be minimal by this technique [13,14].
Availability of tissue adhesive materials allows a sutureless patch technique of repair for oozing type of rupture [9,13]. The glue should be able to provide reliable sealing with high adhesive strength [13]. A wide range of synthetic and biological glues are available for this purpose e.g. fibrin glues, gelatin based glues and cyanoacrylate glue [9]. Several authors have reported good clinical results using tissue adhesive materials to get the pericardial patch or Dacron patch glued to the oedematous friable myocardium [9,13,15]. The advantage of this technique is that it avoids taking sutures through the friable myocardium and it can be done without cardiopulmonary bypass [9]. Some authors recommend fixing the patch with running sutures, even with the glue technique, as it can be more effective in achieving haemostasis and is more likely to prevent rerupture than sutureless techniques [13]. The obvious limitation of the sutureless technique is that it can only be used in cases of oozing type of rupture [9]. Sutureless repair should be avoided in patients with blow-out rupture [15]. Besides, the glue covers over an area of infarct which cannot be resected or excluded. As this tends to be a large diffuse area it may continue to evolve and extend so rupturing or forming an aneurysm later. Several authors have raised concerns about the risk of recurrent rupture and pseudoaneurysm formation with the sutureless techniques [13]. An elective intraoperative insertion of IABP could avoid these complications particularly when a sutureless technique is used [13]. The IABP reduces wall stress and should limit infarct extension and reduce intracavitary pressure [13]. Use of IABP is advocated even in the absence of haemodynamic instability [13].
Repair of defects on the anterior and lateral walls, the most common types encountered, can be achieved with simple closure without cardiopulmonary bypass [3]. A detailed coronary angiography and coronary artery bypass grafting could be performed later [3].
Batts et al. [4] reported that 80% of patients who underwent post-mortem examination had multivessel disease with severe obstruction of at least one major coronary artery. Thus there is a strong theoretical indication for revascularisation in these patients, which might potentially improve the long-term prognosis [3]. A preoperative angiography in such critically ill patients is not advisable [3]. Repairing the ventricular defect and empirically performing CABG based on palpable disease in the coronary artery, as was done in one patient in our series, is a controversial therapeutic option [3]. The other option of quickly relieving the tamponade and repairing the defect without revascularisation is preferred by many other surgeons [13]. Due to the small number of patients involved there are no data to support either approach. The surgeons using sutureless technique should be aware that if a patient required CABG later, identification and exposure of coronary arteries could be difficult due to the wide and deep pile of collagen haemostats [13]. A careful follow up was required as some of these patients will develop ventricular aneurysm or pseudoaneurysm at the site of patch repair [3,4].
5. Conclusion
Left ventricular free wall rupture though uncommon is a catastrophic complication of MI associated with high mortality rate. Surgical techniques to deal with this complication vary and there are no standard guidelines. Due to the widespread availability of portable echocardiography machines more cases were being reported. Patients with an oozing type of rupture located on lateral or anterolateral wall can be treated with sutureless techniques often without cardiopulmonary bypass. Patients with a blow out type of rupture or actively squirting lesions would require a sutured approach. Long term follow up is necessary as there is a risk of formation of ventricular aneurysm or pseudoaneurysm.
References
Zilcher H, Glogar D. Non arrhythmogenic sudden death as complication of coronary heart disease. Acta Med Austriaca 1979; 6:59–66.
Reddy SG, Roberts WC. 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 Apr 15, 1989; 63:906–911.
Sutherland FW, Guell FJ, Pathi VL, Naik SK. Postinfarction ventricular free wall rupture: strategies for diagnosis and treatment. Ann Thorac Surg Apr 1996; 61:1281–1285.
Batts KP, Ackermann DM, Edwards WD. Postinfarction rupture of the left ventricular free wall: clinicopathologic correlates in 100 consecutive autopsy cases. Hum Pathol May 1990; 21:530–535.
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 Vaiss Mar 1987; 80:336–344.
Pedro PG, Pereirinha A, Fiuza M, Correia LC, Dias E, Pinto F, Carvalho M, Vega J, Silva Z, Lacerda A. Thrombolysis in acute myocardial infarction in the aged. A greater risk of cardiac rupture Rev Port Cardiol Feb 1991; 10:133–139.
Nakamura F, Minamino T, Higashino Y, Ito H, Fujii K, Fujita T, Nagano M, Higaki J, Ogihara T. Cardiac free wall rupture in acute myocardial infarction: ameliorative effect of coronary reperfusion. Clin Cardiol Apr 1992; 15:244–250.
Montegut FJ Jr. Left ventricular rupture secondary to myocardial infarction. Report of survival with surgical repair. Ann Thorac Surg Jul 1972; 14:75–78.
Muto A, Nishibe T, Kondo Y, Sato M, Yamashita M, Ando M. Sutureless repair with TachoComb sheets for oozing type postinfarction cardiac rupture. Ann Thorac Surg Jun 2005; 79:2143–2145.
Anagnostopoulos E, Beutler S, Levett JM, Lawrence JM, Lin CY, Replogle RL. Myocardial rupture. Major left ventricular infarct rupture treated by infarctectomy. J Am Med Assoc Dec 19, 1977; 238:2715–2716.
Stiegel M, Zimmern SH, Robicsek F. Left ventricular rupture following coronary occlusion treated by streptokinase infusion: successful surgical repair. Ann Thorac Surg Oct 1987; 44:413–415.
Chemnitius JM, Schmidt T, Wojcik J, Ruschewski W, Kreuzer H, Tebbe U. Successful surgical management of left ventricular free wall rupture in the course of myocardial infarction. Eur J Cardiothorac Surg 1991; 5:51–55.
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 Jan 2001; 71:201–204.
Nunez L, de la Llana R, Lopez Sendon J, Coma I, Gil Aguado M. Diagnosis and treatment of subacute free wall ventricular rupture after infarction. Ann Thorac Surg May 1983; 35:525–529.
Padro JM, Mesa JM, Silvestre J, Larrea JL, Caralps JM, Cerron F, Aris A. Subacute cardiac rupture: repair with a sutureless technique. Ann Jan 1993; 55:20–24.(Pankaj Kumar Mishra,, Vivek Pathi and An)
b Department of Cardiothoracic Surgery, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, UK
Abstract
Occurrence of left ventricular free wall rupture following myocardial infarction is an unpredictable event associated with very high mortality rate. The most appropriate surgical approach remains controversial. With recent advances in portable echocardiography machines there has been a progressive rise in the number of cases of left ventricular free wall rupture diagnosed and reported. Early diagnosis and expeditious relief of tamponade followed by emergency surgery could save many lives. We present a review of six patients treated at our institute for ventricular free wall rupture over the last ten years. A literature review of the optimal management strategy follows. All patients were operated using cardiopulmonary bypass. Two patients died following surgery. Intra-aortic balloon pump was used in all patients. One patient had coronary artery bypass grafting empirically based on palpable disease in the epicardial coronary arteries. None of the surviving patients showed any evidence of neurological deficit. We advocate tailoring the type of repair to the status of the tear at the time of operation.
Key Words: Myocardial infarction; Ventricular free wall rupture
1. Introduction
In recent years major advances in the management of myocardial infarction (MI), including thrombolysis and primary percutaneous intervention, has dramatically improved the outcome [1,2]. However, mortality due to left ventricular (LV) free wall rupture as a complication of MI continues to be high [1,2]. Hence prompt diagnosis and surgical treatment of this condition has gained increasing significance. Accessibility of portable echocardiography coupled with greater awareness of the condition has allowed antemortem diagnosis and emergency operative repair in some cases.
The experience of any surgical team in dealing with this catastrophic complication is likely to be limited. We present six cases that underwent operative repair during the last ten years at our institute and review the literature on the current status of diagnosis and management.
2. Material and methods
2.1. Patients
January 1996 to December 2005 six patients underwent surgical repair of left ventricular free wall rupture post MI. There were three males and three females. Mean age was 61 years (range, 44–71 years). None of the patients had a past history of MI. Four patients had a history of hypertension. Three patients had a history of angina. Only one patient had a history of treatment with thrombolytic agents.
2.2. Clinical presentation, diagnosis and initial management
In four patients rupture developed within 24 h of MI. In one patient it developed on day two and in one patient on day three following admission with chest pain.
The clinical presentation was with cardiogenic shock in Accident and Emergency in four patients. One patient was admitted in coronary care with history and electrocardiographic findings suggestive of acute myocardial infarction. He was thrombolysed and was responding well to treatment. On day three he deteriorated suddenly and had a cardiac arrest. He was successfully resuscitated and an echocardiographic diagnosis of left ventricular free wall rupture was made. One patient was admitted to coronary care with angina and on day two developed unexplained hypotension. Echocardiography revealed fluid in the pericardial cavity with tamponade.
The diagnosis was made on echocardiography in five patients and was noticed at the time of operation in one patient (preoperative diagnosis was aortic dissection). One patient had cardiac catheterisation performed as part of assessment. It revealed severe acute aortic regurgitation and echocardiography reported a suspicious aortic root with a large expanding pericardial effusion. A computed tomography scan raised doubts of aortic dissection with pericardial effusion.
Echocardiography showed normal left ventricular (LV) function (EF50%) in one, an impaired function (EF30–49%) in three and poor (EF<29%) LV function in two patients (Table 1).
All patients were haemodynamically unstable at the time of diagnosis and were treated with fluids, ionotropes and vasoconstrictors. Two patients were treated with pericardiocentesis (one in accident and emergency within 30 min of presentation) for urgent relief of tamponade. Two patients were on IABP (intraortic balloon pump) preoperatively. In the remaining patients IABP was inserted in the operating room after the completion of the surgical procedure
2.3. Surgical procedure
All patients underwent surgery immediately after the rupture was diagnosed. The rupture was localised to anterolateral wall in three, anteroapical in one, inferolateral in one patient and posterior wall in one patient. Only one patient was found to have a blow-out type of rupture while the remaining patients had an oozing type of ventricular wall rupture.
A midline sternotomy was performed. Blood and clots were evacuated from the pericardial cavity followed by establishment of cardiopulmonary bypass (CPB). One patient had massive bleeding on opening the pericardium, which necessitated volume replacement and urgent establishment of CPB. In all but one patient the aorta was cross-clamped and antegrade cardioplegia administered. In one patient the operative repair was undertaken on beating perfused heart.
In the patient with a preoperative diagnosis of dissecting thoracic aneurysm (Type A), intraoperative findings were of a normal aorta with a large haemorrhagic inferolateral infarct. An area of epicardial haematoma surrounding the tear was found in all patients. In three patients the tear was actively oozing while in the remaining three it appeared to have been sealed by the overlying clot. Excision of the infarct and direct closure with interrupted mattress sutures reinforced with Teflon was performed in two patients. In one patient direct closure (without infarct excision) with interrupted pledgetted horizontal mattress sutures was combined with coronary artery bypass grafting to four target vessels (venous grafts). In this patient patchy disease was palpable in all major epicardial arteries and the venous grafts were performed empirically. In one patient a two-layer plication of the LV aneurysm using horizontal mattress sutures through strips of Teflon on either side was performed.
A sutureless glue repair was carried out in one patient. In one patient an autologous pericardial patch closure was performed. The patch was secured to surrounding myocardium with continuous running non-pledgetted prolene sutures. A liberal spray of Tissel glue under the patch towards the end of the procedure was performed. In both these patients compression was applied by the surgeon's fingers after spraying the glue.
3. Results
All patients were successfully weaned from bypass. Two patients died in the postoperative period in the intensive care unit (ICU). Both died within 48 h of surgery due to low output syndrome.
The longest hospital stay following surgery was 12 days (mean nine days). Most of the patients required 2–3 units of blood transfusion except one patient where 13 units of blood were transfused. This patient had prolonged ICU and longest hospital stay. Longest CPB time was 163 min and shortest was 36 min. Ischemia time ranged from 0–42 min. One patient was operated on CPB without cross clamping the aorta. IABP was used in all patients. In two patients it was inserted preoperatively to stabilise haemodynamics. In the rest of the patients IABP was inserted electively before coming off CPB. The longest duration of IABP use (110 h) was in the patient with the longest duration of ischemia time. The same patient had longest ICU and longest hospital stay. Shortest duration (24 h) of IABP use was in the patient who was operated on CPB with warm perfused heart (Table 2).
None of the patients were reopened for bleeding complications. Left ventricular pseudoaneurysms were not detected by echocardiography in any of the surviving patients. None of the surviving patients had any evidence of residual neurologic deficit.
4. Discussion
Left ventricular rupture is usually a fatal complication following MI. Several autopsy series have accurately defined this entity [1,2]. Approximately 4% of myocardial infarctions will develop ventricular free wall rupture [2,3]. It accounts for 12–21% of deaths following myocardial infarction [2,3]. Animal studies on biomechanical strength of myocardium after MI has shown that the myocardium regains its normal strength after about seven days [3,4]. It correlates with the fact that the incidence of rupture was highest in the first seven days following MI [4]. Sometimes rupture of ventricular septum or papillary muscle was associated with ventricular free wall rupture [2].
The reported incidence is increasing with wider availability of noninvasive diagnostic modalities [3]. Common sites of rupture are the anterior or lateral walls [4]. According to Batts et al. [4] a midventricular position along the apex to base axis is most frequent (66%). Four morphologic types of rupture have been described [5]. Type I has little dissection or infiltration of the myocardium. Type II has a multicanalicular trajectory with extensive myocardial dissection. Type III rupture is protected either by a thrombus sitting at the orifice on the ventricular side or by pericardial adhesion. Type IV rupture is incomplete as the trajectory does not traverse through all layers. Various other terms such as blow-out and ooze rupture have been used but these pathologic variations could be easily fitted into the above classification [3].
Usually the patients are older females with long history of hypertension [4]. In our series all but one patient were 60 years or older with no history of past MI which is consistent with the characteristic features described previously [3,4]. There was no female preponderance as described in previous series [4]. The clinical presentation could be with chest pain or with features of cardiac tamponade often with frank electromechanical dissociation [3]. A high index of clinical suspicion coupled with urgent portable echocardiography could clinch the diagnosis. Other investigations like transthoracic echocardiography, cineventriculography and technetium pyrophosphate scanning, though reported to be helpful in diagnosis were more of academic interest [3]. Patients' clinical situations do not usually allow such detailed evaluation.
The role of thrombolysis and reperfusion is controversial [6,7]. Some studies showed that thrombolysis had no impact on the incidence of rupture [6]. Nakamura et al. [7], on the other hand, found a lower incidence of rupture (1.7% vs. 2.7%) in patients receiving thrombolysis. Reperfusion therapy might also decrease the incidence of late rupture (after four days) [3,7]. In our series five patients had not received thrombolysis, which supported the findings of Nakmura et al. [7].
Emergency surgery is usually the only therapeutic option available. However, the most appropriate surgical procedure remains controversial. Successful surgical treatment of this condition was first reported in literature in 1972 [8]. Any individual surgeon will have very limited experience in managing this condition.
The surgical therapy was aimed at urgent relief of tamponade and closure of ventricular wall defect [9]. Several different techniques have been described in the literature [10,11]. These include direct closure without excision; excision of infarct segment and direct closure or closure using a prosthetic or autologous patch [10,11]. Recent reports suggest that the conventional technique of infarctectomy might be avoided and a more conservative approach can give equally good results [3,12]. Simple mattress sutures buttressed with Teflon felt can achieve haemostasis [12]. The suture line in all cases should be along the nonischemic area and deep preferably trasmural stitches are required which can lead to further deterioration in ventricular function due to damage to the nonischemic myocardium [13]. If sutures are placed in the necrotic myocardium, myocardial tearing can occur [13]. The technique described by Nunez et al. [14] was adopted in one of our patients with excellent results. In this technique the patch covering the area of infraction was anchored to normal myocardium with continuous running sutures taking shallow bites through the epicardium and through the superficial layers of myocardium [14]. Myocardial damage could be minimal by this technique [13,14].
Availability of tissue adhesive materials allows a sutureless patch technique of repair for oozing type of rupture [9,13]. The glue should be able to provide reliable sealing with high adhesive strength [13]. A wide range of synthetic and biological glues are available for this purpose e.g. fibrin glues, gelatin based glues and cyanoacrylate glue [9]. Several authors have reported good clinical results using tissue adhesive materials to get the pericardial patch or Dacron patch glued to the oedematous friable myocardium [9,13,15]. The advantage of this technique is that it avoids taking sutures through the friable myocardium and it can be done without cardiopulmonary bypass [9]. Some authors recommend fixing the patch with running sutures, even with the glue technique, as it can be more effective in achieving haemostasis and is more likely to prevent rerupture than sutureless techniques [13]. The obvious limitation of the sutureless technique is that it can only be used in cases of oozing type of rupture [9]. Sutureless repair should be avoided in patients with blow-out rupture [15]. Besides, the glue covers over an area of infarct which cannot be resected or excluded. As this tends to be a large diffuse area it may continue to evolve and extend so rupturing or forming an aneurysm later. Several authors have raised concerns about the risk of recurrent rupture and pseudoaneurysm formation with the sutureless techniques [13]. An elective intraoperative insertion of IABP could avoid these complications particularly when a sutureless technique is used [13]. The IABP reduces wall stress and should limit infarct extension and reduce intracavitary pressure [13]. Use of IABP is advocated even in the absence of haemodynamic instability [13].
Repair of defects on the anterior and lateral walls, the most common types encountered, can be achieved with simple closure without cardiopulmonary bypass [3]. A detailed coronary angiography and coronary artery bypass grafting could be performed later [3].
Batts et al. [4] reported that 80% of patients who underwent post-mortem examination had multivessel disease with severe obstruction of at least one major coronary artery. Thus there is a strong theoretical indication for revascularisation in these patients, which might potentially improve the long-term prognosis [3]. A preoperative angiography in such critically ill patients is not advisable [3]. Repairing the ventricular defect and empirically performing CABG based on palpable disease in the coronary artery, as was done in one patient in our series, is a controversial therapeutic option [3]. The other option of quickly relieving the tamponade and repairing the defect without revascularisation is preferred by many other surgeons [13]. Due to the small number of patients involved there are no data to support either approach. The surgeons using sutureless technique should be aware that if a patient required CABG later, identification and exposure of coronary arteries could be difficult due to the wide and deep pile of collagen haemostats [13]. A careful follow up was required as some of these patients will develop ventricular aneurysm or pseudoaneurysm at the site of patch repair [3,4].
5. Conclusion
Left ventricular free wall rupture though uncommon is a catastrophic complication of MI associated with high mortality rate. Surgical techniques to deal with this complication vary and there are no standard guidelines. Due to the widespread availability of portable echocardiography machines more cases were being reported. Patients with an oozing type of rupture located on lateral or anterolateral wall can be treated with sutureless techniques often without cardiopulmonary bypass. Patients with a blow out type of rupture or actively squirting lesions would require a sutured approach. Long term follow up is necessary as there is a risk of formation of ventricular aneurysm or pseudoaneurysm.
References
Zilcher H, Glogar D. Non arrhythmogenic sudden death as complication of coronary heart disease. Acta Med Austriaca 1979; 6:59–66.
Reddy SG, Roberts WC. 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 Apr 15, 1989; 63:906–911.
Sutherland FW, Guell FJ, Pathi VL, Naik SK. Postinfarction ventricular free wall rupture: strategies for diagnosis and treatment. Ann Thorac Surg Apr 1996; 61:1281–1285.
Batts KP, Ackermann DM, Edwards WD. Postinfarction rupture of the left ventricular free wall: clinicopathologic correlates in 100 consecutive autopsy cases. Hum Pathol May 1990; 21:530–535.
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 Vaiss Mar 1987; 80:336–344.
Pedro PG, Pereirinha A, Fiuza M, Correia LC, Dias E, Pinto F, Carvalho M, Vega J, Silva Z, Lacerda A. Thrombolysis in acute myocardial infarction in the aged. A greater risk of cardiac rupture Rev Port Cardiol Feb 1991; 10:133–139.
Nakamura F, Minamino T, Higashino Y, Ito H, Fujii K, Fujita T, Nagano M, Higaki J, Ogihara T. Cardiac free wall rupture in acute myocardial infarction: ameliorative effect of coronary reperfusion. Clin Cardiol Apr 1992; 15:244–250.
Montegut FJ Jr. Left ventricular rupture secondary to myocardial infarction. Report of survival with surgical repair. Ann Thorac Surg Jul 1972; 14:75–78.
Muto A, Nishibe T, Kondo Y, Sato M, Yamashita M, Ando M. Sutureless repair with TachoComb sheets for oozing type postinfarction cardiac rupture. Ann Thorac Surg Jun 2005; 79:2143–2145.
Anagnostopoulos E, Beutler S, Levett JM, Lawrence JM, Lin CY, Replogle RL. Myocardial rupture. Major left ventricular infarct rupture treated by infarctectomy. J Am Med Assoc Dec 19, 1977; 238:2715–2716.
Stiegel M, Zimmern SH, Robicsek F. Left ventricular rupture following coronary occlusion treated by streptokinase infusion: successful surgical repair. Ann Thorac Surg Oct 1987; 44:413–415.
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