Postinfarction Ventricular Septal Rupture 

Updated: Sep 17, 2021
Author: Shabir Bhimji, MD, PhD; Chief Editor: Dale K Mueller, MD 

Overview

Practice Essentials

Essential features of ventricular septal rupture (VSR) may be summarized as follows:

  • The rupture typically occurs 3-8 days after an MI.

  • VSR is more likely to occur in the anterior septum than in the posterior septum (60% vs 40%).

  • The most consistent finding is a murmur (see Presentation).

  • The differential diagnosis includes ventricular septal rupture and mitral insufficiency secondary to papillary muscle rupture, papillary muscle dysfunction, or left ventricular dilatation.

  • In the differential diagnosis, exclude MR from papillary muscle rupture.

  • Diagnosis is confirmed with the aid of echocardiography and the presence of a left-to-right shunt (see Workup).

  • Catheterization results help determine the extent of coronary artery disease (CAD).

  • Emergent surgery is necessary but the condition still carries a very high mortality (see Treatment).

  • Today, percutaneous means of closure are available.

Background

Postinfarction ventricular septal rupture (VSR) is a rare but lethal complication of myocardial infarction (MI). The event occurs 2-8 days after an infarction and often precipitates cardiogenic shock.[1] The differential diagnosis of postinfarction cardiogenic shock should exclude free ventricular wall rupture and rupture of the papillary muscles. (See the image below.)

Postinfarction ventricular septal rupture. Ventric Postinfarction ventricular septal rupture. Ventricular septal rupture is defect in interventricular septum (wall dividing left and right ventricles of heart).

To avoid the high morbidity and mortality associated with this disorder, patients should undergo emergency surgical treatment.[2, 3, 4, 5] In current practice, postinfarction VSR is recognized as a surgical emergency, and the presence of cardiogenic shock is an indication for intervention.[6] Long-term survival can be achieved in patients who undergo prompt surgery. Concomitant coronary artery bypass grafting (CABG) may be required. The addition of CABG has helped improve long-term survival.[7, 8]

Surgery is performed via a transinfarction approach, and all reconstruction is performed with prosthetic materials to avoid tension. Developments in myocardial protection and improved prosthetic materials have contributed greatly to successful management of VSR.[9] Improved surgical techniques (eg, infarctectomy) and better perioperative mechanical and pharmacologic support have helped lower mortality. In addition, the development of surgical techniques to repair perforations in different areas of the septum has led to improved results. (should discuss the different techniques)

In current practice, patients undergoing VSR repair tend to be older and are more likely to have received thrombolytic agents, which may complicate repair. After successful repair, survival and quality of life are excellent, even in patients older than 70 years.[10]

For information, news, and CME activities on heart failure, see the Heart Failure Resource Center. For patient education resources, see the Heart Health Center, as well as Ventricular Septal Defect and Heart Attack.

Pathophysiology

The septal blood supply comes from branches of the left anterior descending coronary artery, the posterior descending branch of the right coronary artery, or the circumflex artery when it is dominant. Infarction associated with a ventricular septal rupture (VSR) is usually transmural and extensive. About 60% of VSRs occur with infarction of the anterior wall; 40% with infarction of the posterior or inferior wall (see the image below). Posterior VSR may be accompanied by mitral valve insufficiency secondary to papillary muscle infarction or dysfunction.

Postinfarction ventricular septal rupture. Heart s Postinfarction ventricular septal rupture. Heart sectioned transversely at level of middle left ventricle. Posterior ventricular septal defect is visible at site of recent acute myocardial infarction.

At autopsy, patients with VSR usually show complete coronary artery occlusion with little or no collateral flow. The lack of collateral flow may be secondary to associated arterial disease, anatomic anomalies, or myocardial edema. Sometimes, multiple septal perforations occur. These may occur simultaneously or within several days of each other. See the image below.

Postinfarction ventricular septal rupture. A secti Postinfarction ventricular septal rupture. A section of the ventricle indicating location of the VSR (arrow).

VSR may be either anterior or inferior myocardial infarctions (MIs). Studies show that they occur with equal frequency.[11, 12] The anterior infarcts usually cause an apical VSR, which tend to be small and have a defined edge, making them a little simpler to repair. On the other hand, the inferior VSR usually have a thin and uneven edge which is often necrotic, making repair very difficult.

The natural history of postinfarction VSR is greatly influenced by hypertension, anticoagulation therapy, advanced age, and, possibly, thrombolytic therapy. The natural course in patients with postinfarction VSR is well documented and short. Most patients die within the first week, and almost 90% die within the first year; some reports indicate that fewer than 7% of patients are alive after 1 year.

This grim prognosis results from an acute volume overload exacted on both ventricles in a heart already compromised by a large MI and occasionally by extensive coronary artery disease (CAD) in sites other than that already infarcted. In addition, superimposed ischemic mitral valve regurgitation, a ventricular aneurysm, or a combination of these conditions may be present, further compromising heart function. The depressed left ventricular function commonly leads to impaired peripheral organ perfusion and death in most patients.

A few sporadic reports indicate that some patients with medically treated postinfarction VSR live for several years. Although many medical advances have been made in the nonsurgical treatment of these patients, including intra-aortic balloon counterpulsation (IABCP), these methods have not eliminated the need for surgery.

Etiology

Risk factors for postinfarction ventricular septal rupture (VSR) include the following:

  • Female gender

  • Advanced age

  • Higher Killip class

  • Myocardial infarction (MI) associated with ST segment elevation and elevated cardiac markers

  • Preoperative use of an intra-aortic balloon pump

  • Inferior wall MI

  • Renal failure with dialysis

Most studies show that the left anterior descending and right coronary arteries are chiefly involved in an MI that is associated with VSR.

Epidemiology

Rupture of the interventricular septum is an uncommon complication of MI. Although autopsy studies reveal an 11% incidence of myocardial free-wall rupture after MI, septal-wall perforation is much less common, occurring at a rate of approximately 1-2%.

Ventricular septal rupture (VSR) occurs in a zone of necrotic myocardial tissue, usually within the first 10-14 days. Clinical studies report an average time of 2.6 days from MI to VSR. However, some data suggest that initial treatment of MI with thrombolytics may affect both the time between infarction and VSR and the eventual outcome. Early use of thrombolytic agents may lead to reopening of the occluded vessels, thereby reducing the incidence of VSR.

The age range of patients who sustain a postinfarction VSR is wide, from 44 to 81 years. Men are affected more commonly than women are, though VSR is more common in women than would be predicted on the basis of the prevalence of CAD alone.

Prognosis

Operative mortality is directly related to the interval between MI and surgical repair. In a retrospective analysis of 41 patients treated for postinfarction ventricular septal defect (VSD), Serpytis et al confirmed that whereas female sex, advanced age, arterial hypertension, anterior-wall acute MI, absence of previous acute MI, and late arrival at hospital were associated with a higher risk of mortality from acute VSD, the time from the onset of acute MI to operation was the most important factor determining operative mortality and intrahospital survival.[13]

If repair of a postinfarction ventricular septal rupture (VSR) is performed 3 weeks or more after the infarction, mortality is approximately 20%; if it is performed before this time, mortality approaches 50%. The most obvious reason for this is that the greater the degree of myocardial damage and hemodynamic compromise, the more urgent the need for early intervention or the patients being repaired survived and were self selected.

With the use of an early operative approach, most studies show an overall mortality of less than 25%. Mortality tends to be lower for patients with anteriorly located VSRs and lowest for patients with apical VSRs. For anterior defects, mortality ranges from 10% to 15%; for posterior defects, mortality ranges from 30% to 35%.

More than 50% of deaths occurring after surgery for postinfarction VSR are due to cardiac failure. Sudden death is rare, and intractable heart failure can also occur. Other causes of death include cerebral embolism. Most patients who survive the hospital period have good functional status, with the majority falling into New York Heart Association (NYHA) class I or II.[14]

The most important risk factors for death in the early phase are poor hemodynamics and associated right ventricular dysfunction developing before the patient comes to the operating room. The amount and distribution of myocardial necrosis and scarring are responsible for both.

Right ventricular dysfunction results from ischemic damage or frank infarction of the right ventricle and is present when stenosis occurs in the right coronary artery system. The higher mortality observed after repair of defects located inferiorly in the septum is probably related to the higher prevalence of important right coronary artery stenosis.

The severity and distribution of CAD are also risk factors. Similarly, advanced age at operation, diabetes, and preinfarction hypertension are risk factors for death in the early phase.

Risk factors for death in patients with postinfarction VSR may be summarized as follows:

  • Posteriorly located VSRs are technically more difficult to repair and are associated with profound right ventricular dysfunction

  • The presence of multiple organ failure is a poor prognostic factor

  • The presence of cardiogenic shock does not bode well for the patient’s survival

In a retrospective analysis of 52 consecutive patients with surgically repaired postinfarction VSR over a 30-year period (mean follow-up, 7.8±7.7 years), Takahashi et al found that predictors of 30-day mortality on univariate analysis included the following[15] :

  • Renal insufficiency

  • Shock at surgery

  • Emergency surgery

  • Logistic EuroSCORE

  • Three-vessel disease

  • Significant left circumflex coronary arterial stenosis

  • Significant right coronary arterial stenosis

  • Incomplete revascularization

  • Surgical duration

  • Cardiopulmonary bypass time

On multivariate analysis, only incomplete coronary revascularization was an independent risk factor for 30-day mortality.[15]

Complications

Complications of postinfarction VSR include the following:

  • Of patients treated without surgery, 90% die

  • Surgical treatment must be carried out on an emergency basis, even if the patient is stable[3]

  • All VSRs are closed with a patch and associated coronary artery bypass grafting (CABG)

  • Operative mortality is 10-15% for anterior defects and 30-35% for posterior defects

 

Presentation

History and Physical Examination

Upon auscultation, a loud systolic murmur is heard, usually within the first week after an acute myocardial infarction (MI). The left-to-right shunt is often significant and can quickly compromise the cardiopulmonary system. There is sudden overload of the right ventricle and pulmonary arteries, resulting in increased pulmonary venous return. This is the most consistent physical finding of postinfarction ventricular septal rupture (VSR). Before the development of the murmur, the patient may have been stable after the acute MI. Coincident with the onset of the murmur, the patient’s clinical course undergoes a sudden deterioration, with the development of congestive heart failure (CHF) and, often, cardiogenic shock.

The typical harsh systolic murmur is audible over a large area, including the left sternal border and apical area. It sometimes radiates to the left axilla, thereby mimicking mitral regurgitation (MR). A thrill is palpable in approximately 50% of patients.

Because of the sudden increase in right sided blood flow, the second heart sound is accentuated and one may even hear an S3. Depending on the size of the shunt, one may also see signs of right and left heart failure. Signs of cardiogenic shock are common, including cold and clammy skin, cool extremities, unpalpable pulses, hypotension, oliguria, and diffuse rales. If the right ventricle is compromised, one will see elevation in the jugular venous pressure, enlarged/pulsatile liver, and distal extremity swelling. Within a short time, signs of coagulopathy will appear.

Almost 50% of patients have recurrent chest pain.

 

Workup

Approach Considerations

Patients with postinfarction ventricular septal rupture (VSR) are best managed in an ICU setting, even if stable. Close monitoring of the vital signs is mandatory. Fluid should be administered with great caution as the patients often have pulmonary edema.

In the setting of renal dysfunction, a nephrologist should be consulted for optimization prior to surgery.

Laboratory Studies

The following lab studies may be useful in the workup of postinfarction ventricular septal rupture (VSR):

  • Complete blood count

  • Electrolytes

  • Renal and liver function

  • Blood coagulation parameters including platelets, prothrombin time (PT) and partial thromboplastin time (PTT)

  • Cross and type at least 4-8 units of blood

Imaging Studies

On plain chest radiography, 82% of patients with postinfarction ventricular septal rupture (VSR) demonstrate left ventricular enlargement, 78% have pulmonary edema, and 64% have a pleural effusion. These findings are nonspecific and do not exclude other causes, such as a ruptured papillary muscle.

M-mode transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) have been used to help diagnose postinfarction VSR. TTE findings have been improved with the use of color-flow Doppler methods to visualize the VSR. In addition, echocardiography can help assess the presence of any mitral valve pathology. (See the image below.)

Postinfarction ventricular septal rupture. Ventric Postinfarction ventricular septal rupture. Ventricular septal defect on echocardiography.

Electrocardiography

No electrocardiographic (ECG) features are diagnostic of postinfarction VSR, though ECG indeed provides some useful information. Persistent ST-segment elevation associated with ventricular aneurysm is common. ECG may reveal atrioventricular block in one third of patients. ECG can also be used to help predict the anatomic location of the septal rupture. (See the image below.)

Postinfarction ventricular septal rupture. Acute a Postinfarction ventricular septal rupture. Acute anterior myocardial infarction on ECG.

Catheterization and Pressure Measurement

Left-heart catheterization with coronary angiography is recommended in all stable patients. This procedure is time-consuming and carries some degree of morbidity in already compromised patients; accordingly, good judgment is required when this test is ordered.

An important diagnostic test for differentiating ventricular septal rupture (VSR) from mitral valve insufficiency is catheterization of the right heart with a Swan-Ganz catheter. In the presence of a VSR, oxygen concentration between the right atrium and the pulmonary artery is stepped up. In addition, a pulmonary capillary wedge pressure tracing is beneficial for differentiating acute mitral regurgitation (MR) from VSR.

Left- and right-side pressure measurements help estimate the degree of biventricular failure and are useful in monitoring the response to perioperative therapy. Whereas right-side failure is more common in patients with postinfarction VSR, left-side failure and refractory pulmonary edema are more prominent in patients with a ruptured papillary muscle. However, one third of patients with postinfarction VSR also have some degree of MR secondary to left ventricular dysfunction. Only rarely is VSR also associated with ruptured papillary muscle.

Procedures

Most patients will benefit from intra-aortic balloon counterpulsation (IABCP). Because of low ejection fraction, tissue perfusion may be poor. Hence, the patient's distal pulses must be closely monitored to avoid ischemia when the intra-aortic balloon pump (IABP) is inserted.

 

Treatment

Approach Considerations

The timing for postinfarction ventricular septal rupture (VSR) surgery was once debatable but today it is no longer an issue. The key fact is that most patients will need surgery as a life saving treatment. The timing of surgery depends on the hemodynamic status of the patient. If the patient remains stable and is well perfused, then surgery can be delayed. The premise behind this approach is that the extra time will enable the friable tissues to recover and strengthen and hold the stitches better. However, if the patient is declining and is hemodynamically unstable, then immediate surgery may be necessary. Delayed surgery in stable patients can be undertaken anytime between 14-21 days; these patients should not be discharged home as sudden deterioration is not uncommon.

Medical Therapy

Initiate pharmacologic therapy in an attempt to render the patient hemodynamically stable. The goals are to reduce afterload on the heart and to increase forward cardiac output.

Vasodilators may be used in an attempt to decrease the left-to-right shunt associated with the mechanical defect and thereby increase cardiac output. Intravenous (IV) nitroglycerin can be used as a vasodilator and may provide improved myocardial blood flow in patients with significant ischemic cardiac disease.

When used alone, inotropic agents may increase cardiac output; however, without changes in the ratio of pulmonary to systemic flow (Qp-to-Qs ratio), they markedly increase left ventricular work and myocardial oxygen consumption. The profound level of cardiogenic shock in some patients precludes vasodilator treatment, often necessitating vasopressor support.

Vasopressors markedly increase left ventricular work and myocardial oxygen consumption. They also increase systemic afterload and further increase the Qp-to-Qs ratio, thus lowering cardiac output and greatly augmenting myocardial oxygen consumption.

Intra-aortic balloon counterpulsation (IABCP) offers the most important means of temporary hemodynamic support. IABCP reduces left ventricular afterload, thus increasing systemic cardiac output and decreasing the Qp-to-Qs ratio. IABCP also facilitates diastolic augmentation with an increase in coronary blood flow, resulting in an improved oxygen supply.

IABCP is not a substitute for urgent intervention, and in patients with cardiogenic shock, it should be followed by immediate intervention. Patients with ventricular septal rupture (VSR) do not die of cardiac failure; they die as a result of end-organ failure. Only by shortening the duration of shock can the high risk of mortality be prevented.

Achieving hemodynamic stability before surgery is very beneficial, but prolonged attempts to improve the patient’s hemodynamic status can be hazardous.[16]

This aggressive approach often results in temporary stability of these extremely ill patients. As a rule, however, these benefits are brief, and patients may deteriorate rapidly. Therefore, early diagnosis and rapid surgical intervention should be planned. Only about 10-15% of patients can be treated with conservative measures for a period of 2-4 weeks, after which surgical treatment can be provided at a greatly reduced risk.

Surgical Therapy

Indications and contraindications

In view of the grim prognosis for medically treated patients, the diagnosis of postinfarction ventricular septal rupture (VSR), by itself, constitutes an indication for operation. The controversy that once surrounded the timing of surgical intervention is no longer an issue, and most surgeons now agree that early surgery is indicated to minimize the risk of mortality and morbidity. The success of surgical therapy depends on prompt medical stabilization of the patient and prevention of cardiogenic shock.

The relative safety of repair 2-3 weeks or more after perforation has been established. Because the edges of the defect have become more fibrotic, repair is more secure and is easily accomplished. A successful clinical outcome is related to the adequacy of the closure of the VSR; therefore, if possible, search for multiple defects both preoperatively and at the time of surgery.

Only when the patient is hemodynamically stable should repair be initially delayed, but there must be a high degree of certainty that the patient is in fact stable. These patients can suddenly deteriorate and die. The criteria for a delay in surgical treatment include the following:

  • Adequate cardiac output
  • No evidence of cardiogenic shock
  • Absence of signs and symptoms of congestive heart failure (CHF) or minimal use of pressor agents to control initial symptoms
  • Absence of fluid retention
  • Good renal function

The natural history of the disease is such that few patients present with these signs and symptoms. In most patients, postinfarction VSR rapidly leads to a worsening of the hemodynamic state, with cardiogenic shock, marked and intractable symptoms of CHF, and fluid retention. Immediate surgery is usually indicated.[6] The high surgical risk of early repair is accepted because of the even higher risk of death without surgery under such circumstances.

Occasionally, a delay in diagnosis and referral occurs. These patients are usually critically ill, and the prognosis is very grim; thus, allowing the natural history of the disease to take its course is prudent.[6]

Although most patients who experience postinfarction VSR need emergency surgery, an occasional patient, because a delay in either diagnosis or referral, may be in a state of multiorgan failure and may not be a candidate for surgery. The chances of such a patient surviving an operation are minimal; in these circumstances, supportive medical therapy may be adequate.[6] Patients who are comatose and in cardiogenic shock have a particularly poor prognosis after surgery, and surgery is best avoided in such circumstances.

Repair Techniques

There are currently two techniques of repairing a VSR. The first one has been used the longest and is the simplest. A pericardial or prosthetic patch is used to cover the septal defect by suturing the patch circumferentially to the septum wall. The two key limitations of this technique include 1) the sutures are often placed in friable and ischemic tissue; hence, the patch may become loose, and 2) the repair is made through a zone of infarct, which will continue to be subjected to high ventricular pressures after the surgery; hence, bleeding may be an issue.

To circumvent these problems, a second method pioneered by David uses an infarct exclusion technique. A small is created using a pericardial patch. The area of infarction and the septal defect are then excluded from the high pressures of the left ventricle.[17]

Choice of operative approach

The first operations for repair of postinfarction VSR used an approach through the right ventricle, with an incision of the right ventricular outflow tract such as was used to repair some congenital ventriculoseptal defects (VSDs). This approach proved inadequate because of limited exposure for lesions at the apex of the heart, injury to normal right ventricular muscle, interruption of coronary collateral vessels, and failure to excise the infarcted tissue.

Subsequently, a transinfarction approach was described, which incorporated infarctectomy, and repair of the ventricular septal perforation. Several techniques have been used to close these defects. The choice of procedure is determined by the location of the defect.

Most defects are anteroapical and are closed by buttressing the defect with viable muscle from the adjacent anterior left ventricular wall. Smaller defects located high in the ventricular septum are closed with a Dacron patch.

High posterior septal or inferior defects, which are less common, are approached through the inferior portion of the heart, usually in the distribution of the posterior descending coronary branch of the right coronary artery. The incision is made in the area of maximal infarction. A well-proven principle of repair for these defects is the use of a synthetic patch closure to prevent tension.

A triple-patch approach has been described, with acceptable early and midterm outcomes.[18]

Additional procedures that may be considered in the treatment of postinfarction VSR include the following:

  • Concomitant coronary artery bypass grafting (CABG)
  • Mitral valve replacement

Controversy surrounds the issue of whether to perform CABG in patients undergoing emergency postinfarction VSR repair. Some authors have found no benefit to CABG in this setting and have concluded that cardiac catheterization in ill patients is time-consuming and poses a risk of contrast injury to the kidney. Others, however, have used a selective approach to cardiac catheterization.

In patients who probably do not have a history of angina or previous myocardial infarction (MI), cardiac catheterization is deferred. Cardiac catheterization findings help confirm and quantitate the presence of a shunt and reveal pulmonary artery pressure and resistance values. The left ventriculogram helps in determining the location and number of VSDs, defining left ventricular function, and assessing mitral valve function. Most surgeons perform bypass in patients with VSR, with significant improvements in survival.

Occasionally, significant mitral regurgitation (MR) may be associated with acute VSR, particularly when the infarction is posterior. In such circumstances, the mitral valve must be repaired or replaced.

When a left ventricular aneurysm is associated with postinfarction VSR, it is excised as the initial step in surgical therapy. After repair of the VSR, the aneurysm is generally repaired.

Preparation for surgery

Preoperative management is directed toward rapid resuscitation and stabilization of the patient and preparation for surgery. The goals are as follows:

  • To reduce systemic vascular resistance (thereby decreasing the left-to-right shunt)
  • To maintain a stable cardiac output and blood pressure
  • To maintain coronary artery blood flow

Preoperative treatment of patients with postinfarction VSR may be summarized as follows:

  • Transfer patients to an intensive care unit (ICU) for resuscitation

  • Place a Swan-Ganz catheter to assist with hemodynamic management

  • Decrease the systemic vascular resistance and the left-to-right shunt with vasodilators

  • Maintain cardiac output and organ perfusion with inotropic agents

  • Maintain coronary artery blood flow

  • Use IABCP to decrease myocardial oxygen consumption, decrease afterload, and increase coronary artery perfusion

  • Use mechanical ventilation as required

  • Use echocardiography to help determine the site of septal rupture (see the image below) 

    Postinfarction ventricular septal rupture. An echo Postinfarction ventricular septal rupture. An echocardiogram of a 69-year-old patient with a postinfarction VSR who decompensated very quickly.
  • Use cardiac catheterization to help determine the presence of coronary artery disease (CAD)

Closure of defect

Principles associated with the evolution of techniques for the closure of postinfarction VSR may be summarized as follows:

  • Determine and understand the anatomy and location of the VSR and any associated coronary artery pathology

  • Expeditiously establish hypothermic total cardiopulmonary bypass, and pay attention to myocardial protection with cardioplegia

  • Use a transinfarction approach to the VSR, with the site of ventriculotomy determined by the location of the transmural infarction

  • Inspect the papillary muscles, and concomitantly replace the mitral valve only if frank papillary muscle rupture is present

  • Close the VSR without tension using prosthetic material and buttress the suture line with Teflon pledgets depending on the closure technique

An alternative technique included percutaneous techniques similar to those used to close some congenital VSDs. Technical improvements in experimental devices for closing intracardiac shunts are being made to treat postinfarction VSR or residual shunts after primary repair. A balloon catheter introduced percutaneously has been used to abolish the shunt in poor-risk patients.

Patients who require IABPC preoperatively appear to benefit from postoperative support with the pump for 24-72 hours. Some of these patients demonstrate a small persistent or recurrent left-to-right shunt. Because of the large amount of prosthetic material used to repair the septal perforation, anticoagulation therapy in these patients is recommended by some surgeons for a period of 6-8 weeks.

Residual VSDs have been noted early or late after operative treatment in 10-25% of patients. These residual defects are easily diagnosed with the aid of color-flow Doppler investigations. Residual VSDs may be attributable to the reopening of a closed defect, the presence of an overlooked VSD, or the development of a new septal perforation during the early postoperative period.

Reoperation is required for closure of such residual VSDs when the Qp-to-Qs ratio is greater than 2. When the VSDs are small and asymptomatic, a conservative approach may be recommended because spontaneous closure can occur. Alternative techniques include percutaneous methods.

Postoperative complications include the following:

  • Death 30 day mortality rates vary from 20%-70%

  • Multiple organ failure

  • Recurrence of VSR due to loosening of stitches/patch

  • Bleeding

Interventional Therapy

Data collected by the Society of Thoracic Surgeons National Database indicate that postinfarction ventricular septal defect (VSD) is a lethal disorder, even with treatment.[19] There is considerable interest in the development of percutaneous interventional techniques for closing the ruptured VSD and lowering the mortality.

Isolated reports with the Amplatzer Septal Occluder (St Jude Medical, St Paul, MN) found the technique to be safe for closure of small lesions.[20]

Schlotter et al carried out a comprehensive systematic literature search (13 studies; N=273) to evaluate the existing evidence regarding percutaneous closure of postinfarction VSD.[21] Overall, the technical success rate was greater than 75%, and the device implantation success rate was 89%; however, the overall in-hospital/30-day mortality remained substantial, at 32%. Device embolization, ventricular perforation, and arrhythmias were the major complications of the procedure.

ECMO in adult cardiac surgery can be used for postoperative support with refractory cardiogenic shock. Alternatively, ECMO can be used preoperatively as a bridge to definitive surgical closure when postinfarction ventricular septal rupture with refractory cardiogenic shock are encountered.[22]

It is very important to understand that not every patient with VSR will be a surgical candidate and good clinical judgement should be exercised before proceeding to the operating room. In some cases, only supportive care may be the best solution.