Posterior Ventricular Septal Defect Research Articles

'Double patch and glue' technique for early repair of posterior post-infarction ventricular septal defect

A surgical procedure that reduces the recurrence of post-infarction posterior ventricular septal defects is described. This technique is based on a double ventriculotomy without an infarctectomy, the use of two patches, and glue, which is applied between the two patches. Excellent results have been obtained in 18 consecutives patients with this simple and reliable technique.

Post infarction ventricular septal defect – can we do better?✩

To identify predictors of early and late outcome among 117 consecutive patients who underwent postinfarction ventricular septal defect (VSD) repair over a period of 12 years. A retrospective analysis of clinical data was performed. Mean age was 65.5+/-7.8. There were 43 females. Full data were obtained in 110 patients. Of these, 76 patients presented with anterior and 34 with posterior VSD. Thirty-three patients were operated in cardiogenic shock. Mean time between myocardial infarction (MI) and VSD development was 5.6+/-7.8 days (median 4) and from VSD to surgery 9. 0+/-28.1 (median 2). Sixty-six patients had intraaortic balloon pump (IABP) inserted, and 15 were ventilated preoperatively. Logistic regression and Cox regression were used for multivariate analysis. Thirty days mortality was 37%. Among 110 patients, in whom complete analysis was possible, 38 died within 30 days (35%). Mortality in the posterior VSD group was 35% and in the anterior VSD group 34% (NS). In 44 patients (40%) a residual shunt was found on postoperative echocardiography. This required reoperation in 13 patients (four deaths). Cardiogenic shock prior to surgery adversely influenced early survival - odds ratio (OR) 5.7 (confidence interval (CI) 2.1-16.0) (P=0.0008). Deterioration of haemodynamic status in between admission and surgery was stronger predictor of mortality than shock on admission - OR 6.0 (CI 1.6-22.6) (P=0.008) vs. 3.1 (CI 1.0-9.3) (P=0.049). A longer time between MI and surgery favoured survival - OR 0.1 (CI 0.03-0.4) (P=0.002). The time period from the infarct to the septal rupture, but not from the rupture to surgery, appeared to be a significant predictor of survival - OR 0.2 (CI 0. 05-0.6) (P=0.008). Five years survival was 46+/-5%. Preoperative cardiogenic shock affected late survival - OR 2.7 (CI 1.5-4.9) (P=0. 001). Of 72 patients who survived 30 postoperative days, 12 (17%) were in New York Heart Association (NYHA) class III or IV and five (6.9%) in Canadian Cardiovascular Soceity (CCS) class III or IV at the last follow-up. Preoperative cardiogenic shock and early postinfarction septal rupture carry a grave prognosis. Achieving haemodynamic stability prior to surgery may be beneficial but prolonged attempts to improve patients' cardiovascular state are hazardous.

Surgical repair of postinfarction ventricular septal defect by infarct exclusion.

Repair of postinfarction ventricular septal defect (VSD) by infarct exclusion has been used for a decade in our unit. It involves securing a glutaraldehyde-preserved bovine pericardial patch to the endocardium of the left ventricle all around the necrotic myocardium to exclude the VSD and the infarct from the left ventricular cavity. Fifty-two patients with postinfarction VSD underwent this type of repair from 1987 to 1996. Thirty-four patients were in shock when undergoing operation; 26 had anterior VSD and 26 had posterior. Ten patients died perioperatively, for surgical mortality of 19%. Three patients developed recurrent VSD; one died and two survived. Preoperative cardiogenic shock and age older than 70 years were associated with an increased operative mortality. Operative survivors were followed up from 6 to 135 months, mean of 65 months. The actuarial survival at 8 years was 59% +/- 6%. Repair of postinfarction VSD by infarct exclusion is a relatively simple operative procedure and seems to have improved the results of surgery in patients with posterior VSD.

Sandwich repair with two sheets of equine pericardial patch for acute posterior post-infarction ventricular septal defect.

A 74-year-old man, who had posterior post-infarction ventricular septal defect, was treated successfully by early surgical repair with a sandwich technique involving two sheets of equine pericardial patch. In this technique the ventricular septal defect (VSD) was exposed through a trans-infarction approach. The inside patch covered the VSD and ventriculotomy from the inside. The outside patch generously covered the infarcted myocardium. The two patches completely sandwiched the infarcted myocardium including the VSD and ventriculotomy with eighteen interrupted sutures. This technique ensures strong fixation of the VSD, reducing the risk of bleeding and recurrence of VSD, and also maintains the proper shape and size of the left ventricle without the danger of ventricular aneurysm formation.

Transaxial Repair of Postinfarction Posterior Ventricular Septal Defect

Repair of a postinfarction posterior ventricular septal defect generally has been performed by ventriculotomy in the infarct zone. This approach carries a significant mortality and morbidity from hemorrhage, extending infarction, or further compromise of ventricular function secondary to suture placement. A successful transatrial repair of a postinfarction posterior ventricular septal defect is presented. The simplicity of this operation and the patient's rapid recovery contrasted remarkably with the transventricular approach used in previous patients.

Repair of complete atrioventricular canal in infancy

AbstractResults of operative repair of complete atrioventricular canal defects (CAVCD) are improving due to: general advances in pre‐, intra‐, and postoperative care; a better understanding of the relevant pathological factors, principally of the left atrioventricular (A‐V) valve; a clearer definition of the path of the specialized conduction tissue; and the recognition of associated defects such as single left ventricular papillary muscles, ventricular hypoplasia, with or without malalignment of the common A‐V valve, coexistent ventricular septal defects, and double orifice left A‐V valves. Forty‐eight patients underwent repair from July 1980 through July 1984. Three patients died early and 2 late after the operation. One patient with an additional posterior ventricular septal defect (VSD) remained in complete heart block. Three patients required reoperation for residual left A‐V valve regurgitation and 1 for a residual VSD. In 20 recatheterized patients, mitral regurgitation was moderate in 4 and severe in 2. Pulmonary artery pressure (pulmonary/systemic arterial systolic pressure ratio) remained unchanged in only 1 patient with significant A‐V valve regurgitation. To avoid the development of pulmonary vascular obstructive disease, and based also on the trend of decreasing operative mortality and morbidity rates, primary repair of CAVCD is recommended within the first year of life.

Axial cineangiographic evaluation of the posterior ventricular septal defect

The posterior or inlet ventricular septal defect may occur as an isolated anomaly or in combination with other defects. Axial clneanglography is the best means to delineate the anatomy of this defect as well as to exclude the presence of other ventricular septal defects. The posterior ventricular septal defect can be recognized in the four chamber view by obliteration of the septum by contrast medium flowing across the defect. Anterosuperior extension into the perimembranous region is identified by obliteration of the septum In the long axial oblique view. The presence of a posterior ventricular septal defect can be suspected on the basis of a two dimensional echocardiogram or electrocardiographic left axis deviation. When this is the case, the four chamber view should be performed first so that contrast material in the liver blood pool from a previous injection does not interfere with image quality.

Surgical treatment of post-myocardial infarction ventricular septal defects

Ventricular septal defect (VSD) following myocardial infarction has long been recognized as a lethal complication of severe coronary artery disease. Between 1969 and 1978, 13 patients underwent operative repair of post-myocardial infarction VSDs associated with large left-to-right shunts and markedly impaired left ventricular performance. Emergency cardiac catheterization in 12, coronary cineangiography in 11, and operative repair in 13 were performed 1 to 15 days after ventricular septal perforation. The surgical approach consisted of left ventricular aneurysmectomy or infarctectomy with VSD repair and with coronary revascularization when indicated. Survival could not be predicted on the basis of preoperative hemodynamics, extent of coronary artery disease, age, time from the appearance of the VSD or myocardial infarction to definitive surgical therapy, or preoperative functional class. There were six survivors, all of whom had anterior septal defects. All but one of the nonsurvivors had posterior VSDs. The one patient who died with anterior VSD had the highest left-to-right shunt--2.6 L/min/m2. Emergency operative repair of acute post-myocardial infarction VSD is warranted in this high-risk group of patients who otherwise have little chance of survival.

Posterior Rupture of the Interventricular Septum after Acute Myocardial Infarction: Successful Early Surgical Repair

A patient with a large posterior ventricular septal defect complicating an acute inferior myocardial infarction is reported. Because of medically intractable biventricular failure, temporary circulatory assistance was initiated using intraaortic balloon pumping. Emergency coronary angiography, ventriculography, and subsequent operation were carried out. Operative repair involved closure of the septal defect with the use of a Dacron patch, infarctectomy, and aortocoronary bypass grafting and resulted in long-term survival of the patient.

Surgical injury to the conduction system in ventricular septal defect

The conduction systems of 9 hearts with ventricular septal defect coming to autopsy after open heart surgery were studied by serial section. In 2 cases severe A-V block was present; in 2, complete right bundle branch block; and in the remainder there was no clinical evidence of A-V block after surgery. The severe A-V block in both cases could be ascribed to injury of the penetrating portion of the A-V bundle. An alternate explanation in 1 case was the injury to the branching bundle and the posterior radiation of the left bundle branch. The right bundle branch block in 2 cases for which a postoperative electrocardiogram was available was associated with severe injury to the right bundle. In double outlet right ventricle with an anterior ventricular septal defect, the branching portion of the A-V bundle may lie considerably to the left of the summit of the ventricular septum as in some cases of tetralogy. In a case of double outlet right ventricle with a massive posterior ventricular septal defect, the conduction system resembled that of common A-V orifice or single ventricle.