Jessica G.Y. Luc and James G. Abel
This chapter is a revision and update of that included in previous editions of the TSRA Review written by Daniel P. Logsdon (2nd edition) and Leo M. Gazoni (1st edition).
Mechanical complications after myocardial infarction (MI) are uncommon in the era of culprit vessel revascularization and thrombolytic protocols, accounting for approximately 15% of deaths following acute MI. Mechanical complications in order of decreasing incidence include: left ventricular free wall rupture, left ventricular aneurysm, ventricular septal rupture, and papillary muscle rupture with acute ischemic mitral regurgitation. Mechanical complications of MI constitute a class I indication for emergent coronary artery bypass grafting surgery (CABG) with repair of structural defects as per the American Heart Association 2011 CABG guidelines.
Immediate goals preoperatively are afterload reduction to increase non-regurgitant cardiac output and maintaining organ perfusion. In general, consider pharmacological therapy such as vasodilators (nitrites, sodium nitroprusside), inodilators (milrinone, dobutamine, and enoximone), and non-pharmacological therapy such as an intra-aortic balloon pump (IABP). Extracorporeal membrane oxygenation (ECMO) insertion or other modalities of mechanical circulatory support may be needed emergently as a short-term bridge to definitive surgical repair.
Key principles of surgical repair of mechanical complications of acute MI are that sutures should be placed through non-infarcted tissue to maximize suture-line integrity in a tension-free closure. Retrograde cardioplegia can be a useful adjunct in addition to antegrade cardioplegia in acute coronary occlusion to improve myocardial protection. For patients requiring concomitant CABG, left internal mammary harvest may not be appropriate in the unstable patient, and in such scenarios, one should consider utilizing saphenous vein conduit. These patients are often acutely unwell, and one should have a low threshold to seek help.
Ischemic Ventricular Free Wall Rupture
Incidence and survival
Free wall rupture occurs in 0.5-1.5% of patients presenting with an acute MI, and usually within the first 14 days post-transmural infarction. Free wall rupture is the third most common cause of mortality following acute MI (1st: cardiogenic shock; 2nd: congestive heart failure). Mortality at 90 days without surgical intervention has been reported at 63%. With surgical intervention, mortality at 7 years is reduced to 32% with an operative mortality ranging from 12-30%.
Pathophysiology
Free wall rupture most commonly occurs in the left ventricle but can also occur in the right ventricle. The anterior and lateral walls of the left ventricle are the highest risk for rupture. The coronary lesion associated with free wall rupture is most commonly the left anterior descending artery (42%), followed by the circumflex artery in 40%, and right coronary artery in 18% of patients. Free wall rupture occurs secondary to extension of the infarction with thinning and dilation of the necrotic zone post-transmural infarction.
Free wall rupture has been categorized into three different types based on pathologic findings:
- Type I = abrupt myocardial tear without myocardial thinning
- Type II = erosion of infarcted myocardium with subsequent dehiscence and covering by thrombus
- Type III = myocardial thinning with perforation at the center of ventricular aneurysm
Although there are three types of free wall rupture, the treatment and management all necessitate surgical repair. Pseudoaneurysm of the left ventricle can also occur if the free wall rupture is contained, most commonly by pericardial adhesions and/or thrombosis.
Presentation and Diagnosis
Patients with free wall rupture can present with either acute or subacute symptoms. Acute rupture presents with sudden onset of chest pain and shortness of breath with immediate hemodynamic compromise from cardiac tamponade, leading to shock, jugular venous distention, pulsus paradoxus, and sudden death (pulseless electrical activity). Patients with a contained rupture often present sub-acutely with pleuritic chest pain due to pericarditis, persistent ST elevation, nausea, and hypotension.
Echocardiography – signs of tamponade with right-sided diastolic collapse and a dilated inferior vena cava.
Pulmonary Artery Catheter (not necessary) – signs of tamponade with equalization of the right atrial, right ventricular diastolic, and pulmonary capillary wedge pressure.
Treatment
For ventricular free wall ruptures, pericardiocentesis can be used as a temporizing measure emergently while preparing patient for surgical repair. Additionally, an IABP may be necessary to stabilize the patient preoperatively.
Ventricular pseudoaneurysm portend a high risk of rupture and hemopericardium, as such, the treatment strategy is the same as that of ventricular free wall rupture via surgical repair.
Traditionally, surgical repair requires the suturing of healthy myocardium on either side of infarcted area to close the ventricle, most commonly with a horizontal mattress suture buttressed with pledgets or Teflon felt. A bovine pericardial, Dacron, or PTFE patch reinforced with surgical glue can also be used.
Post-Infarction Ventricular Aneurysms
Post-infarction ventricular aneurysms develop via thinning of the myocardium. They are differentiated from pseudoaneurysms in that pseudoaneurysms are contained ruptures, whereas post-infarction ventricular aneurysms have a low risk of rupture and hemopericardium.
Left ventricular aneurysms are addressed in more detail in a subsequent chapter of this book.
Ischemic Ventricular Septal Defect
Incidence and survival
Ischemic ventricular septal defect (VSD) is a defect in the interventricular septum caused by ruptured infarcted myocardium. The occurrence of a VSD after acute MI has markedly decreased from 1-2% in the pre-reperfusion (PCI and thrombolytic) era to approximately 0.2% in the contemporary era and happen around 5 days post MI. VSDs are best treated surgically but still carry a high mortality rate. Treated with medical therapy alone, 24% of patients die by 24 hours, 46% at 1 month, and 80% at 2 months. With surgical repair, mortality at 30 days is 41% with 5-year survival of 38%. If patients survive the first 30 days, their 5-year survival is 67%.
Ischemic VSDs occur in the following sites:
- Anterior infarction -> anterior VSD in the anterior / apical interventricular septum (2/3 of patients with ischemic VSDs)
- Caused by occlusion of the left anterior descending coronary artery
- Inferior infarction -> posterior VSD in the inferobasal interventricular septum (1/3 of patients with ischemic VSDs)
- Caused by occlusion of the dominant right coronary or, less frequently, of a dominant circumflex artery
Mortality after closure occurs more often with inferior VSDs compared with anterior VSDs (73% vs. 30%, respectively). This difference is attributed to the complicated nature of inferior VSD repair given the often impaired right ventricular function and potential mitral valve regurgitation secondary to papillary muscle infarction.
Presentation and Diagnosis
Patients with acute ischemic VSD may present with increasing dyspnea progressing to cardiogenic shock, signs of right heart failure, and a harsh holosystolic murmur best heard at the left sternal border radiating to the axilla.
Echocardiography – Left to right shunt is often large with pulmonary to systemic blood flow ratio (Qp/Qs) of >2.0. Can also help delineate associated valvular pathology.
Pulmonary Artery Catheter or Right Heart Catheterization – Elevated pulmonary artery wedge pressure, left atrial pressure, left ventricular end diastolic pressure, and pulmonary artery pressure. The right ventricular function is often impaired. Step-up in oxygen saturation between the right atrium and pulmonary artery (>9%) further supports the diagnosis. Prominent V wave.
Treatment
Repair of ischemic VSDs is urgently indicated given the poor survival with medical therapy alone. The greatest predictor of postoperative mortality in patients with ischemic VSDs is the time spent in cardiogenic shock preoperatively. The goal of preoperative management is to (1) reduce the left to right shunt by reducing the systematic vascular resistance and left ventricular pressure, and (2) maintain cardiac output and end-organ perfusion. These patients are often treated with inotropes, IABP, and/or mechanical circulatory support to achieve these preoperative goals.
Cardiogenic shock in the setting of an ischemic VSD is an indication for operation. However, if a patient is already in multisystem organ failure and survival from emergent surgery is unlikely, mechanical circulatory support or catheter closure can be considered to bridge the patient to a more stable state for intervention in the future.
Two main techniques are utilized in VSD repair and include either primary repair (more common) or infarct exclusion. The benefit of infarct exclusion is that it excludes the VSD from the highly pressurized left ventricle and maintains ventricular geometry to preserve ventricular function. CABG if needed, is often performed prior to VSD repair, to administer cardioplegia via the grafts and optimize myocardial protection.
A left ventriculotomy is made through the infarcted area adjacent to the septum. Primary repair can be accomplished with debridement of necrotic septal myocardium and patch repair with PTFE, Dacron, autologous or bovine pericardium sutured to healthy endocardium to close the VSD. Patch repair is accomplished with interrupted mattress sutures using pledgeted 3-0 Prolene sutures passed from the right ventricle through the intraventricular septum and then through the patch material. Infarct exclusion aims to exclude the left ventricular cavity from the infarcted myocardium by suturing a larger patch so that it spans the entire area of the infarcted endocardium, suturing to non-infarcted endocardium of the septum and left ventricular wall. No debridement is performed. In cases of papillary muscle rupture, a mitral valve replacement would need to be performed after patch placement either by a left atriotomy, transseptal approach via the dome of the left atrium, or through the ventriculotomy itself. The patch can then be incorporated into a 2-layer ventricular closure for support with interrupted horizontal mattress sutures of 2-0 Prolene buttressed with Teflon felt strips, with reinforcement with continuous 2-0 Prolene over and over stitch. With a posterior-inferior infarct, the posterior papillary muscle may be involved, requiring concomitant replacement of the mitral valve.
Percutaneous closure of ischemic VSDs have also been described using the Amplatzer Muscular VSD Occluder (St. Jude Medical, St. Paul, MN) in those of extremely high-risk as an interim measure before surgery, in those with delayed presentations, or recurrent defects after surgical repair. However, percutaneous closure is limited by friable tissue, size of the VSD, and proximity to the mitral valve or papillary muscles.
Ischemic Mitral Regurgitation
Incidence and survival
Acute severe mitral regurgitation after an MI is a life-threatening condition with improved outcomes if intervened surgically. The reported incidence of mild-moderate chronic mitral regurgitation is 13-45% in patients following an acute MI. Mild-moderate mitral regurgitation is usually well tolerated by patients and is often asymptomatic. However, acute severe mitral regurgitation due to papillary muscle rupture occurs less often, in approximately 0.25% of patients following an acute MI, but has in-hospital mortality of 70-80% if treated medically. With surgical intervention the outcomes are much improved, carrying an expected operative mortality of 27% with 5-year survival of patients after surgery of approximately 79%. Long-term survival at 15 years demonstrates an almost 3-fold increase in survival when concomitant CABG is performed during papillary muscle repair (CABG 64% vs. no CABG 23%).
Pathophysiology
Papillary muscle rupture is more common (75% of cases) in patients with inferior MI affecting the posteromedial papillary muscle, which has a single blood supply from the posterior descending artery. Anterolateral papillary muscle rupture is less common (25% of cases) owing to its dual blood supply from the left anterior descending and circumflex artery.
Median time to rupture after MI is 13 hours and is typically diagnosed between 2 to 7 days. In the setting of acute papillary muscle rupture, immediate pulmonary edema may occur with hypotension and cardiogenic shock. Mitral regurgitation following MI is a strong predictor of mortality.
Presentation and Diagnosis
The patient will likely present with shock, acute pulmonary edema, and a new pansystolic murmur, heard loudest at the apex and radiating to the axilla. The systolic murmur may be less audible with more severe mitral regurgitation with early systolic equalization of transvalvular pressures.
Echocardiography – Demonstrates partial or complete rupture of papillary muscle or chordae tendinae, leaflet eversion, severe mitral regurgitation on doppler, hyperdynamic left ventricle, and pulmonary hypertension. Importantly, the severity of mitral regurgitation is underestimated on intraoperative echocardiography due to general anesthesia and the accompanying physiological responses with left ventricular unloading and vasodilation.
Pulmonary Artery Catheter or Right Cardiac Catheterization – Prominent V wave and increased pulmonary artery pressures.
Treatment
Medical therapy as previously mentioned is aimed at reducing afterload and can be augmented with short term mechanical circulatory support, such as an IABP or ECMO.
Acute severe mitral regurgitation following MI is an indication for urgent surgery. Surgical intervention can include repair, but due to concerns with ongoing necrosis or failing mitral valve apparatus, the preferred choice of surgery is often mitral valve replacement with chordal preservation. There are rare circumstances where the papillary muscle can be reimplanted or where neochords can be used. Appropriate coronary revascularization should also occur at the time of surgery. The survival benefit is controversial for surgical treatment of moderate or severe chronic ischemic mitral regurgitation; however, patients who underwent surgical repair or replacement and concomitant CABG had lower rates of postoperative mitral regurgitation and increased functional status based on a clinical trial performed by the Cardiothoracic Surgical Trials Network (CTSN) on 2-years of follow-up.
Suggested Readings
- Watson J, Louis C. TSRA Clinical Scenarios in Cardiothoracic Surgery: 3rd Edition. Independently published. August 2020.
- Chikwe J, Cooke D, Weiss A. Cardiothoracic Surgery, Oxford Handbooks in Surgery. 2nd Edition. Oxford University Press. March 2013.
- Cohn LH, Adams DH. Cardiac Surgery in the Adult Fifth Edition. McGraw-Hill Education / Medical. August 2017.
- Raja SG. Cardiac Surgery: A Complete Guide. Springer. February 2020.
- Moorjani N, Viola N, Ohri SK. Key Questions in Cardiac Surgery. TFM Publishing. March 2011.
