Ventricular septal defect (VSD) is a rare but deadly mechanical complication of acute myocardial infarction (AMI). Before thrombolysis, post-AMI VSD occurred in as many as 1–3 % of patients. With the advent of early reperfusion strategies, the incidence of this complication has dropped significantly to less than 0.2 %. Septal rupture tends to occur 3–8 days after the AMI, but it may occur within 24 h or as late as 2 weeks afterward. Three mechanisms are reported, which, of course, may merge in individual patients: septal rupture occurring in the first 24 h is usually due to a large intramural hematoma that dissects into the tissue, leading to an abrupt laceration. Later ruptures may result from erosion of the infarcted septal wall (with subsequent tear) by lytic enzymes produced by neutrophils in the infarcted area. A third mechanism involves the formation of a thin septal aneurysm, with perforation occurring in its central portion.

In most patients, the defect consists of a discrete hole with a direct, through-and-through communication across the septum. Complex defects are characterized by serpiginous, convoluted tracts within the necrotic tissue. Less commonly, the post-AMI VSD may be associated with a dissection of the interventricular septum or right ventricular free wall. Septal rupture in a patient with anterior AMI tends to be apical, with a discrete simple hole. In patients with inferoposterior AMI, the defect involves the basal inferoposterior septum and often has a more complex geometry. The size of the defect may vary from few millimeters to several centimeters and is the primary cause of the magnitude of the left-to-right shunt. Large defects lead to the development of right ventricular dysfunction, pulmonary hypertension, congestive heart failure, low cardiac output, and fatal cardiogenic shock. Some decades ago, there was a tendency to treat patients with post-AMI VSD nonsurgically in the acute phase. A waiting period of 3–6 weeks was supposed to be necessary to allow the necrotic and friable margins of the defect to be replaced by robust connective tissue that would be more receptive to sutures. The mortality rate with this strategy was as high as 50 % at 1 week and up to 94 % at 1 month. Even apparently stable patients with small defects, when treated conservatively, may experience an unpredictable deterioration (due to extension of the defect, abrupt right ventricular failure, or both) leading to cardiogenic shock and death. Thus, current American and European guidelines suggest immediate operative intervention regardless of the patient’s clinical status. In the past two decades, developments in myocardial protection, improved prosthetic materials, and refined surgical techniques (i.e., infarctectomy, excision of all necrotic and friable margins, and reconstruction of the ventricular septum with Dacron patches) have certainly contributed to an improved surgical outcome (Fig. 7.1).

Inotropic support and, when necessary, the use of intra-aortic balloon counterpulsation may stabilize the patient during transportation or preparation for surgery. Coronary artery bypass grafting is recommended for patients with multivessel coronary artery disease. Although in-hospital mortality is significantly lower than with conservative management, it remains as high as 47 % after surgery (see GUSTO trial), and dehiscence of the patch requiring a second operation is not infrequent because the sutures may tear out of the friable support around the defect.

In today’s era of percutaneous interventions, some patients may benefit from catheter-based percutaneous closure of the septal rupture, but the role of percutaneous intervention in these patients is yet to be clarified. Unlike closure of congenital VSD, percutaneous closure of post-AMI VSD has several drawbacks. Although the procedure does not require the direct manipulation of the necrotic tissue surrounding the defect, any attempt to pass the stiff closure device through the defect may tear its fragile borders and thus increase the size of the hole. In patients with very basal defects, positioning and expanding the device may impinge on tricuspid or mitral valve leaflets, causing an unacceptable valve malfunction. Finally, in patients with inferior/posterior AMI, the septal rupture is usually near the base of the right and left ventricular free wall, which may be at least partially involved in the necrotic process; when the device is expanded, it may place excessive tension on the free wall, with risk of further tearing and defect expansion, or free wall distortion and rupture.

Currently, percutaneous closure is considered a valid alternative to surgical repair in patients with small to medium VSDs, in whom the occlusion device may provide a definitive treatment. Conversely, patients with very large defects should undergo immediate operation because of a high risk of device embolization. The procedure may also be accomplished in patients with residual leak after surgical closure, as bridge to a safer surgical correction, or in patients with unacceptable surgical risk because of age, comorbidity, or end-organ dysfunction.

Two-dimensional transthoracic/transesophageal echocardiographic (TTE/TEE) color Doppler provides the most rapid diagnosis by demonstrating a discontinuity in the ventricular septum with left-to-right shunt. Color Doppler may discover the abnormal shunt from the left ventricle to the right ventricle even when the anatomic grey-scale image does not show any distinct interruption in the septal contour. The scanning plane may in fact not correspond to the site of the defect, which can be revealed only by nonconventional, off-axis planes. Furthermore, the size and the shape of the defect are difficult to appreciate with a tomographic technique. In this respect, three-dimensional (3D) TEE and 3D color Doppler appear to be very valuable tools in showing the defect as it anatomically is—a hole through the septum.

This chapter reviews the 3D TEE anatomy of the ventricular septum, 3D TEE imaging of post-AMI VSDs, and the current use of 3D TEE during percutaneous closure with catheter-based devices.