Postinfarction Ventricular Septal Rupture Treatment & Management

Updated: Mar 09, 2017
  • Author: Shabir Bhimji, MD, PhD; Chief Editor: Brett C Sheridan, MD, FACS  more...
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Treatment

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. [12]

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.

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Surgical Therapy

Indications and contraindications

In view of the grim prognosis for medically treated patients, the diagnosis of postinfarction 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 firmer and 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.

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, aneurysmectomy, 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, which is usually on the right ventricular side of the septum. 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. [13]

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

  • Concomitant coronary artery bypass grafting (CABG)
  • Mitral valve replacement
  • Excision of left ventricular aneurysm

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 replaced. Replacement is usually best accomplished through the left ventriculotomy by using interrupted, pledgeted mattress sutures.

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
  • 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
  • Trim the left ventricular margins back to viable muscle
  • Conservatively trim the right ventricular muscle
  • Close the VSR without tension, using prosthetic material
  • Buttress the suture line with Teflon pledgets

Percutaneous techniques have been used successfully 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.

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Interventional Therapy

Data collected by the Society of Thoracic Surgeons National Database indicate that postinfarction VSD is a lethal disorder, even with treatment. [14] 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. [15]

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. [16] 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.

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