pediagenosis: Cardiovascular
Article Update
Showing posts with label Cardiovascular. Show all posts
Showing posts with label Cardiovascular. Show all posts

Friday, September 11, 2020

Percutaneous Mitral Valve Repair Techniques

Percutaneous Mitral Valve Repair Techniques

Percutaneous Mitral Valve Repair Techniques
This chapter describes established and emerging percutaneous mitral valve repair techniques. The goal of any percutaneous procedure is to achieve a durable correction of mitral disease with clinical efficacy similar to that of well-established open surgical interventions. Knowing which patients will benefit most from percutaneous approach and which approach to apply is exceedingly challenging given the complex and varied pathophysiology and anatomy of mitral valve disease. Surgical risk is often prohibitive given that mitral valve disease is both caused by and develops in parallel to many comorbidities that increase surgical risk. By applying concepts that have made surgical repair successful to the engineering of percutaneous technologies, restoring proper mitral valve function with catheter based techniques can be performed without many of the risks inherent to surgery. Percutaneous therapies therefore represent an expanding toolbox for the modern valvular heart disease center that strives to repair mitral valve disease in patients at all levels of surgical risk. Although catheter based repairs for MR are only approved in patients at prohibitive surgical risk, as more data is collected, percutaneous repair may one day be used as a viable option to surgical candidates who wish to avoid surgery.
 Robotic Mitral Valve Surgery

Robotic Mitral Valve Surgery

 Robotic Mitral Valve Surgery
Keywords : mitral valve, repair, replacement, prolapse, robotic
Robotic mitral valve surgery was introduced in 1998 to reproduce excellent conventional sternotomy results with less invasive techniques. This technology is now routinely performed for delivering complete anatomic correction of all categories of mitral valve prolapse, regardless of disease complexity, with or without concomitant tricuspid valve repair and atrial fibrillation ablation procedures. Recent studies have demonstrated broad advantages of robotic mitral valve surgery, including reduced bleeding, extubation on the operating room table, shorter hospital length of stay, quicker return to normal activities, and a superior cosmetic result. Here we discuss the current status of robotic mitral valve surgery techniques.

Tuesday, July 28, 2020

Minimally Invasive Mitral Valve Surgery: Partial Sternotomy Approach

Minimally Invasive Mitral Valve Surgery: Partial Sternotomy Approach

Minimally Invasive Mitral Valve Surgery: Partial Sternotomy Approach
Keywords : minimally invasive cardiac surgery, minimally invasive mitral valve replacement

·   Mitral valve dysfunction is a common pathologic process. The process may involve any component of the valve or subvalvular structures, including the valve leaflets, the annulus, the papillary muscles, the chordae tendineae, and the left ventricular wall.
Mitral Valve Replacement

Mitral Valve Replacement

Mitral Valve Replacement
Keywords : mitral valve, mitral valve replacement
Step 1. Anatomy
·    The mitral valve is a complex structure comprised of an anterior and posterior leaflet that is connected to the left ventricle via attachments to papillary muscles through the chordae tendineae.
Repairing Degenerative Mitral Valve Disease

Repairing Degenerative Mitral Valve Disease

Repairing Degenerative Mitral Valve Disease
Keywords : Mitral valve repair, myxomatous mitral valve disease, degenerative mitral valve disease
Degenerative mitral valve disease is a common cause of mitral regurgitation and results in significant morbidity and mortality. Mitral valve repair is preferred over valve replacement given improvements in survival, left ventricular function, and freedom from reoperation. The purpose of this chapter is to provide surgeons with a comprehensive overview of various strategies available to successfully repair degenerative mitral valve disease. A brief overview of pertinent surgical anatomy is followed by a discussion on operative strategy and approach, with emphasis on minimally invasive techniques. Techniques to repair posterior, anterior, and bileaflet prolapse are discussed, along with some special scenarios. The chapter concludes with an overview on evaluating the repair, postoperative care, and pearls and pitfalls.
Ross Procedure

Ross Procedure

Ross Procedure
Keywords: autograft, aortic root, pulmonary root, inclusion technique, aortic valve replacement

The Ross procedure uses the pulmonary autograft to replace the diseased aortic valve and root. With appropriate patient selection and technical modifications, the durability of the autograft can be significantly improved. The Ross procedure continues to be a safe, effective and coumadinfree alternative for aortic valve replacement across all age groups.
Transcatheter Aortic Valve Replacement

Transcatheter Aortic Valve Replacement

Keywords: Transcatheter aortic valve replacement

Transcatheter Aortic Valve Replacement
Transcatheter aortic valve replacement (TAVR) is a relatively new technique that has been clinically applied mostly in higher risk older patients in the past 10 years. Major differences in comparison to conventional aortic valve replacement (AVR) are as follows:

Thursday, June 25, 2020

Bentall Procedure

Bentall Procedure

Bentall Procedure
Keywords: Bentall Procedure, Operations for Valvular Heart Disease, bentall, aortic replacement, valve replacement, composite aortic valve, aortic replacement

Monday, June 1, 2020

Aortic Valve Repair

Aortic Valve Repair

Aortic Valve Repair

Keywords: Aortic Valve Repair, Operations for Valvular Heart Disease, aortic valve Repair, aortic valve surgery, cardiac surgery

Aortic valve repair has been shown to yield good outcomes for select patients when performed by trained surgeons. In this chapter, we will discuss the surgical anatomy of the aortic valve, the surgical steps to aortic valve repair, as well as the pre-, intra-, and postoperative considerations that need to be addressed for a successful repair.
Aortic Root Enlargement Techniques

Aortic Root Enlargement Techniques

Aortic Root Enlargement Techniques
Keywords: Aortic Root Enlargement Techniques, Operations for Valvular Heart Disease

This chapter discusses the commonly used aortic root enlargement techniques that increase the diameter of the aorta with small annulus and allow the implantation of larger prosthetic valves with better hemodynamic performance. In addition, some other surgical considerations in patients with small aortic root will also be discussed.

Monday, December 23, 2019

Aortic Valve Replacement

Aortic Valve Replacement

Aortic Valve Replacement

Aortic valve replacement remains the gold standard for the treatment of patients with significant aortic valve stenosis and regurgitation. Successful aortic valve replacement requires careful preoperative assessment of the patient and an intimate understating of the aortic root anatomy. The authors understand that the operative steps may vary among surgeons; however, certain core principals exist that will ensure an optimal outcome.

Keywords: aortic valve, aortic stenosis, valve replacement, Operations for Valvular Heart Disease

Introductory Considerations
Step 1. Surgical Anatomy
·    The aortic valve is the last valve in the heart through which the blood is pumped before it goes to the body. The purpose of the aortic valve is to prevent backflow of blood from the aorta into the left ventricle.
·   The normal aortic valve is tricuspid, with left coronary, right coronary, and noncoronary leaflets. Each leaflet is supported by a fibrous skeleton with a shallow U-shaped configuration. The portion of this skeleton that supports the left coronary leaflet is continuous with the anterior leaflet of the mitral valve, forming the aortic-mitral curtain (annulus fibrosa).
·    Each leaflet is attached just beneath their corresponding sinus of Valsalva. The sinuses of Valsalva are slight dilations of the aorta above the valve that act to create the vortex of blood required for valve closure. The sinuses end at the sinotubular junction, which is the narrowest portion of the ascending aorta.
·    The left main coronary artery arises from the left sinus of Valsalva. Its ostium lies directly posterior, below the level of the sinotubular junction. The left main coronary artery runs to the left, beneath the pulmonary artery. The right coronary ostium is an anterior structure located above the right coronary cusp. Its location tends to be more variable than that of the left main coronary artery.
·  The ventricular septum is located beneath the right coronary cusp and contains the atrioventricular conduction system, which passes below the noncoronary cusp near the right-noncoronary commissure (Fig. 9.1).

Step 2. Preoperative Considerations
Indications for Aortic Valve Replacement for Aortic Stenosis
·       In the vast majority of adults, aortic valve replacement (AVR) is the only effective treatment for severe aortic stenosis (AS). Although there is some lack of agreement about the optimal timing of surgery, particularly in asymptomatic patients, it is possible to develop rational guidelines for most patients.
·      In the absence of serious comorbid conditions, AVR is indicated in virtually all symptomatic patients with severe AS. There are many ways in which AVR benefits these patients. These depend partly on the patient’s left ventricular (LV) function. The outcome is similar in patients with normal LV function and in those with moderate ventricular dysfunction. The depressed ejection fraction in many of these patients is caused by excessive afterload, and LV function improves after AVR. If LV dysfunction is not caused by afterload mismatch, improvement in LV function and resolution of symptoms may not be complete after valve replacement,1 but survival is still improved in this setting.2
·    Symptomatic patients with angina, dyspnea, or syncope exhibit symptomatic improvement and an increase in survival after AVR.1-6
·       In patients who have severe AS, even those with a low transvalvular pressure gradient, AVR results in hemodynamic improvement and better overall patient functional status.
·       In summary, symptomatic patients with severe AS should undergo AVR. These patients will have improved LV function, reduced or resolved symptoms, and increased survival.
·   Many clinicians are reluctant to proceed with AVR in an asymptomatic patient, whereas others are concerned about conservative treatment of a patient with severe AS. Insertion of a prosthetic aortic valve is associated with low perioperative morbidity and mortality. Despite this, some difference of opinion persists among clinicians regarding the indications for corrective surgery in asymptomatic patients. Irreversible myocardial depression or fibrosis may develop during a prolonged asymptomatic stage, and this may preclude an optimal outcome.5,7 Still others attempt to identify patients who may be at especially high risk of sudden death without surgery, although evidence supporting this approach is limited. Patients in this subgroup include those who have an abnormal response to exercise (e.g., hypotension), those with LV systolic dysfunction, those with marked or excessive LV hypertrophy, and those with evidence of very severe AS.
·    We recommend that asymptomatic patients with an aortic valve area of less than 0.8 cm2 undergo valve replacement. Similarly, any evidence of impaired LV function (e.g., decreased ejection fraction, LV dilation, or significantly elevated LV diastolic pressure at rest or with exercise) is an indication for AVR. In the absence of symptoms, a peak aortic gradient of 70 mm Hg may be an indication for surgery, but this is controversial.
·       Patients with moderate or more AS (mean gradient of 20 mm Hg or higher), with or without symptoms, who are undergoing coronary artery bypass grafting should undergo AVR at the time of the revascularization procedure.
·    Similarly, patients with moderate or more severe AS undergoing surgery on other valves (e.g., mitral valve repair) or the aortic root should also undergo AVR as part of the surgical procedure.

Indications for Aortic Valve Replacement in Aortic Regurgitation
·       AVR is recommended for patients with severe regurgitation in the presence of symptoms or any evidence of pathologic LV remodeling (e.g., impairment of LV function, LV dilation, significant elevation of LV end-diastolic pressure).
·    Symptomatic patients with advanced LV dysfunction (ejection fraction < 0.25 or end-systolic dimension > 60 mm) present difficult management issues. Some patients manifest meaningful recovery of LV function after operation, but many will have developed irreversible myocardial changes. The mortality rate associated with valve replacement approaches 10% in these patients, and the postoperative mortality rate over the subsequent few years is high.
·   AVR should be considered more strongly for patients with New York Heart Association (NYHA) functional class II and III symptoms, especially if symptoms and evidence of LV dysfunction are of recent onset, and intensive short-term therapy with vasodilators, diuretics, or intravenous positive inotropic agents results in substantial improvement in hemodynamics or systolic function. However, even in patients with NYHA functional class IV symptoms and an ejection fraction less than 0.25, the high risks associated with AVR and subsequent medical management of LV dysfunction are usually a better alternative than the higher risks of long-term medical management alone.8
·     AVR in asymptomatic patients remains a controversial topic, but it is generally agreed that valve replacement is indicated for patients with LV systolic dysfunction.8-14 As noted previously, for the purposes of these guidelines, LV systolic dysfunction is defined as an ejection fraction below normal at rest.
·     Valve replacement is also recommended for patients with severe LV dilation (end-diastolic dimension > 75 mm or end-systolic dimension > 55 mm), even if the ejection fraction is normal. Most patients with this degree of dilation have already developed systolic dysfunction because of afterload mismatch and thus are candidates for valve replacement on the basis of the depressed ejection fraction. The elevated end-systolic dimension in this regard is often a surrogate for systolic dysfunction. The relatively small number of asymptomatic patients with preserved systolic function, despite severe increases in end-systolic and end-diastolic chamber size, should be considered for surgery because they appear to represent a high-risk group with an increased incidence of sudden death15,16; the results of valve replacement in these patients have thus far been excellent. In contrast, postoperative mortality is considerable once patients with severe LV dilation develop symptoms or LV systolic dysfunction.17

Step 3. Operative Steps
·    Once the cardiac structures have been exposed, the patient is heparinized, and the distal ascending aorta and right atrial appendage are cannulated. If the aorta is heavily calcified, the surgeon may consider femoral or axillary cannulation and deep hypothermia with circulatory arrest without cross-clamping to avoid stroke. Transesophageal or epiaortic echocardiography can be useful if there is some uncertainty about the state of the aorta.18 A retrograde cardioplegia cannula is placed into the coronary sinus. Cardiopulmonary bypass is instituted, and a LV vent is placed through the right superior pulmonary vein. A cannula is placed in the mid ascending aorta for the delivery of cardioplegia into the aortic root and later de-airing. The aorta is cross-clamped, and the heart is arrested with antegrade and retrograde cardioplegia. Intermittent doses of cardioplegia are given throughout the procedure. In patients with significant aortic insufficiency, antegrade cardioplegia is often not effective, and arrest can be initiated with retrograde cardioplegia, followed by direct injection of cardioplegia into the coronary ostia.
·   Access to the aortic valve can be through an oblique or a transverse aortotomy. The aortotomy is placed at least 1 cm above the sinotubular junction, above the right coronary ostium. This circumvents compromising or injuring the right coronary artery during closure of the aortotomy. The aortotomy can be extended to the noncoronary sinus of Valsalva for greater exposure (Fig. 9.2).

·   Traction sutures can be placed at the sinotubular junction above the commissures. This provides maximum exposure of the annulus. The instillation of carbon dioxide into the operative field while the aorta is open may reduce intracardiac air when the cross-clamp is removed.
·    With the aortic valve exposed, the leaflets are resected, and the annulus is débrided of calcium. The surgeon must leave a thin rim of valve tissue and not excise the annulus completely. Resection of the valve is initiated at the commissure between the right and noncoronary sinuses. The commissure is excised from the aortic wall, and the right coronary cusp is excised (Fig. 9.3). The commissure between the left and right coronary cusps is excised, and the left coronary cusp is removed. Resection is completed with excision of the noncoronary cusp, performed toward the commissure between the left and noncoronary cusps (Fig. 9.4). When calcification is encountered, careful débridement is required to avoid detaching the aorta from the ventricle. A rongeur can be used to crush the calcium into smaller pieces to facilitate removal. All debris must be accounted for; this will minimize the possibility of stroke and coronary ostial occlusion of embolization. Extensive and vigorous irrigation must be performed after valve excision. A small gauze cloth may be placed into the left ventricle to prevent calcified particulate matter from entering the cavity, especially if the valve is severely calcified. Retrograde cardioplegia is given during irrigation to prevent debris from entering the coronary ostia.
·       The annulus is measured, and the appropriate-sized valve is selected for the replacement. If the annulus is too small, various aortic root enlargement techniques can be used (see Chapter 11).
·      Several suturing techniques have been used, but the most common technique uses horizontal pledgeted sutures with pledgets on the aortic or ventricular aspect of the annulus, depending on the type of valve being inserted.
·   We use an interrupted suture technique that affords maximum strength of the prosthetic attachment and has a low incidence of perivalvular leak. We place sutures from below the annulus, exiting slightly above it into the aorta. Double-needle, pledgeted 2-0 Dacron sutures are used, with little space between them. The sutures are alternating green and white to simplify identification of the suture pairs. The pledgets are placed below the annulus in the LV outflow tract. This secures the prosthesis by compressing the annulus between the sutures and prosthesis (Fig. 9.5).

·     Sutures are placed in the right coronary annulus toward the commissure between the right and noncoronary sinuses. In a similar fashion, the left coronary annulus is sutured toward the noncoronary sinus. Finally, the noncoronary sutures are placed (Fig. 9.6). Deep sutures along the posterior annulus, under the left main artery, should be avoided, given that the left main artery runs for a short distance along the posterior aspect of the aorta. Deep sutures in the muscle below the right coronary leaflet may damage the conduction system—in particular the left bundle and bundle of His, and should once again be avoided (see Fig. 9.1).
·    The sutures are then passed through the sewing ring of the prosthesis, which is tied down in the supraannular position (Fig. 9.7). Supraannular valves allow for a larger orifice area and tend to seat well in the annulus. We prefer to tie down the commissure sutures first, followed by the left, right, and noncoronary sinuses.
·   The use of sutureless prosthetic heart valves, initially developed in the 1960s, has been abandoned, due to multiple complications, such as paravalvular leaks and valve-related thromboembolic events.19 The rapid development of transcatheter technology, however, has fueled a reemergence of the sutureless strategy in an effort to accelerate the surgical procedure and potentially reduce adverse outcomes.20 Depending on the manufacturer, these valves may be contraindicated in bicuspid aortic valves, along with irregular or heavily calcified valves.
·       The implantation of sutureless valves varies in technique. As with traditional sutured valves, the leaflets must be excised. The degree to which the annulus is débrided depends on the particular valve that is chosen. From one to three guiding sutures are used to ensure proper orientation of the valve relative to the annulus.
·    Valves are deployed by releasing self-expanding Nitinol stents or balloon inflation of the valve, once positioned in the native annulus. The inflow portion of the valves are wrapped in cloth or pericardial tissue to promote adaptation of the prosthesis to the native annulus and prevent paravalvular leaks.
·      Once the prosthesis has been secured into place, the aortotomy is closed. Pledgeted, double- needle polypropylene sutures are placed at the lateral aspects of the aortotomy and tied down. A horizontal mattress stitch is used from the lateral aortotomy toward the middle. A second continuous stitch is placed as a second layer for the closure (Fig. 9.8). When a friable or thin aorta is encountered, consideration should be given to using felt strips for closure.
·     After release of the cross-clamp, transesophageal echocardiography (TEE) is used to assess the position of the prosthesis and evaluate for the possibility of perivalvular leak. Intraventricular air volume can also be determined. If a significant quantity of air remains in the ventricle, this can be aspirated using a needle in the ventricular apex. Right atrial and right ventricular pacing wires are placed. After recovery of a suitable heart rhythm, the patient is weaned from cardiopulmonary bypass, and TEE is used to monitor ventricular function. Cannulae are removed, heparin is reversed with protamine, and the incision is closed.

Step 4. Postoperative Care
·     The postoperative management for a patient having undergone AVR is routine and standard for most postcardiac surgical patients.
·   However, several points should be addressed. A patient with AS has a hypertrophied left ventricle and thus will likely be very sensitive to the preload state. In addition, atrial fibrillation is often not well tolerated in patients with a stiff, hypertrophic left ventricle. Although a Swan-Ganz catheter may not always be required, it may help assess the degree of volume loading and should be considered in complex cases.
·    Wide fluctuations in blood pressure are not uncommon. Any sudden increase in bleeding from the chest tubes or mediastinal tubes should alert the surgeon to the possibility of aortotomy suture line bleeding.
·     In patients in whom a mechanical valve has been placed, warfarin is started on the first or second postoperative day. If the international normalized ratio (INR) has not increased by the fourth day, we recommend intravenous heparin until the patient has achieved a therapeutic INR. The pacing wires are removed when clinically appropriate and prior to achieving an INR higher than 2.

Step 5. Pearls and Pitfalls
·    Solitary AVR is usually a straightforward procedure. However, attention to several points can improve the outcome. Because the aortic valve is often calcified, the surgeon should take care not to lose calcified debris in the ventricle or down the coronary arteries. A gauze pad can be placed in the ventricle during débridement to prevent embolization, and the ventricle should be copiously irrigated with cold saline after débridement. In addition, retrograde cardioplegia should be administered during irrigation.
·      When implanting any prosthetic valve, the surgeon needs to ensure that the coronary arteries are not occluded by the sewing ring, pledgets, or sutures. In case of a regional wall motion abnormality after bypass, it may be necessary to rearrest the heart and inspect the coronary ostia or to bypass the vessel supplying the dysfunctional region.
·     In the presence of a small aortic root, it is not advised to force a valve into the root. This may result in a paravalvular leak or, worse, aortic or ventricular disruption. This is especially true in older frail patients with a calcified annulus. If the surgeon is concerned with the possibility of a patient-prosthesis mismatch (predicted aortic valve area index < 0.8 cm2/m2), he or she should consider enlarging the aortic root annulus (see Chapter 11).
·       TEE has become a standard part of the procedure. It allows the surgeon and anesthesiologist to assess the adequacy of replacement in terms of possible paravalvular leak, abnormal leaflet motion, or regional or global myocardial dysfunction. In our opinion, it should be used in every case of valve replacement or repair unless contraindicated.

1.       Connolly HM, Oh JK, Orszulak TA, et al. Aortic valve replacement for aortic stenosis with severe left ventricular dysfunction: prognostic indicators. Circulation. 1997;95:2395–2400.
2.         Smith N, McAnulty JH, Rahimtoola SH. Severe aortic stenosis with impaired left ventricular function and clinical heart failure: results of valve replacement. Circulation. 1978;58:255–264.
3.           Schwartz F, Baumann P, Manthey J, et al. The effect of aortic valve replacement on survival. Circulation. 1982;66:1105–1110.
4.        Murphy ES, Lawson RM, Starr A, Rahimtoola SH. Severe aortic stenosis in patients 60 years of age or older: left ventricular function and 10-year survival after valve replacement. Circulation. 1981;64:II184–II188.
5.       Lund O. Preoperative risk evaluation and stratification of long-term survival after valve replacement for aortic stenosis: reasons for earlier operative intervention. Circulation. 1990;82:124–139.
6.         Kouchoukos NT, Davila-Roman VG, Spray TL, et al. Replacement or the aortic root with a pulmonary autograft in children and young adults with aortic-valve disease. N Engl J Med. 1994;330:1–6.
7.          Lund O, Larsen KE. Cardiac pathology after isolated valve replacement for aortic stenosis in relation to preoperative patient status: early and late autopsy findings. Scand J Thorac Cardiovasc Surg. 1989;23:263–270.
8.           Bonow RO, Nikas D, Elefteriades JA. Valve replacement for regurgitant lesions of the aortic or mitral valve in advanced left ventricular dysfunction. Cardiol Clin. 1995;13:73–83.
9.           Ross J Jr. Afterload mismatch in aortic and mitral valve disease: implications for surgical therapy. J Am Coll Cardiol. 1985;5:811–826.
10.        Nishimura RA, McGoon MD, Schaff HV, Giuliani ER. Chronic aortic regurgitation: Indications for operation—1988. Mayo Clin Proc. 1988;63:270–280.
11.        Bonow RO. Asymptomatic aortic regurgitation: indications for operation. J Card Surg. 1994;9:170–173.
12.        Rahimtoola SH. Valve replacement should not be performed in all asymptomatic patients with severe aortic incompetence. J Thorac Cardiovasc Surg. 1980;79:163–172.
13.        Carabello BA. The changing unnatural history of valvular regurgitation. Ann Thorac Surg. 1992;53:191–199.
14.        Gaasch WH, Sundaram M, Meyer TE. Managing asymptomatic patients with chronic aortic regurgitation. Chest. 1997;111:1702–1709.
15.        Turina J, Turina M, Rothlin M, Krayenbuehl HP. Improved late survival in patients with chronic aortic regurgitation by earlier operation. Circulation. 1984;70:I147–I152.
16.        Bonow RO, Lakatos E, Maron BJ, Epstein SE. Serial long-term assessment of the natural history of asymptomatic patients with chronic aortic regurgitation and normal left ventricular systolic function. Circulation. 1991;84:1625–1635.
17.        Klodas E, Enriquez-Sarano M, Tajik AJ, et al. Aortic regurgitation complicated by extreme left ventricular dilation: long-term outcome after surgical correction. J Am Coll Cardiol. 1996;27:670–677.
18.        Byrne JG, Aranki SF, Cohn LH. Aortic valve operations under deep hypothermic circulatory arrest for the porcelain aorta: “no-touch” technique. Ann Thorac Surg. 1998;65:1313–1315.
19.        Magovern GJ, Cromie HW. Sutureless prosthetic heart valves. J Thorac Cardiovasc Surg. 1963;46:726–736.
20.    Carrell T, Englberger L, Stalder M. Recent developments for surgical aortic valve replacement: the concept of sutureless valve technology. p 2013.

Postinfarction Ventricular Septal Defect Repair

Postinfarction Ventricular Septal Defect Repair

Keywords : postinfarct ventricular septal defect, Operations for Coronary Artery Disease

Postinfarction Ventricular Septal Defect Repair
Step 1. Surgical Anatomy
·    Postinfarction ventricular septal defects (VSDs) are classified as occurring in three locations apical, anterior, and posteroinferior (Fig. 8.1). Most common is an anterior or apical defect caused by anterior septal myocardial infarction after occlusion of the left anterior descending coronary artery. In about one-third of patients, the rupture occurs in the posterior septum after an inferior septal infarction. The inferior septal infarction is usually due to occlusion of a dominant right coronary or, less frequently, of a dominant circumflex artery. An apical septal defect can be considered a variant of an anterior defect, but it presents the opportunity for a modified, and less involved, surgical technique.1,2
·    Associated with the septal defect is a variable amount of adjacent myocardial damage, both septal and free wall. In addition, the posterior papillary muscle is often involved in a posterior postinfarction septal defect. When the free wall infarction involves the papillary muscle, special techniques must be used to anchor the repair, or a mitral valve replacement should be undertaken.1,2

Step 2. Preoperative Considerations
·  Without surgery, 50% of patients with a postinfarction VSD will die within 24 hours, and 80% will die within 4 weeks. Therefore, the presence of this defect is considered an urgent indication for operation. The goal of preoperative management is to reduce the left-to-right shunt by reducing both the systemic vascular resistance and left ventricular pressure.
·    In addition, efforts are made to maintain cardiac output and arterial pressure to aid in end- organ perfusion. Placement of an intraaortic balloon pump is greatly beneficial and should be done as soon as the diagnosis is made. Patients in severe failure who are deemed hopeless candidates for immediate operation can be managed with an intraaortic balloon pump or with mechanical circulatory support in an attempt to delay surgery.
·    The use of a ventricular assist devices and extracorporeal membrane oxygenation (ECMO) with staged repair of the postinfarct VSD has been described. Left ventricular assist devices may result in a greater degree of right-to-left shunting; therefore, biventricular assist devices are preferred. ECMO may allow for support and resuscitation of critically ill patients in cardiogenic shock. ECMO can be instituted using central or peripheral cannulation. The type of cannulation should be determined on a case by case basis. Mechanical circulatory support for a short amount of time can be used to reverse end-organ damage. In addition, it can provide some time for infarct maturation, allowing for firmer tissue at the time of surgical repair.3,4
·  In select patients, percutaneous closure is possible. The primary limitation is the friable condition of the surrounding septal muscle and proximity to the mitral valve or papillary muscles. Given reports of frequent early failure, this approach may best be used as an interim measure before surgery. The approach is more likely to be successful in delayed presentations or as treatment for recurrent defects that may occur between a repair patch and adjacent noninfarcted myocardium.5 The advent of the Amplatzer Muscular VSD Occluder (St. Jude Medical, St. Paul, MN) has shown potential for being an effective percutaneous treatment for extremely high-risk patients with postinfarct VSD.6
·  Controversy exists over the role of preoperative coronary angiography and concomitant bypass surgery. Those who argue against preoperative catheterization have noted that there is no survival benefit and that it is a time-consuming procedure. In addition, because all patients present with a completed full-thickness infarction, revascularization of the infarcted territory is of limited value. A selective approach is appropriate, with catheterization performed in the subset of patients who are not in shock or severe failure before surgery,7 because some patients may benefit from revascularization to noninfarcted territories in which flow-limiting coronary lesions exist.

Step 3. Operative Steps
1. General Principles
·   A standard median sternotomy is performed. Cardiopulmonary bypass is accomplished through the distal ascending aorta, with bicaval venous drainage. A variety of myocardial protection strategies are available. Satisfactory protection has been demonstrated with moderate hypothermia and frequent administration (every 15 to 20 minutes) of cold oxygenated blood cardioplegia with a combination of antegrade and retrograde perfusion through the coronary sinus. Other strategies, including continuous warm cardioplegia, have been used. A flexible left ventricular vent is placed through the right superior pulmonary vein. To prevent postbypass coagulopathy, an antifibrinolytic is administered before commencing cardiopulmonary bypass and is continued as an infusion. The use of surgical sealants on the epicardial surface of the heart at the location of felt buttresses may be recommended.
·  Areas of full-thickness myocardial infarction will not hold sutures against pressure. Regardless of the operative technique or location of the defect, it is critical to anchor suture lines to noninfarcted tissue. In the endocardium, this is done by taking stitches at least 5 mm from the zone of necrosis. When this is not possible, stitches are taken through the full thickness of the free wall, and a buttress of Teflon felt is used. In this way, strength is afforded by the epicardial portion of the ventricular wall, and the stress is distributed.7
·   There are two general approaches to the treatment of the necrotic muscle. The first approach emphasizes débridement of necrotic tissue and tension-free repair, and it usually involves a prosthetic patch to replace excised tissue. The second approach is to leave the necrotic tissue in place, but to exclude it by placing a bovine pericardial patch that circumscribes the infarction. Both techniques are described.

2. Standard Technique: Débridement of Necrotic Tissue
Anterior Apical Defects
  The VSD is approached through an incision through the anterior apical left ventricle (LV), passing through the area of necrosis. After débridement of necrotic tissue, smaller defects, particularly at the apex, can be closed by approximating the free walls of the right ventricle (RV) and LV with the septum using interrupted size 0 polypropylene sutures over Teflon felt strips (Fig. 8.2). It is critical that the stitches pass through healthy muscle.7
  Usually, the size of the necrotic tissue prevents a primary tension-free repair, requiring the use of prosthetic patch material. Low-porosity Dacron is generally used, although glutaraldehydetreated bovine pericardium is an alternative. The patch is fashioned to be larger than the defect. Pledgeted sutures of 1-0 Tevdek are passed from the RV through the intraventricular septum and then through the patch material (Fig. 8.3A). In the apical portion, pledgeted sutures are taken through the free wall of the RV (see Fig. 8.3B). The ventriculotomy is then closed with Teflon felt strips and no. 1 Tevdek, first using interrupted mattress sutures and then a running suture as a second layer7  (see Fig. 8.3C).

Posteroinferior Defects
·    Closure of posteroinferior septal defects poses a greater technical challenge. Simple plication of these defects is rarely possible. With large defects, this results in unacceptable tension and reopening or catastrophic disruption. Depending on the size and location of the defect, one or two patches may be required. In addition, rupture of the posterior papillary muscle occasionally requires replacement of the mitral valve.
·  A transinfarct posterior incision is made just to the left ventricular side of the posterior descending coronary artery (Fig. 8.4A). This incision is started at the midportion of the posterior wall and extended toward the mitral annulus and apically. Most commonly, rupture is found in the proximal half of the posterior septum (see Fig. 8.4B) and involves the pos- teromedial papillary muscle. The necrotic portion of the ventricular septum is excised, along with the involved portion of the posterior ventricular free wall (Fig. 8.5A). The free edge of the RV is shaved back to expose the margins of the defect clearly.
·   Rarely, repair of a small septal rupture can be undertaken primarily. An appropriate lesion would appear as an unhinging of the posterior attachment to the septum, with little adjacent myocardial necrosis. The repair is accomplished by approximating the posterior septum to the free wall of the RV with felt-buttressed mattress sutures of 1-0 Tevdek. The LV can then be closed with a separate suture line, again with interrupted mattress sutures of no. 1 Tevdek buttressed with felt. A second running suture line is then taken to reinforce the ventriculotomy closure.

·    More commonly, patches are required. A single patch can be added to aid in a tension-free closure of the LV after primary closure of the septum (see Fig. 8.5B). When the defect in the septum is larger, a two-patch technique is used. Interrupted mattress sutures of buttressed 2-0 Tevdek are placed circumferentially around the defect. The sutures are placed on the right ventricular side of the septum and then transitioned to the epicardial surface of the diaphragmatic right ventricular free wall. An appropriately shaped Dacron patch is parachuted down after passage of the stitches. Use of additional felt on the exterior of the patch cushions the sutures and aids in the even distribution of forces (Fig. 8.6A). A second patch is now required for closure of the remaining defect into the LV.
·    Mattress sutures of buttressed 2-0 Tevdek are placed circumferentially around the margins of the posterior left ventricular free wall. The stitches are taken from the endocardial surface through the ventricular wall so that the patch will lie on the epicardial surface when the repair is complete (Fig. 8.7; see Fig. 8.6B). Again, use of additional felt on the outside of the patch may be advantageous (Fig. 8.8).
·    Involvement of the posterior medial papillary muscle may preclude the placement of stitches through infarcted tissue. In these cases, as in the case of papillary muscle rupture, a mitral valve replacement is performed after patch placement. The mitral valve is exposed through a left atriotomy. On occasion, a transseptal approach via the dome of the left atrium may be required. The valve is excised and replaced with a low-profile prosthesis. Interrupted, felted 2-0 Tevdek sutures are used, with the needle passing from the left atrium through the annulus.

3. Modification of Technique: Infarct Exclusion
Anterior Apical Defects
·     The apical portion of the ventricle is opened through the infarction, with extension onto the anterior LV. A glutaraldehyde-preserved bovine pericardial patch is secured to noninfarcted areas of the left ventricular septum using running 3-0 polypropylene sutures. The stitches should be inserted 5 to 7 mm deep in the muscle and 4 to 5 mm apart. The stitches in the patch should be 5 mm from its free margin to allow the patch to cover the area between the entrance and exit of the sutures (Fig. 8.9A).
·   The suture line is begun at the most proximal part of the septum, and suturing begins traveling toward the apex. The suture line continues from the septum onto the left ventricular free wall. If the infarct involves the anterior papillary muscle at its base, the suture is brought outside the heart at this point and continued as full-thickness interrupted 2-0 polypropylene sutures buttressed on the epicardial surface with a strip of bovine pericardium or Teflon felt. The LV is then closed with interrupted mattress sutures of 2-0 polypropylene buttressed by Teflon felt strips, followed by a running 2-0 polypropylene stitch (see Fig. 8.9B).8
Posteroinferior Defects
   A transinfarct incision is made in the inferior wall of the LV, just lateral to the posterior descending coronary artery, to expose the defect and is extended toward both the mitral valve and apex. Care is taken to avoid damage to the posterior lateral papillary muscle. A bovine pericardial patch is tailored in a triangular shape. Its size will be approximately 4 × 7 cm in most patients. The base of the triangle is sutured to the mitral valve annulus with continuous 3-0 polypropylene sutures. The medial suture line then transitions from the mitral annulus to the endocardium of the ventricular septum and is continued along that structure apically. Laterally, the suture line transitions to the endocardium of the posterior LV.
     After several stitches, the posterior papillary muscle is encountered. If the area of necrosis is small, and if healthy tissue allows for continuation, the running sutures are continued toward the apex. Usually, on reaching the posterior papillary muscle, it is necessary to bring the running stitch through the muscle to the outside of the LV. The suture line is then continued with interrupted, full-thickness, 2-0 polypropylene sutures and buttressed with felt on the outside (Fig. 8.10A). The suture line continues until the patch is completely secured, and then the ventriculotomy is closed in two layers of full-thickness sutures buttressed on strips of Teflon felt. The infarcted right ventricular wall is left undisturbed8  (Fig. 8.10B).

Right Ventricular Approach
Hosoba et al.9 have described repairing postinfarct VSDs using a right ventricular approach and two Dacron patches. For anterior septal defects, an incision is made in the RV wall parallel to the distal left anterior descending artery. Sutures are placed transseptally from the LV cavity via the VSD and into the octagonally shaped patch. The patch is placed through the VSD, into the LV, and secured into place. A second Dacron patch is secured over the defect in the RV. For posterior VSDs, a similar two-patch technique is used, with an incision in the RV parallel to the midportion of the posterior descending artery.

Step 4. Postoperative Care
·  If an intraaortic balloon pump was not inserted before surgery, one should be placed. Inotropic support is instituted with milrinone (phosphodiesterase inhibitor). This drug is preferred because, in addition to its inotropic properties, it has vasodilatory properties in the pulmonary vascular bed.
·    Posterior defects are associated with a right ventricular infarction and more often result in right heart failure on separation from bypass. In such a case, inhaled nitric oxide (20 ppm) is instituted before attempted separation. Additional maneuvers may include right-sided infusion of prostaglandin E1 (0.5 µg/kg/min) and left-sided norepinephrine infusion through a left atrial line.7,10
·  For patients who are still in cardiogenic shock despite these maneuvers, mechanical circulatory support may be warranted.11 ECMO may allow for support and resuscitation of these patients in the postoperative stage. Central cannulation may be preferred postcardiotomy but the cannula location should be individualized based on the clinical picture.
·    Extubation usually requires aggressive early postoperative diuresis. After fully rewarming, intravenous infusion of furosemide at doses of 5 to 20 mg/hr is used to maintain urine output greater than 100 mL/hr. Continuous venovenous hemofiltration is used for nonresponders.

Step 5. Pearls and Pitfalls
·   The common problems during separation from bypass are low cardiac output, with or without right ventricular failure and bleeding.
·  Recurrent or severe ventricular ectopy is common. Before attempted separation from cardiopulmonary bypass, amiodarone is begun with a bolus of 150 mg, followed by ongoing infusion at 1 mg/min. The bolus may be repeated up to six times for malignant ectopy.
· Inadequate hemodynamics on separation from cardiopulmonary bypass may require placement of a ventricular assist device or ECMO. Left ventricular assist devices may result in increased right-to-left shunting, and biventricular devices may be preferable.

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2.  Daggett WM. Postinfarction ventricular septal defect repair: Retrospective thoughts and historical perspectives. Ann Thorac Surg. 1990;50:1006–1009.
3.      Pitsis A, Kelpis T, Visouli A, et al. Left ventricular assist device as a bridge to surgery in postinfarction septal defect. J Thorac Cardiovasc Surg. 2008;135:951–952.
4.   Conradi L, Treede H, Brickwedel J, et al. Use of initial biventricular mechanical support in a case of postinfarction ventricular septal rupture as a bridge to surgery. Ann Thorac Surg. 2009;87:e37–e39.
5.  Michel-Behnke I, Trong-Phi L, Waldecker B, et al. Percutaneous closure of congenital and acquired ventricular septal defects: Considerations on selection of the occlusion device. J Interv Cardiol. 2005;18:89–99.
6.     Calvert PA, Cockburn JC, Wynne D, et al. Percutaneous closure of post-infarction ventricular septal defect: in-hospital outcomes and long-term follow-up of UK Experience. Circulation. 2014;129:2395–2401.
7.    Agnihotri AK, Madsen JC, Daggett WM Jr. Surgical treatment of complications of acute myocardial infarction: postinfarction ventricular septal defect and free wall rupture. In: Cohn LH, ed. Cardiac Surgery in the Adult. 3rd ed. New York: McGraw-Hill; 2008:753–784.
8.    David TE, Armstrong S. Surgical repair of postinfarction ventricular septal defect by infarct exclusion. Semin Thorac Cardiovasc Surg. 1998;10:105–110.
9.   Hosoba S, Asai T, Suzuki T, Nota H, et al. Mid-term results for the use of the textended sandwich patch technique through right ventriculotomy for postinfarction ventricular septal defects. Eur J Cardiothorac Surg. 2013;e116-e120.
10.   Taghavi S, Mangi AA. Postinfarction ventricular septal defect and ventricular rupture. In: Selke F, del Nido SJ, Swanson SJ, eds.
11.   Sabiston and Spencer Surgery of the Chest. 9th ed. Philadelphia: Elsevier; 2016:1653–1662.
12.   Firstenberg MS, Blais D, Crestanello J, et al. Long-term mechanical support for complex left ventricular postinfarct pseudoaneurysms.
13.   Heart Surg Forum. 2009;12:E291–E293.

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