Complete myocardial revascularization and sutureless technique for left ventricular free wall rupture: clinical and echocardiographic result
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《交互式心脏血管和胸部手术》
Department of Cardiac Surgery, Ospedale Civile di Legnano, Via Candiani 2, 20025 Legnano (MI), Italy
Abstract
Left ventricular free wall rupture (LVFWR) is one of the most dramatic complications of myocardial infarction. We present our mid-term clinical and echocardiographic results of LVFWR with patch and complete myocardial revascularization on viable tissue. From August 2000 to July 2005, 9 patients underwent surgery for LVFWR. Mean age was 68±S.D. 9.3 years. Mean interval time between AMI and LVFWR was 122.2±154.9 h. All patients presented for emergency surgery with cardiac tamponade at echocardiography. Three patients received IABP preoperatively. Eight had coronarography. Effective control of bleeding was achieved in all cases with a Teflon patch applied with Bioglue?. Four patients had myocardial revascularization, all in ECC; two of them with cross-clamping. There was no operative death. Mean follow-up was 38.8±22.2 S.D. months. One further death occurred from myocardial infarction. All patients were in NYHA I–II. Survivors had follow-up transthoracic echocardiography: all patients had preserved left ventricular function with absence of restricted motion. There was no evidence of mitral regurgitation. Sutureless covering technique for LVFWR is related to excellent early and long-term clinical and echocardiographic results. Complete coronary artery bypass grafting improves long-term symptom-free survival. We have demonstrated that ECC and cross-clamping do not affect early survival.
Key Words: Myocardial infarction; Cardiac rupture; Cardiac surgery; Cardiac tamponade
1. Introduction
Left ventricular free wall rupture (LVFWR) is a well-recognized complication of myocardial infarction. Clinical studies reported a frequency of 1 to 4% of patients after myocardial infarction [1], while in an autopsy study this complication occurred in 7–24% [1]. Surgical repair is the only life-treating option, accounting for an operative mortality between 24 and 35% [2].
The most appropriate surgical management remains controversial because each report's experience in treating this pathology is very small, so no one revealed unequivocal results. Many different surgical approaches have been proposed in literature: infarctectomy and ventricle reconstruction with patch [3], interrupted pledged sutures, reinforced linear Teflon strips, glutaraldehyde-treated bovine pericardial patch secured to the heart with biological glues utilizing or not anchoring epicardial sutures [3].
We here describe our experience and follow-up in 9 patients adopting the sutureless technique, using a Teflon patch and biological glue to treat postinfarction LVFWR.
2. Patients and methods
2.1. Patients
This study is a follow-up series of nine patients (mean age 68±S.D. 9.3 years; range 53–79) referred for surgery for LVFWR after transmural myocardial infarction from August 2000 to July 2005. Four patients were male. Table 1 shows patients data and pre-operative clinical status. The mean interval between myocardial infarction (MI) and rupture was 122.2±154.9 h (range 12–432). In one patient (11.1%) the LVFWR followed the first MI. Four patients (patient # 1, 4, 5) received thrombolysis according to the ACC/AHA guidelines [4]. Eight patients (88.9%) underwent coronary angiography, only one patients was excluded from this clinical diagnosis for hemodynamic instability. Six patients (75%) underwent coronary angiography before LVFWR, two (25%) after diagnosis for relatively hemodynamic stability was reached with inotropic agents. Three-vessel disease was present in three patients (37.5%), two-vessel disease in one patient (12.5%) and single-vessel disease in four patients (50%). Three patients (33.3%) received percutaneous transluminal coronary angioplasty on the culpit lesion (patient # 4, 5, 7) according to the criteria of the ACC/AHA [4].
Clinical diagnosis was based on the sign of cardiac tamponade, persistent pain. In all patients the diagnosis was made first by transthoracic echocardiography. All patients had pericardial effusion and sign of cardiac tamponade. Clinical signs of cardiac tamponade were observed in 5 patients (5.6%), 4 had cardiogenic shock and one patient (# 4) had atrio-ventricular block needing an intraventricular pace-maker.
Once diagnosed, all patients received volume support and inotropic therapy (dobutamine preferentially and dopamine, 5–7 /kg/min). Three patients (30%) received an intra-aortic balloon pump preoperatively.
2.2. Surgical management
Median sternotomy was performed in all patients. In all an obvious area of necrosis with an epicardial hematoma in the area of infarction was identified. All patients demonstrated only minor oozing. The location of the site was the free wall of the left ventricle in all cases, occurring at the following sites: infero-apical in two patients (22.2%) and postero-lateral in seven (77.8%). All operative data are shown in Table 2 and discussed above. Cardiopulmonary bypass was instituted in 7 patients (mean time 94.3±57.1 h) because of exsanguination, hemodynamic collapse, to locate the tear or to reach graftable vessels. In two of them the extracorporeal circulation was established with femoro-femoral bypass to raise hemodynamic stability before pericardial opening. In all cases, an elliptical patch of polytetrafluoroethylene felt (Teflon; PTFE felt, Boston Scientific, Meadox Medical Inc, Oakland, NJ) was fashioned to be circumferentially 1 cm larger than the macroscopical area of hematoma and muscle necrosis such that the whole perimeter of the patch lies on healthy myocardium and the area of the infarct is covered.
The patch was placed over the infarcted area and then soaked with biocompatible glue (Byoglue?, Cryolife?, Inc., Kennesaw, GA, USA). After 2 to 3 min the patch is firm and hemostatic.
Three cases (patients # 3, 7, 9) were operated with heart arrest utilizing Buckberg protocol (mean time 57.7±43.9 min): in patient # 3 it was impossible to obtain complete cessation of bleeding with beating heart, in the other patients clamping of the aorta was needed to perform anastomosis in difficult to reach diseased vessels.
In addition to patch/glue repair of the rupture, four patients (44.4%) underwent concomitant coronary artery grafting to obtain complete revascularization of diseased vessels supplying non-infarcted area; in two patients (# 1, 6) distal anastomoses were performed with beating heart during ECC, and in the others during cross clamp.
2.3. Follow-up
Follow-up information was obtained by direct contact with the patient and post-mortem reports. Follow-up on November 30, 2005 was 100% complete (mean follow-up: 38.8±22.2 months, range: 9–63). Survivors were invited for transthoracic echocardiography organized specifically for the purpose of this study.
2.4. Statistical analysis
Statistical analysis was performed with SPSS statistical package (SPSS Inc). All means in the text are expressed as ±S.D. mean. Univariate analysis was performed with the Fisher exact test. Two-tailed Student's t-test was used for statistical analysis of continuous variables. Statistical significance was determined at a P-value less than 0.05.
3. Results
Neither on-table nor operative (30-day) deaths occurred. No patients required IABP insertion post-operatively; the three patients with preoperative IABP maintained it for 2.3±0.9 days after surgery. Complications that occurred and length of hospital stay are listed in Table 3.
During follow-up one patient (# 5) died of AMI 35 months after surgery. On follow-up all patients were free from angina, six were in NYAH class I (75% of survivors) and two in class II.
In Table 4 are shown: the mean left ventricular ejection fraction (LVEF), left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic dimension (LVESD), mitral regurgitation (MR) and New York Heart Association (NYHA) functional class collected at discharge and at follow-up. Variations without statistical significance were observed for all the echocardiographic findings analyzed and the NYHA functional class data between the two time spans. So it was not possible to demonstrate restriction of left ventricular free wall motion, evolution towards left ventricular dilatation or left ventricular aneurismal formation during the follow-up. Dynamic function was preserved in all patients. There was no evidence of mitral regurgitation improvement in any of the patients during the follow-up period.
It was not possible to identify the patch on transtoracic echo.
4. Discussion
Surgical treatment of ventricular rupture has varied over time and is often individualized depending on the state of the tear and the presence of concomitant lesions. Two clinico-pathological entities are described: the ‘oozing’ type characterized by a smaller tear, which may be temporarily sealed by a clot or fibrinous pericardial adhesion; the ‘blow-out’ characterized by sudden recurrent chest pain, electrical mechanical dissociation, shock and death within a few minutes due to massive hemorrhages into the pericardial cavity.
In literature there is not univocity in considering those as two different anatomo-pathologic entities or as two stages of the same process: first moderate pericardic effusion (oozing) and a later progression to full-blown condition (blow-out). We consider that all the blow-out postinfarction free wall ruptures followed a subacute course, according to Padro et al. [5] who used the term of ‘subacute rupture’ to describe this event. In our five years clinical experience we had only the ‘oozing’ type rupture. Considering what was above mentined, it could be reasonably related to a correct thrombolytic timing and a prompt diagnosis in high-risk patients. Myocardial rupture occurs in the region of transmural myocardial necrosis, usually after extensive conversion of a bland infarct into a hemorrhagic infarct, so thrombolysis timing plays an important role in the evolution toward LVFWR. Honan and coworkers [6] performed a meta-analysis of four large clinical trials concluding that the risk of cardiac rupture was directly related to late thrombolytic therapy (after 17 h). Our Hospital's thrombolysis management is in accordance to the ACC/AHA guidelines and a rapid rupture diagnosis could be the reason why we had no ‘blow-out’ rupture.
Traditional LVFWR repair techniques, such as infarctectomy and ventricular reconstruction with patch, interrupted pledged sutures, reinforced linear Teflon strips are reported and advocated by some authors [7], if the rupture is of ‘blow-out’ type and is related to a higher mortality rate ranging from 35 to 61% [8]. In contrast to those, the sutureless epicardial patch technique represents an alternative option demonstrating better outcome results controlling hemorrhage [9] in the case of ‘oozing rupture’ compared to the above-mentioned techniques which demonstrated excellent surveillance [8]. Biological glue transforms the patch and the underlying epicardium and myocardium into a single, resistant tissue so that the infarcted myocardium near the rupture is reinforced. Due to the high adhesive power of the glue, a large contact surface is not necessary, therefore the patch in contact with the rupture can have a relatively small dimension. The sutureless option demonstrates distinct advantages as simplicity, speedy and theoretically preserves the ventricular geometry compared with distortion that can result from linear plication [10], or from ventricular remodelling [11]. In conclusion, the limitations of the biological glues are that they are only effective in the absence of active bleeding. So glues should be used if the tear is sealed or the lesion is of the oozing type [8].
We have reported our experience utilizing the sutureless technique to repair postinfarction LVFWR in 9 unselected patients. All patients who demonstrated an ‘oozing’ type rupture with concomitant ventricular septal defect or papillary muscle rupture were excluded.
The most important diagnostic tool for LVFWR is transthoracic echocardiography, with sensitivity and specificity of the diagnosis between 93 and 98% [13]. Data on segmental contractility can help in predicting the lesion.
We prefer to remove the pericardial effusion in the operating theater, once it is diagnosed, because this procedure can cause a dangerous increase in blood pressure, which consequently produces more tension on the lesioned myocardium, and resulting dramatically in increasing the tear diameter in a closed chest. We prefer using a rational administration of inotropic support to improve hemodynamic disbalance. Intra-aortic balloon pump should be used preoperatively in hemodynamically unstable patients with acute myocardial infarction. The balloon pump decreases after load, end-systolic pressure, and myocardial oxygen demand, thus preventing wall rupture and evolution of myocardial necrosis [13], three patients in our cohort of patients needed the IABP preoperatively, and the others after operation.
Different opinions are published regarding the opportunity to perform coronary angiograms [14] or avoiding this investigation to save time and eventually to perform a ‘blind’ coronary artery bypass grafting. We believe that cardiac catheterization is indicated in stable patients even when LVWFR is suspected, before they deteriorate. It is difficult to know if such a rupture will allow enough time to accomplish this objective safely. But we believe, like other authors [15], that a prompt angiographic exam giving the coronary status, results in a proper revascularization related to a positive impact on survival and freedom from angina. It should be also considered that, as demonstrated by Mantovani [15], this clinical entity is not strictly related to a single diseased vessel, in our experience almost half of the patients demonstrated multiple coronaropathy. Our policy is to bypass the majority of diseased vessels supplying the non-infarcted area.
Our first choice is complete myocardial revascularization in the non-infarcted area without cardiopulmonary bypass. Some reports demonstrated that off-pump sutureless epicardial repair contributes positively to the outcome, but we believe in the importance of complete myocardial revascularization improving mid- and long-term mortality and morbidity. The necessity for circulatory support of CPB or with cross-clamping, when indispensable, should be individualized and depends on the hemodynamic state of the patient, the location of the tear and the coronary anatomy of graftable vessels just to achieve complete myocardial grafting on viable myocardium.
No hemodynamic mitral regurgitation was present preoperatively in our patients; postoperatively no one developed moderate or severe mitral insufficiency. We could not find in the literature specific addresses to this topic, and our suggestion is not to treat mitral regurgitation unless its moderate grade is moderate or more.
We had no 30-day mortality. Only one death at follow-up was shown. On follow-up all survival patients were free from angina and in New York Heart Association functional class between I and II, however not increased over time. Transtoracic echocardiography confirmed that the patch was intact, the visual examination was used to screen for regional wall motion abnormalities, no restricted left ventricular free wall motion was noted and dynamic function was preserved in all patients. There was no evidence of mitral regurgitation in any patient. Despite the limitation of the retrospective approach and small number of patients, our study shows that clinical outcome in the case of subacute left ventricle free wall rupture could be improved by prompt diagnosis, emergent surgical treatment and complete myocardial revascularization, regardless of the utilization of CPB and cross-clamping.
In conclusion, surgical repair of post-ischemic ventricular free wall rupture is related to acceptable early mortality and excellent long term results. In other reports the recommended choice is a less aggressive approach with epicardial patching and off-clamping myocardial revascularization of the non-infarcted area. We have demonstrated that complete coronary artery bypass grafting improves long term symptom-free survival and ‘on-pump’ and the cross-clamping technique does not affect early mortality. So cardiopulmonary bypass with cross-clamping should be suggested to achieve complete myocardial revascularization.
References
Pollak H, Nobis H, Mlczoch J. Frequency of left ventricular free wall rupture complicating acute myocardial infarction since the advent of thrombolysis. Am J Cardiol Jul 15, 1994; 74:184–186.
Lopez Sendon J, Gonzales A, Lopez de Sa E, Coma-Canella I, Roldan I, Dominguez F, Maqueda I, Martin Jadrague L. Diagnosis of subacute ventricular wall rupture after acute myocardial infarction: sensitivity and specificity of clinical, hemodynamic and echocardiographic criteria. J Am Coll Cardiol May 1992; 19:1145–1153.
Kirklin JW. Left ventricular aneurysm. In: Kirklin JW, Barrat-Boyes BG. eds. Cardiac Surgery 1993;New York: Churchill Livingstone 398: 383–402. In:.
American College of Cardiology/American Heart Association Guidelines for the Management of Patients With Acute Myocardial Infarction – part VI (6.3.1.6.4.). Approved by ACC: May 7, 2004. Approved by AHA: May 5, 2004 Antman EM.
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 Jan 1993; 55:20–23. discussion 23–24.
Honan MB, Harrell Jr FE, Reimer KA, Califf RM, Mark DB, Pryor DB, Hlatky MA. Cardiac rupture, mortality and timing of thrombolytic therapy: a meta-analysis. J Am Coll Cardiol 1990; 16:359.
Pretre R, Benedikt P, Turina MI. Experience with postinfarction left ventricular free wall rupture. Ann Thorac Surg May 2000; 69:1342–1345.
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.
Feneley MP, Chang VP, O'Rourke MF. Myocardial rupture after acute myocardial infarction. Ten year review. Br Heart J Jun 1983; 49:550–556.
McMullan MH, Kilgore Jr TL, Dear Jr HD, Hindman SH. Sudden blowout rupture of the myocardium after infarction: urgent management. Report of four cases. J Thorac Cardiovasc Surg Feb 1985; 89:259–263.
Sinatra R, Macrina F, Braccio M, Melina G, Luzi G, Ruvolo G, Marino B. Left ventricular aneurysmectomy; comparison between two techniques; early and late results. Eur J Cardiothorac Surg Aug 1997; 12:291–297.
Imagawa H, Nakano S, Akagi H, Yagura A, Fujita T. Pericardial hood repair of cardiac rupture secondary to extended myocardial infarction. Ann Thorac Surg Jun 2000; 69:1959–1960.
Pollak H, Diez W, Spiel R, Enenkel W, Mlczoch J. Early diagnosis of subacute free wall rupture complicating acute myocardial infarction. Eur Heart J May 1993; 14:640–648.
Figueras J, Juncal A, Carballo J, Cortadellas J, Soler JS. Nature and progression of pericardial effusion in patients with a first myocardial infarction: relationship to age and free wall rupture. Am Heart J Aug 2002; 144:251–258.
Mantovani V, Vanoli D, Chelazzi P, Lepore V, Ferrarese S, Sala A. Post-infarction cardiac rupture: surgical treatment. Eur J Cardiothorac Surg Nov 2002; 22:777–780.(Cristian Leva, Pier Giorg)
Abstract
Left ventricular free wall rupture (LVFWR) is one of the most dramatic complications of myocardial infarction. We present our mid-term clinical and echocardiographic results of LVFWR with patch and complete myocardial revascularization on viable tissue. From August 2000 to July 2005, 9 patients underwent surgery for LVFWR. Mean age was 68±S.D. 9.3 years. Mean interval time between AMI and LVFWR was 122.2±154.9 h. All patients presented for emergency surgery with cardiac tamponade at echocardiography. Three patients received IABP preoperatively. Eight had coronarography. Effective control of bleeding was achieved in all cases with a Teflon patch applied with Bioglue?. Four patients had myocardial revascularization, all in ECC; two of them with cross-clamping. There was no operative death. Mean follow-up was 38.8±22.2 S.D. months. One further death occurred from myocardial infarction. All patients were in NYHA I–II. Survivors had follow-up transthoracic echocardiography: all patients had preserved left ventricular function with absence of restricted motion. There was no evidence of mitral regurgitation. Sutureless covering technique for LVFWR is related to excellent early and long-term clinical and echocardiographic results. Complete coronary artery bypass grafting improves long-term symptom-free survival. We have demonstrated that ECC and cross-clamping do not affect early survival.
Key Words: Myocardial infarction; Cardiac rupture; Cardiac surgery; Cardiac tamponade
1. Introduction
Left ventricular free wall rupture (LVFWR) is a well-recognized complication of myocardial infarction. Clinical studies reported a frequency of 1 to 4% of patients after myocardial infarction [1], while in an autopsy study this complication occurred in 7–24% [1]. Surgical repair is the only life-treating option, accounting for an operative mortality between 24 and 35% [2].
The most appropriate surgical management remains controversial because each report's experience in treating this pathology is very small, so no one revealed unequivocal results. Many different surgical approaches have been proposed in literature: infarctectomy and ventricle reconstruction with patch [3], interrupted pledged sutures, reinforced linear Teflon strips, glutaraldehyde-treated bovine pericardial patch secured to the heart with biological glues utilizing or not anchoring epicardial sutures [3].
We here describe our experience and follow-up in 9 patients adopting the sutureless technique, using a Teflon patch and biological glue to treat postinfarction LVFWR.
2. Patients and methods
2.1. Patients
This study is a follow-up series of nine patients (mean age 68±S.D. 9.3 years; range 53–79) referred for surgery for LVFWR after transmural myocardial infarction from August 2000 to July 2005. Four patients were male. Table 1 shows patients data and pre-operative clinical status. The mean interval between myocardial infarction (MI) and rupture was 122.2±154.9 h (range 12–432). In one patient (11.1%) the LVFWR followed the first MI. Four patients (patient # 1, 4, 5) received thrombolysis according to the ACC/AHA guidelines [4]. Eight patients (88.9%) underwent coronary angiography, only one patients was excluded from this clinical diagnosis for hemodynamic instability. Six patients (75%) underwent coronary angiography before LVFWR, two (25%) after diagnosis for relatively hemodynamic stability was reached with inotropic agents. Three-vessel disease was present in three patients (37.5%), two-vessel disease in one patient (12.5%) and single-vessel disease in four patients (50%). Three patients (33.3%) received percutaneous transluminal coronary angioplasty on the culpit lesion (patient # 4, 5, 7) according to the criteria of the ACC/AHA [4].
Clinical diagnosis was based on the sign of cardiac tamponade, persistent pain. In all patients the diagnosis was made first by transthoracic echocardiography. All patients had pericardial effusion and sign of cardiac tamponade. Clinical signs of cardiac tamponade were observed in 5 patients (5.6%), 4 had cardiogenic shock and one patient (# 4) had atrio-ventricular block needing an intraventricular pace-maker.
Once diagnosed, all patients received volume support and inotropic therapy (dobutamine preferentially and dopamine, 5–7 /kg/min). Three patients (30%) received an intra-aortic balloon pump preoperatively.
2.2. Surgical management
Median sternotomy was performed in all patients. In all an obvious area of necrosis with an epicardial hematoma in the area of infarction was identified. All patients demonstrated only minor oozing. The location of the site was the free wall of the left ventricle in all cases, occurring at the following sites: infero-apical in two patients (22.2%) and postero-lateral in seven (77.8%). All operative data are shown in Table 2 and discussed above. Cardiopulmonary bypass was instituted in 7 patients (mean time 94.3±57.1 h) because of exsanguination, hemodynamic collapse, to locate the tear or to reach graftable vessels. In two of them the extracorporeal circulation was established with femoro-femoral bypass to raise hemodynamic stability before pericardial opening. In all cases, an elliptical patch of polytetrafluoroethylene felt (Teflon; PTFE felt, Boston Scientific, Meadox Medical Inc, Oakland, NJ) was fashioned to be circumferentially 1 cm larger than the macroscopical area of hematoma and muscle necrosis such that the whole perimeter of the patch lies on healthy myocardium and the area of the infarct is covered.
The patch was placed over the infarcted area and then soaked with biocompatible glue (Byoglue?, Cryolife?, Inc., Kennesaw, GA, USA). After 2 to 3 min the patch is firm and hemostatic.
Three cases (patients # 3, 7, 9) were operated with heart arrest utilizing Buckberg protocol (mean time 57.7±43.9 min): in patient # 3 it was impossible to obtain complete cessation of bleeding with beating heart, in the other patients clamping of the aorta was needed to perform anastomosis in difficult to reach diseased vessels.
In addition to patch/glue repair of the rupture, four patients (44.4%) underwent concomitant coronary artery grafting to obtain complete revascularization of diseased vessels supplying non-infarcted area; in two patients (# 1, 6) distal anastomoses were performed with beating heart during ECC, and in the others during cross clamp.
2.3. Follow-up
Follow-up information was obtained by direct contact with the patient and post-mortem reports. Follow-up on November 30, 2005 was 100% complete (mean follow-up: 38.8±22.2 months, range: 9–63). Survivors were invited for transthoracic echocardiography organized specifically for the purpose of this study.
2.4. Statistical analysis
Statistical analysis was performed with SPSS statistical package (SPSS Inc). All means in the text are expressed as ±S.D. mean. Univariate analysis was performed with the Fisher exact test. Two-tailed Student's t-test was used for statistical analysis of continuous variables. Statistical significance was determined at a P-value less than 0.05.
3. Results
Neither on-table nor operative (30-day) deaths occurred. No patients required IABP insertion post-operatively; the three patients with preoperative IABP maintained it for 2.3±0.9 days after surgery. Complications that occurred and length of hospital stay are listed in Table 3.
During follow-up one patient (# 5) died of AMI 35 months after surgery. On follow-up all patients were free from angina, six were in NYAH class I (75% of survivors) and two in class II.
In Table 4 are shown: the mean left ventricular ejection fraction (LVEF), left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic dimension (LVESD), mitral regurgitation (MR) and New York Heart Association (NYHA) functional class collected at discharge and at follow-up. Variations without statistical significance were observed for all the echocardiographic findings analyzed and the NYHA functional class data between the two time spans. So it was not possible to demonstrate restriction of left ventricular free wall motion, evolution towards left ventricular dilatation or left ventricular aneurismal formation during the follow-up. Dynamic function was preserved in all patients. There was no evidence of mitral regurgitation improvement in any of the patients during the follow-up period.
It was not possible to identify the patch on transtoracic echo.
4. Discussion
Surgical treatment of ventricular rupture has varied over time and is often individualized depending on the state of the tear and the presence of concomitant lesions. Two clinico-pathological entities are described: the ‘oozing’ type characterized by a smaller tear, which may be temporarily sealed by a clot or fibrinous pericardial adhesion; the ‘blow-out’ characterized by sudden recurrent chest pain, electrical mechanical dissociation, shock and death within a few minutes due to massive hemorrhages into the pericardial cavity.
In literature there is not univocity in considering those as two different anatomo-pathologic entities or as two stages of the same process: first moderate pericardic effusion (oozing) and a later progression to full-blown condition (blow-out). We consider that all the blow-out postinfarction free wall ruptures followed a subacute course, according to Padro et al. [5] who used the term of ‘subacute rupture’ to describe this event. In our five years clinical experience we had only the ‘oozing’ type rupture. Considering what was above mentined, it could be reasonably related to a correct thrombolytic timing and a prompt diagnosis in high-risk patients. Myocardial rupture occurs in the region of transmural myocardial necrosis, usually after extensive conversion of a bland infarct into a hemorrhagic infarct, so thrombolysis timing plays an important role in the evolution toward LVFWR. Honan and coworkers [6] performed a meta-analysis of four large clinical trials concluding that the risk of cardiac rupture was directly related to late thrombolytic therapy (after 17 h). Our Hospital's thrombolysis management is in accordance to the ACC/AHA guidelines and a rapid rupture diagnosis could be the reason why we had no ‘blow-out’ rupture.
Traditional LVFWR repair techniques, such as infarctectomy and ventricular reconstruction with patch, interrupted pledged sutures, reinforced linear Teflon strips are reported and advocated by some authors [7], if the rupture is of ‘blow-out’ type and is related to a higher mortality rate ranging from 35 to 61% [8]. In contrast to those, the sutureless epicardial patch technique represents an alternative option demonstrating better outcome results controlling hemorrhage [9] in the case of ‘oozing rupture’ compared to the above-mentioned techniques which demonstrated excellent surveillance [8]. Biological glue transforms the patch and the underlying epicardium and myocardium into a single, resistant tissue so that the infarcted myocardium near the rupture is reinforced. Due to the high adhesive power of the glue, a large contact surface is not necessary, therefore the patch in contact with the rupture can have a relatively small dimension. The sutureless option demonstrates distinct advantages as simplicity, speedy and theoretically preserves the ventricular geometry compared with distortion that can result from linear plication [10], or from ventricular remodelling [11]. In conclusion, the limitations of the biological glues are that they are only effective in the absence of active bleeding. So glues should be used if the tear is sealed or the lesion is of the oozing type [8].
We have reported our experience utilizing the sutureless technique to repair postinfarction LVFWR in 9 unselected patients. All patients who demonstrated an ‘oozing’ type rupture with concomitant ventricular septal defect or papillary muscle rupture were excluded.
The most important diagnostic tool for LVFWR is transthoracic echocardiography, with sensitivity and specificity of the diagnosis between 93 and 98% [13]. Data on segmental contractility can help in predicting the lesion.
We prefer to remove the pericardial effusion in the operating theater, once it is diagnosed, because this procedure can cause a dangerous increase in blood pressure, which consequently produces more tension on the lesioned myocardium, and resulting dramatically in increasing the tear diameter in a closed chest. We prefer using a rational administration of inotropic support to improve hemodynamic disbalance. Intra-aortic balloon pump should be used preoperatively in hemodynamically unstable patients with acute myocardial infarction. The balloon pump decreases after load, end-systolic pressure, and myocardial oxygen demand, thus preventing wall rupture and evolution of myocardial necrosis [13], three patients in our cohort of patients needed the IABP preoperatively, and the others after operation.
Different opinions are published regarding the opportunity to perform coronary angiograms [14] or avoiding this investigation to save time and eventually to perform a ‘blind’ coronary artery bypass grafting. We believe that cardiac catheterization is indicated in stable patients even when LVWFR is suspected, before they deteriorate. It is difficult to know if such a rupture will allow enough time to accomplish this objective safely. But we believe, like other authors [15], that a prompt angiographic exam giving the coronary status, results in a proper revascularization related to a positive impact on survival and freedom from angina. It should be also considered that, as demonstrated by Mantovani [15], this clinical entity is not strictly related to a single diseased vessel, in our experience almost half of the patients demonstrated multiple coronaropathy. Our policy is to bypass the majority of diseased vessels supplying the non-infarcted area.
Our first choice is complete myocardial revascularization in the non-infarcted area without cardiopulmonary bypass. Some reports demonstrated that off-pump sutureless epicardial repair contributes positively to the outcome, but we believe in the importance of complete myocardial revascularization improving mid- and long-term mortality and morbidity. The necessity for circulatory support of CPB or with cross-clamping, when indispensable, should be individualized and depends on the hemodynamic state of the patient, the location of the tear and the coronary anatomy of graftable vessels just to achieve complete myocardial grafting on viable myocardium.
No hemodynamic mitral regurgitation was present preoperatively in our patients; postoperatively no one developed moderate or severe mitral insufficiency. We could not find in the literature specific addresses to this topic, and our suggestion is not to treat mitral regurgitation unless its moderate grade is moderate or more.
We had no 30-day mortality. Only one death at follow-up was shown. On follow-up all survival patients were free from angina and in New York Heart Association functional class between I and II, however not increased over time. Transtoracic echocardiography confirmed that the patch was intact, the visual examination was used to screen for regional wall motion abnormalities, no restricted left ventricular free wall motion was noted and dynamic function was preserved in all patients. There was no evidence of mitral regurgitation in any patient. Despite the limitation of the retrospective approach and small number of patients, our study shows that clinical outcome in the case of subacute left ventricle free wall rupture could be improved by prompt diagnosis, emergent surgical treatment and complete myocardial revascularization, regardless of the utilization of CPB and cross-clamping.
In conclusion, surgical repair of post-ischemic ventricular free wall rupture is related to acceptable early mortality and excellent long term results. In other reports the recommended choice is a less aggressive approach with epicardial patching and off-clamping myocardial revascularization of the non-infarcted area. We have demonstrated that complete coronary artery bypass grafting improves long term symptom-free survival and ‘on-pump’ and the cross-clamping technique does not affect early mortality. So cardiopulmonary bypass with cross-clamping should be suggested to achieve complete myocardial revascularization.
References
Pollak H, Nobis H, Mlczoch J. Frequency of left ventricular free wall rupture complicating acute myocardial infarction since the advent of thrombolysis. Am J Cardiol Jul 15, 1994; 74:184–186.
Lopez Sendon J, Gonzales A, Lopez de Sa E, Coma-Canella I, Roldan I, Dominguez F, Maqueda I, Martin Jadrague L. Diagnosis of subacute ventricular wall rupture after acute myocardial infarction: sensitivity and specificity of clinical, hemodynamic and echocardiographic criteria. J Am Coll Cardiol May 1992; 19:1145–1153.
Kirklin JW. Left ventricular aneurysm. In: Kirklin JW, Barrat-Boyes BG. eds. Cardiac Surgery 1993;New York: Churchill Livingstone 398: 383–402. In:.
American College of Cardiology/American Heart Association Guidelines for the Management of Patients With Acute Myocardial Infarction – part VI (6.3.1.6.4.). Approved by ACC: May 7, 2004. Approved by AHA: May 5, 2004 Antman EM.
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 Jan 1993; 55:20–23. discussion 23–24.
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