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1/16. Post-infarction ventricular septal defect: percutaneous transvenous temporary closure using a Swan-Ganz catheter.

    We report on a case of temporary closure of a post-infarction ventricular septal defect (VSD) using a Swan-Ganz catheter through a femoral transvenous approach. This resulted in substantial improvement in the hemodynamic status of the patient. Six hr later, the patient underwent surgery for VSD closure. When immediate surgical intervention is not possible, it may be helpful to stabilize the patient until surgery can be performed. Thus, such a treatment has potential as a temporary measure for patients awaiting surgical repair of post-infarction VSD.
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2/16. Transatrial repair of ventricular septal rupture under preoperative localization by transesophageal echocardiography.

    We report about a 71-year-old woman with postinfarction ventricular septal rupture who was successfully treated by the transatrial closure under preoperative localization by transesophageal echocardiography. In an attempt at transatrial repair of the ventricular septal rupture, the most important thing is preoperative localization of the defect in the septum, which is located high and posterior, where it is smooth with relatively few trabeculations and can be readily exposed by retraction of the tricuspid valve.
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3/16. review of ventricular rupture: key concepts and diagnostic tools for success.

    Although a rare complication of acute myocardial infarction (AMI), ventricular rupture is a serious event associated with significant mortality and morbidity. patients normally present with hemodynamic instability, often in cardiogenic shock. Despite improvements in surgical techniques and diagnostic tools, post-myocardial infarction ventricular rupture remains a difficult therapeutic challenge. There are three categories of ventricular rupture: free wall rupture (FWR), ventricular septal rupture (VSR), and papillary muscle rupture (PWR). The incidence of FWR occurs following up to 10% of myocardial infarctions. VSR and PWR have a lower incidence of 1-2% and 0.5-5%, respectively. patients often present with single-vessel coronary artery disease and usually do not have a positive history for a previous myocardial infarction. The incidence of post infarction angina in these patients is significantly greater than in patients without ventricular rupture. Delay in treatment and continued physical activity post infarction increases the risk of ventricular rupture. Diagnostic tools such as two-dimensional echocardiography and cardiac catheterization confirm the diagnosis of ventricular rupture in only 45-88% of cases. knowledge of the disease progression is necessary to insure accurate and timely diagnosis. Due to the rapid deterioration of these patients, there is a 50-80% mortality rate within the first week if untreated. With surgical correction, patients can extend their 5-year survival rates to 65%. A good example of the complex course of ventricular rupture is the case of a 71-year-old patient at our institution. The patient presented in cardiogenic shock following an AMI. Preoperative diagnosis was unsuccessful in determining the extent of the ventricular rupture. The correct diagnosis was determined in the operating room, and both a mitral valve replacement and closure of a ventricular septal defect were completed. The patient was successfully treated with this difficult pathology.
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4/16. Repair of a postinfarct ventricular septal defect on the beating heart. Surgical considerations.

    Postinfarct ventricular septal defect (VSD) still remains associated with a high mortality and morbidity. Despite the development of modern surgical techniques and medical care it continues to be a difficult therapeutic challenge. This report describes a case of a 70-year-old female patient, who presented with a postinfarct VSD after having anterior wall infarction. She presented with left heart failure, pulmonary hypertension and left to right shunt of 78% (Qp/Qs=4.3). The patient was operated on using cardiopulmonary bypass on the beating heart. The closure was performed with a Dacron-patch and a single bypass to the diagonal branch using the left internal thoracic artery. Postoperatively the patient did well and was discharged in good condition on the 13th postoperative day. We conclude that postinfarction VSD can be repaired on cardiopulmonary bypass avoiding cross-clamping. This method is helpful for the outcome as well as for the early postoperative recovery of elderly patients.
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5/16. Spontaneous closure of an acquired ventricular septal defect.

    Ventricular septal defect (VSD) is a rare but serious complication of acute myocardial infarction requiring early surgical intervention. A patient with acquired VSD that spontaneously closed over three months is presented. The literature on spontaneous closure of acquired VSDs is also reviewed.
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6/16. Double-patch closure using gelatin resorcine formol glue of a ventricular septal perforation following acute myocardial infarction.

    Complete closure is most important when attempting acute-phase closure of a ventricular septal perforation following acute myocardial infarction. Here, we present a case of a 76-year-old male with a ventricular septal perforation following acute myocardial infarction. The ventricular septal perforation was repaired by stitching small and large bovine pericardial patches onto the affected septum from the side of the left ventricle, then cementing the two patches together with gelatin resorcine formol glue injected into the space between them. Complete closure of the ventricular septal perforation was accomplished. Simultaneously, right coronary artery bypass grafting was performed using a saphenous vein. The postoperative course was uneventful, and the patient was discharged, with a favorable post-discharge course for 24 months to date after surgery.
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keywords = closure
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7/16. Compassionate use of the amplatzer ASD closure device for residual postinfarction ventricular septal rupture following surgical repair.

    We report successful transcatheter closure of a post-MI ventricular septal rupture acutely following unsuccessful surgical repair. Catheter closure was accomplished by the use of a 26-mm Amplatzer atrial septal occluder. Initial attempts to close the defect with the use of 28-mm and 33-mm CARDIOSEAL were unsuccessful. Closure technique, immediate and long-term follow-up outcomes are reported.
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8/16. Transcatheter closure of a ruptured ventricular septum following inferior myocardial infarction and cardiogenic shock.

    Elective transcatheter closure of congenital septal defects has emerged as a valuable method, but the clinical experience on occlusion of ventricular septal rupture after myocardial infarction is very limited. We report a case of fatal outcome in a patient with inferior myocardial infarction and cardiogenic shock despite technically successful transcatheter closure of a large complex ventricular septal defect.
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9/16. Spontaneous closure of postinfarction ventricular septal rupture. A case report.

    Spontaneous closure of a postinfarction ventricular septal rupture is extremely rare. We present such a case in which the postinfarction ventricular septal rupture closed spontaneously during follow-up. We postulate that the spontaneous closure of the ventricular septal rupture was probably due to thrombosis in the apical and septal aneurysm.
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10/16. Subepicardial aneurysm following ventriculotomy closure of ventricular septal rupture due to acute myocardial infarction.

    We report an unusual case of subepicardial aneurysm (SEA) of the left ventricle. An 82-year-old man had undergone patch closure of a ventricular septal rupture due to anterior acute myocardial infarction. A postoperative left ventriculogram showed the presence of contrast medium outside the left ventricle, and urgent surgery was performed. The lesion was diagnosed as SEA, and was repaired before rupture.
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