Aaron J. Weiss, MD, and Joanna Chikwe, MD
Concept
- Presentation of post-infarction VSD and LV aneurysm
- Diagnosis and workup
- Operative timing and approaches
- Pitfalls and alternative solutions
Chief complaint
“A 65-year-old man was admitted to the hospital with chest pain and diagnosed with an acute anteroseptal myocardial infarction for which he underwent percutaneous coronary intervention. He was recovering on the floor four days later when he developed new chest pain and breathlessness.”
Differential
Post-myocardial infarction ventricular septal defect, free wall rupture, tamponade, acute papillary muscle rupture, pulmonary embolism, aortic dissection/rupture, and ongoing ischemia/infarction.
History and physical
If patient is stable and alert, a short and focused history to elicit chest pain and dyspnea, calf or leg pain (possible deep vein thrombosis leading to a pulmonary embolism). Focused physical exam should include vital signs, a full neurological, cardiac with attention to new murmurs, lung, and extremities exam. In addition, one should focus on signs of right-sided heart failure (jugular venous distention (JVD), peripheral edema, etc.).
Tests
- EKG. Rule out ongoing or additional ischemic events, any arrhythmias.
- Echo. This is diagnostic. Color flow Doppler echocardiography shows the size and location of the VSD, ventricular function, mitral regurgitation, pulmonary artery and right-sided pressures, and rules out free wall rupture/tamponade.
- Right heart catheterization. Right heart catheterization shows a step-up in oxygenation between the right atrium and pulmonary artery (> 9% is diagnostic). Other information obtained includes an elevated pulmonary-to-systemic flow ratio (ranges from 1.4:1 to 8:1 and correlates with size of defect).
- Left heart catheterization. Most patients undergo this at the time of their initial presentation with acute myocardial infarction. In stable patients without a recent cardiac catheterization left heart catheterization will guide the decision to perform concomitant surgical revascularization. In unstable patients it is reasonable to omit this diagnostic modality.
Index scenario (additional information)
“On physical exam, patient is found to be hypotensive. There is a new harsh holosystolic murmur most prominent at the left lateral sternal border that radiates to the axilla and is associated with a thrill. Coarse breath sounds heard bilaterally. No JVD or peripheral edema noted. EKG shows no new changes from the EKGs performed since admission. Emergent echocardiogram performed at the bedside shows a large new anterior VSD.”
Treatment/management
The natural history of untreated postinfarction VSD is poor (25% mortality rate within 24 hours, 50% mortality rate within one week, 80% within one month, 97% at 1 year). Postinfarction VSD is therefore an indication for urgent surgery.
Preoperatively, management should include reducing afterload to decrease the left-to-right shunt, maintain cardiac output and peripheral perfusion so as to avoid end-organ damage, and increase coronary perfusion pressure. These goals can be accomplished through the use of an intra-aortic balloon pump (IABP) as well as pharmacologic therapy with inotropic agents. As surgical mortality is directly proportional to duration of cardiogenic shock and multi-organ failure pre-operatively, current emphasis is on early surgical intervention. A small percentage of patients severely compromised by multi-organ failure may benefit from mechanical assistance such as biventricular support or ECMO for temporary salvage before more definitive surgery can be performed.
Operative steps
Repair of anterior septal rupture
- Arterial line, general endotracheal anesthesia, central line with large bore access (no pulmonary artery catheter), urinary catheter, transesophageal echocardiography (TEE).
- Median sternotomy, conduit harvest (saphenous vein, and left internal mammary artery in stable patients if coronary revascularization is planned), heparin 400 mg/kg, ascending aorta cannulation, bicaval cannulation, antegrade cardioplegia cannula, retrograde cardioplegia cannula, left ventricular vent through the right superior pulmonary vein, +/- systemic cooling to 25° C, once ACT is 480 initiate cardiopulmonary bypass (CPB), CO2 insufflation.
- Deair antegrade line and run antegrade induction, followed by retrograde perfusion via the coronary sinus. Additional myocardial protection can be obtained by running cold blood cardioplegia during the VSD repair via retrograde coronary sinus catheter.
- Perform coronary bypasses: cardioplegia can be administered via the grafts prior to completion of the proximal anastomoses.
- Left ventricular transinfarct incision with infarctectomy is performed. Debride necrotic septal myocardium even enlarging the defect if needed. Place pledgeted interrupted horizontal mattress sutures around the defect. Pass the sutures through a felt strip then through the septum from right to left and then snap. Continue along the posterior rim. Along the anterior rim, pass the sutures from epicardium to endocardium. Then pass all the sutures symmetrically through a Dacron prosthetic patch. All sutures are pledgeted again and then tied down. Reapproximate the edges of the ventriculotomy with a double layer closure buttressed with Teflon felt or glutaraldehyde-preserved bovine pericardium.
- If used, biological glue is most effective if applied on dry myocardium in the decompressed, arrested heart i.e., prior to cross-clamp removal.
- Deair, wean from CPB, intraoperative TEE to assess for any residual VSD/shunt/left ventricular function/mitral regurgitation, if not already in place, an IABP may be necessary to help wean off bypass.
Potential questions/alternative scenarios
“On intraoperative TEE, the VSD appears to be apical. How would your operative technique differ?”
The same basic set-up as for an anterior septal rupture. Incision is made through the infarcted ventricular apex and the surgeon should debride any necrotic myocardium involving the left ventricle, right ventricle, and septum. Reapproximate the remaining apical portions to the apical septum using interrupted mattress sutures of 1-0 Tevdek passed sequentially through a buttressing strip of Teflon felt, the left ventricle, a second strip of felt, the septum, a third strip of felt, the right ventricle, and a fourth strip of felt. Tie these sutures down and then reinforce the closure with an over-and-over suture to ensure hemostasis.
“On intraoperative TEE, the VSD appears to be posteroinferior. How would your operative technique differ?”
Place the patient on CPB and arrest the heart. Retract the heart out of the pericardial well as you would for a bypass graft to the PDA. Trans-infarct incision is made through the left ventricle 1 cm lateral to the PDA. Debridement of necrotic left ventricular septal myocardium is performed. Inspect the mitral apparatus for any papillary muscle infarct. Less aggressive debridement of the right ventricle is performed as you only want to resect as much as necessary to achieve adequate visualization of the defect. If the posterior septum has separated from the free wall, it can be re-approximated primarily using a double-layered buttressed closure. Larger defects require patch closure as described earlier with the only difference being that the sutures are placed from the right side of the septum and from the epicardial side of the right ventricular free wall. Afterwards, a separate patch closure of the infarctectomy using Dacron graft maybe required versus a buttressed double layer primary repair depending on the size of the free wall defect. Primary closure of a large tissue defect has historically resulted in very poor outcomes. Check for hemostasis, deair, and wean from CPB.
“Is preoperative left heart catheterization necessary? And if CAD is found that necessitates bypass grafts, when should this be performed?”
It is controversial whether or not preoperative coronary catheterization is necessary. In patients with multivessel coronary disease, bypass grafts may increase both early and long-term survival. However, often the patient is too unstable to undergo a catheterization prior to surgery and thus necessitates an individual assessment of patient’s hemodynamics and clinical situation. If bypass grafts are performed, they should be done before the repair of the VSD to optimize myocardial protection.
“Are there any other surgical techniques that might warrant consideration for repair of a VSD?”
Endocardial patch repair with infarct exclusion involves intracavitary placement of an endocardial patch to exclude infarcted myocardium while maintaining ventricular geometry. This technique excludes the VSD from the highly pressured left ventricle instead of closing it. Proponents of this approach argue that maintaining ventricular geometry enhances or at least preserves ventricular function.
“When would delayed repair of a VSD be acceptable?”
Patients with severe end-organ damage deemed too sick to undergo operative repair may be candidates for a delayed repair. Interval treatment may involve placement of a left ventricular assist device (LVAD) that theoretically will help improve end-organ dysfunction and allow for maturation of the infarcted tissue. A biventricular mechanical assist device may be necessary if the LVAD worsens the right-to-left shunt.
“What interventions may help a difficult wean from CPB following VSD repair?”
If an IABP was not inserted preoperatively, one should be inserted at this time to help reduce the afterload and improve coronary perfusion pressure. Pharmacologic adjuncts such as epinephrine and milrinone may help to augment contractility. Milrinone also improves diastolic function and reduces afterload. Other afterload reducing agents may be used as needed. If the patient is having decreased right heart function, the patient may benefit from inhaled prostaglandin or nitric oxide to help dilate the pulmonary vasculature and decrease the work of the right ventricle. A small percentage of patients may require a temporary ventricular assist device.
Pearls/pitfalls
- Discovery of a new onset post-infarction VSD requires urgent surgery.
- The greatest predictor of post-operative mortality is the length of time patients spend in cardiogenic shock pre-operatively.
- Echocardiography is the diagnostic test and is essential to adequately plan the surgical approach.
- The chances of successfully weaning from CPB are improved by expeditious institution of CPB with meticulous myocardial protection.
- The VSD should be approached via a transinfarct incision with meticulous debridement of necrotic myocardium to prevent delayed rupture.
- Inspect the mitral apparatus for any coexisting dysfunction or infarct of the papillary muscles.
- A tension-free closure is important, and therefore patch closure techniques are required for larger defects.
Suggested readings
- Mangi AA and Agnihotri AK. Postinfarction Ventricular Septal Defect. Spencer and Sabiston – Surgery of the Chest. 2010; 1449-1456.
- Gazoni LM. Mechanical complications of coronary artery disease. Mery CM and Turek JW. TSRA Review of Cardiothoracic Surgery. 2011. 282-289.
- Madsen JC and Daggett WM Jr. Repair of postinfarction ventricular septal defect. Semin Thorac Cardiovasc Surg. 1998. Apr;10(2):117-127.
- Arnaoutakis GJ, Zhao Y, George TJ et al. Surgical repair of ventricular septal defect after myocardial infarction: outcomes from the Society of Thoracic Surgeons National Database. Ann Thorac Surg 2012; 94: 436-44.
