The wall of a mature aneurysm is a white fibrous scar, visible externally on the cut surface as well as endocardially. Characteristically, the aneurysmal portion of the LV wall is thin, the endocardial surface is smooth and nontrabeculated, and the area of scar is clearly demarcated. In more than half of patients, varying amounts of mural thrombus are attached to the endocardial surface. The mural thrombus may calcify, as may the overlying pericardium, which is often densely adherent to the aneurysm’s epicardial surface. ^, Such classic LV aneurysms are at one end of the spectrum of postinfarction LV scars. At the other end are diffuse, scattered, and at times sparse punctate scars, frequently visible at operation in areas of previous MI. These scars are usually not transmural, and the LV wall is not thinned or only minimally so. The endocardium beneath retains its trabeculations, and the area of scarring is not clearly demarcated from the rest of the wall. Mural thrombi are not commonly present, and the pericardium is not commonly adherent to the area. Between these extremes is a continuous spectrum of postinfarction LV scarring, as myocardial necrosis is rarely homogeneous in an area of infarction.

A mature aneurysm consists almost entirely of hyalinized fibrous tissue. However, a small number of viable muscle cells are usually present. Fibrous tissue of the type present in aneurysms takes at least 1 month to form, although collagen is present within 10 days of infarction. Thus, when an aneurysm is said to be present (based on wall thinning and dilation) within 1 week or so of a first infarction, the wall is composed largely of necrotic muscle and is, not, therefore, by definition, a true (mature) aneurysm.

About 85% of LV aneurysms are located anterolaterally near the apex of the heart. Few are confined to the lateral (obtuse marginal) area, and only 5% to 10% are posterior, near the base of the heart. Posterior or inferior aneurysms (i.e., those occurring in the diaphragmatic portion of the left ventricle) are in some ways different from apical and anterolateral aneurysms. Nearly half of posterior aneurysms are false aneurysms (see “ False Left Ventricular Aneurysm ” under Special Situations and Controversies), whereas nearly all anterolateral and apical aneurysms are true aneurysms. True posterior wall postinfarction aneurysms are associated with a high prevalence of postinfarction mitral regurgitation secondary to ischemia and dilation of the posterior wall. ^, (see “ Section III Mitral Regurgitation from Ischemic Heart Disease ”). Mitral regurgitation associated with posterior dilation is almost uniformly linked to a focal dilation and contrasts with mitral regurgitation present following anterior MI that is associated with a diffuse dilation affecting more than five segments in the anteroapical region for the mitral regurgitation to be present. ^,

Somewhat less than half of patients undergoing resection of classic LV aneurysms or scars have stenotic coronary artery disease confined to the LAD. ^, More often, diffuse coronary artery disease is present. The discrepancy between the reported prevalence of single- and multivessel disease may be related to differences in the definition of LV aneurysm; to different sources of the material (clinical, surgical, or postmortem); and in the case of surgical material, to case selection. A patient with single-vessel disease is more apt to survive an acute infarction and appear in a surgical series than a patient with multivessel disease. In the present era, with the widespread use of primary PCI, a certain number of patients have patent coronary arteries despite deep injury of the ventricles (no-reflow phenomenon). ^,

Postmortem studies indicate that most patients with classic LV aneurysms have increased cardiac volume and weight. ^{, ,} The increase in volume is, in part, the result of simple thinning and bulging of the aneurysmal portion of the LV wall. However, nonaneurysmal portions of the left ventricle also increase in volume and thickness secondary to hemodynamic stress placed on them by akinesia of the aneurysmal segment (remodeling) and by the Laplace law. Inactivation (by akinesis or dyskinesis) of at least 20% of the LV wall area is required for LV enlargement to occur. ^, The larger the akinetic or dyskinetic area, the greater the enlargement of the rest of the ventricle. The time course of these events has not been clearly defined, ranging from a few days to years after the AMI.

Historically, about 10% to 30% of patients who survived a major MI developed an LV aneurysm. ^, Today, the prevalence has decreased as a result of the improved treatment of patients presenting with AMI. The widespread use of PCI has reduced the prevalence of permanently occluded LADs. Further improvements include better management of hypertension and avoidance of corticosteroids, both of which are risk factors for development of aneurysms. ^, The mechanisms by which LV aneurysms form are not completely elucidated. Occurrence of a large transmural infarction is a prerequisite. It has been suggested that patients who develop LV aneurysms have few intercoronary collateral arteries. It is postulated that a rich collateral blood supply to an area of MI tends to increase the number and size of the islands of viable myocardial cells in the area and decrease the probability that the necrosis is extensive enough to result in a thin-walled transmural scar. This hypothesis is supported by Forman and colleagues, who studied 79 patients undergoing cardiac catheterization 6 months after a first MI. They found total occlusion of the LAD and poorly developed collateral flow to be the determinants of LV aneurysm formation. Apparently, normal or supranormal systolic function in adjacent ventricular segments is necessary for generating sufficiently high intraventricular pressure and wall tension in the infarcted area to result in aneurysm formation.

Whether large LV aneurysms are large because of inception or gradually enlarge once formed is uncertain. The mechanism for increasing symptomatology that characterizes the natural history of many patients with large LV aneurysms has not been clearly established. ^{, ,} It may be due to a gradual increase in the size of the area of akinesia or dyskinesia and to a consequent gradual reduction in stroke volume and global ejection fraction. ^, The non-aneurysmal portion of the LV wall is subjected to increased systolic wall stress as ventricular size increases (as described by the Laplace law) and may ultimately lose its systolic reserve and contribute to LV enlargement and failure. This process is worsened by any myocardial ischemia involving the non-aneurysmal portion of the ventricular wall.

An aneurysm changes the curvature and thickness of the LV wall, and because these are determinants of LV afterload (wall stress), global LV performance is altered. ^, Also, a large LV aneurysm leads to global cardiac remodeling with generalized dilation ( Fig. 10.3 ). Variations in intrinsic properties of scar, muscle, and border-zone tissue can affect both systolic and diastolic function. Finally, paradoxical movement in the aneurysmal portion of the wall reduces efficiency of the ventricle because systolic work is wasted on expansion of the aneurysm.

Gadolinium late enhancement of cardiac MR showing a global dilation of the left ventricle.

Function in uninvolved segments of the left ventricle per se (segmental ejection fraction) has been difficult to study because of the complexities of assessing ventricular function in this setting. When wall thickening is used as a measure of regional systolic function, it appears that systolic function is maintained in the remote nonaneurysmal portions of the ventricle. Moreover, a baseline geometric pattern of LV “dilated” remodeling, indicated by a low relative wall thickness, is associated with a worse diastolic function. However, analysis of the function of the LV wall with speckle tracking technology in all segments before and after surgical ventricular restoration demonstrated that the remote zone (far from the scar) has a lower contractility reserve, an increased mechanical dispersion, and a decreased longitudinal strain. Early in systole, the aneurysm and border zones bulge outward (paradoxical movement) as systolic intraventricular pressure rises to a maximum. After the surgical procedure, all these parameters improve in every region, mostly in the basal region. ^,

Right ventricular (RV) function may be impaired in patients with LV aneurysm. This may result from akinesis or dyskinesis of the ventricular septum, impaired RV wall motion near the apex, increased pulmonary artery pressure, occlusive disease of the right coronary artery, and increased volume of the left ventricle within the pericardial cavity. Involvement of the right ventricle is a major risk factor of mortality after the surgical treatment of LV aneurysm.

The complexities of ischemic heart disease in general and the difficulties in identifying true LV aneurysms have mitigated achieving a clear understanding of survival and risk factors for death of patients with LV aneurysms. Patients with an LV akinetic area (not all of which are true aneurysms) are reported to have a 5-year survival without operation of 69%, perhaps only a little less than that dictated by their coexisting coronary artery disease. Patients with a dyskinetic area of LV wall (many of which are probably aneurysms) have a 54% 5-year survival, which is reduced to 36% when myocardial function in the ventricle is reduced. Size of the aneurysm is a risk factor for premature death in surgically untreated patients. In patients with small aneurysms (usually without symptoms of heart failure [HF]), the probability of surviving is dictated primarily by severity and extent of the coronary arterial stenosis and is greater in asymptomatic than in symptomatic patients. Left ventricle volume after an AMI is one of the most important risk factors for mortality. In a post hoc analysis of the STICH trial, a postoperative left end-systolic volume index (ESVI) less than 70 mL/m ² was associated with improved survival, as well as global LV function and natriuretic markers ( Fig. 10.4 ). In contrast, an ESVI > 70 mL/m ² increases mortality. The functional characteristics of the remaining ventricle are also major determinants of survival. Diastolic dysfunction with increased markers of HF (N terminal [NT]-pro-Brain naturetic peptide [BNP]) is a risk factor for mortality. ^, In addition, all the usual risk factors for premature death in patients with ischemic heart disease ( Chapter 9 ) pertain to patients with LV aneurysms.

Cardiac MR images from a patient with extensive LV remodeling before (A) and after surgical ventricular reconstruction (B) showing significant left volume reduction. Improved ejection fraction (EF) is associated with a significant decrease in circulating natriuretic peptides.

The following principles should be observed to obtain optimal results in the treatment of LV aneurysms and chronic scars.

• •

  Complete revascularization, also in the territory of LAD, with the idea that septal branches are important to the function of the basal septum;

• •

  Exclusion from the cavity of all diseased tissue;

• •

  Reconstruction, respecting the physiologic ellipsoid shape of the LV, avoiding distortion and sphericalization, with the possibility to increase diastolic dysfunction and impair mitral valve (MV) function;

• •

  Sizing the new LV cavity to obtain a target ESVI below 60 mL/m ² .

Anterior aneurysm.

Different techniques have been described to treat an anterior aneurysm. All the techniques are effective if the criteria previously described are achieved. The results are determined also by the anatomic presentation. Small dilation can be treated by plication using a double layer, continuous suture of 2-0 polypropylene. This situation is very rare, especially because small dilations normally do not impact quality of life and life expectancy. Patients with large ventricles and increased values of HF biomarkers, such as NT-proBNP, have high mortality. A standardized surgical technique fitting all types of dilation is advisable.

With extracorporeal circulation with the empty beating heart, the ventricle is freed from the pericardial adhesions, and the target vessels are visualized. The aorta is cross-clamped, the heart is arrested with cold cardioplegic solution, and the distal anastomoses of coronary bypass grafts are completed. Some surgeons believe that it is useful to have a continuous CO ₂ flow in the surgical field to avoid air embolism. The LV is open parallel to the LAD, starting in the scarred anterior spot. Sometimes scar is not visible because of a layer of normal-looking myocardium that is present over the scar, despite the transmural nature of the MI ( Fig. 10.5 ).

The ventricle is unloaded, showing a collapsing anterior wall.

With gentle palpation, it is possible to detect a thinner spot. The ventricle is opened parallel to LAD for a few centimeters toward the apex and inspected, and loose thrombus is sought and removed; the papillary muscle position is identified, and the incision is enlarged toward the basal region of the left ventricle until the transition zone is reached. The cavity is inspected and cleaned of all clots. With the index finger in the cavity and the thumb outside, it is possible to palpate the anterior wall and the septum. This is a simple way to identify the limit between the normal wall and the diseased tissue, which is always thinner. This limit represents the transition zone, which is the line where the suture will run, excluding the scar from the new LV cavity ( Fig. 10.6 ).

After the opening of the left ventricle, the transitional zone is visible near the origin of the papillary muscles.

Four stay sutures are placed at the extremity of the ventriculotomy, and a preshaped sizer is inserted ( Fig. 10.7 ). The sizer is chosen with a volume of 50 mL per meter of the patient’s body surface area. The sizer has a physiologic shape with a normal sphericity index; the longitudinal diameter/transverse diameter is equal to 0.5 ( Fig. 10.8 ). The use of a sizer or mannequin is important because the size will determine the final shape and volume of the new cavity and will avoid restriction, distortion, and amputation. Particularly when the transition zone is not clearly represented (in case of global dilation), the sizer acts as a scaffold, and the cavity is closed over the sizer. The apex of the sizer points out the position of the new apex of the ventricle.

Ventriculotomy is performed with four stay sutures, allowing complete visualization of the cavity.

The sizer is inserted in the cavity with its apex pointing in the direction of the new apex.

In the case of involvement of the inferior wall in the scarred tissue, a gap is present between the transition zone, which often is near the base of papillary muscles, and the site of the new apex points out by the apex of the sizer. This portion of apical inferior dilation must be reduced. To achieve a physiologic longitudinal diameter, a suture of 2-0 polypropylene fixing the inferior dilation is conducted from the transition zone to the site pointed out by the apex of the sizer ( Fig. 10.9 ).

The gap between the new apex and the transitional zone is plicated, obliterating the inferior component of the left ventricle aneurysm and avoiding amputation of the new apex.

When the target is reached, the stitch is secured external to the cavity using a Teflon pledget. A second suture, starting at the transition zone in the basal region near the aortic valve, brings the lateral transition zone against the septum. This suture goes deep into the septum, ensuring all scarred tissue is excluded from the cavity. The remnant tissue is closed over a Teflon strip to reinforce the closure of the ventricle ( Fig. 10.10 ). The MV can be approached through the ventriculotomy if the dilation is large enough to have easy access.

The anterior plication starts near the aortic valve and continues to meet the inferior plication. The sizer acts as a scaffold over which the new cavity is reconstructed.

An alternative procedure is ventricle reconstruction using a patch ( Fig. 10.11 ). This technique has been termed “endoaneurysmorrhaphy” by Cooley and “endoventricular circular patch plasty repair” by Dor. When a patch is used for closure, the area of septal scarring can be excluded from the reconstructed left ventricle. This may result in improved LV function. ^{, ,} Furthermore, curvature of the anterior wall of the left ventricle may be maintained. Based on echocardiographic measurements in normal hearts, Fontan determined that the patch should be oval and should have a long diameter from 2 to 2.5 cm in situ. Thus, it should be made 2.5 to 3 cm in length to compensate for the space taken up by the suture line. A patch that is too large may result in an end-diastolic LV volume that is too large and, thus, a reduced global ejection fraction. A patch that is too small may reduce LV volume and compliance. A balloon of known volume (50 to 60 mL) can be inserted into the opened LV cavity to facilitate creating a chamber of appropriate size and shape. A purse-string suture of No. 2-0 polypropylene is placed at the junction of scar and contractile septal and free wall myocardium. The longitudinal and transverse dimensions of the resulting defect are measured. A patch of gelatin or collagen-impregnated Dacron with slightly larger (0.5 cm) dimensions is fashioned and then sutured into place with a continuous 2-0 polypropylene suture. Before completing the suture line, air is evacuated from the left ventricle by infusing volume from the pump-oxygenator, gently inflating the lungs, and injecting saline into the ventricle. This suture line must be watertight to avoid formation of a false aneurysm. The remnant of the aneurysm is trimmed, if necessary, and is closed securely over the patch with a continuous 2-0 polypropylene suture.

Reconstruction of the left ventricle using a Dacron patch. The patch is sewn deeply on the septum, excluding the scarred tissue. The plane of the patch must be orthogonal to the mitral valve to avoid amputation of the cavity.

With this technique, the shape of the new ventricle is determined by the anatomic position of the line of demarcation from scar and contractile myocardium. If this line is parallel to the mitral plane, a deformation of the cavity is unavoidable ( Fig. 10.12 ), with sphericalization and amputation of the apex, which in turn worsens the LV diastolic function and impairs the MV function. ^, This technique is effective in cases of well-defined LV aneurysms, but results can be suboptimal in the presence of large ventricles without clear transitional zones. An alternative procedure was described for patients without a calcified aneurysm or in patients with a small LV cavity. LV reconstruction is performed using multiple concentric purse-string sutures without a patch. ^, This technique is easy to perform, but it can produce an important distortion of the LV cavity, responsible for the worsening of diastolic function leading up to important arrhythmias.

An example of amputation of the LV cavity. As seen in (A) the patch is oriented parallel to the mitral plane, resulting in a final suboptimal result, as seen in the frame of the left ventriculogram in (B).

Posterior aneurysm.

The techniques described for repairing anterior LV aneurysms are also applicable to posterior aneurysms. The dilation involving the LV inferior wall can be located between the two papillary muscles or between the posteromedial papillary muscle and the septum. The site of incision must be chosen very carefully to avoid injury to papillary muscles. After the identification of the relationship between the aneurysm and papillary muscles, the ventriculotomy is extended to all scarred tissue ( Fig. 10.13 ). In some cases, this incision can start from the mitral anulus and ends at the apex of the left ventricle. More frequently, the incision reaches the base of papillary muscles.

Surgical reconstruction of the posterior LV wall. The margin of the ventriculotomy is brought against the septum, starting from the mitral anulus and reaching the base of the papillary muscles. All the scarred tissue is excluded from the cavity (from left to right).

Associated mitral regurgitation.

Mitral regurgitation of variable degree is often present in patients with LV aneurysm. By changing the shape of the left ventricle, ventricular reconstruction can correct the lateral displacement of papillary muscles and improve the function of the MV, particularly in cases of moderate mitral regurgitation.

In the presence of important LV dilation and severe mitral insufficiency, just the reconstruction of the left ventricle is not sufficient, and the valve must be approached. If repair of the valve is possible, it may be accomplished with standard techniques through a standard left atriotomy. Alternatively, the “edge-to-edge” repair technique proposed by Alfieri and colleagues can be performed through the ventriculotomy.

An alternative technique to repair the MV from the ventricle with a lower rate of recurrence was described by Menicanti and colleagues.

In case of severe mitral regurgitation with dilation of the left ventricle, the replacement of the MV is probably a better strategy (see “ Section III Mitral Regurgitation from Ischemic Heart Disease ”). If valve replacement is indicated, it can be performed through the opened left ventricle for posterior as well as anterior aneurysms. The ventricle is opened through the aneurysm as previously described, and the MV is examined. Due to low ejection fraction of these ventricles, the mitral apparatus should be preserved if possible; the prosthetic valve is inverted and suspended by two hemostats. Interrupted pledgeted mattress sutures of No. 2-0 polyester are placed through the mitral anulus, with the pledgets positioned on the atrial side. These sutures are placed through the sewing ring of the prosthesis on the undersurface of the flanged portion. The valve is then lowered into the anulus, and the sutures tied ( Fig. 10.14 ). A soft rubber catheter is used to keep the prosthesis leaflets in the open position until air is evacuated from the pulmonary veins and left atrium. The left ventricle is then reconstructed using one of the techniques previously described.

Replacement of mitral valve through left ventricle. (A) Valve holder apparatus is removed from the mechanical valve or bioprosthesis, and the valve is inverted and suspended by two hemostats. Interrupted, pledgeted mattress sutures of No. 2-0 polyester are placed through the mitral anulus, with pledgets on the atrial side of the anulus. These sutures are then placed through the sewing ring of the prosthesis on the underside of the flanged portion. (B) The valve is lowered into the anulus, and the sutures tied. The left ventricle is reconstructed using one of the techniques described in the section on “Reconstruction of the Left Ventricle” under “Surgical Technique”.

The most common mode of death early after the operation is acute cardiac failure. ^{, ,} Ranucci and colleagues described a mortality risk score for this procedure. Late postoperatively, the mode of death is progressive chronic HF in about one-third of patients and acute HF after another MI in another third. Intractable ventricular tachycardia and sudden death have been the mode in about 15% of patients in the past, but the prevalence may be lower now as a result of more effective intraoperative management and medical and surgical treatment. Di Donato reported an incidence of 2.5% of sudden death, accounting for 18% of all-cause mortality.

In patients undergoing LV aneurysmectomy, risk factors for premature death and other unfavorable outcomes are generally the same as those in other patients with ischemic heart disease. The lower probability of time-related survival of patients undergoing LV aneurysmectomy (with or without concomitant CABG) is explained, for the most part, by their greater likelihood of having risk factors relating to myocardial scarring.

Most long-term survivors have substantial improvement in symptoms. The majority are in NYHA functional class I or II. ^{, , ,} Improvement has also been demonstrated with exercise testing. The rate of rehospitalization, as a measure of quality of life, is low. Several ^{, ,} but not all comparative studies have demonstrated greater symptomatic improvement among patients undergoing patch closure than among those who had linear closure of the ventriculotomy.

Determining LV function late after resection of LV aneurysms presents the same problems and complexities as it does in the case of the aneurysmal LV before operation (see “ Left Ventricular Function ” under Natural History earlier in this chapter). However, a reasonable amount of information is available. The relationship between improvement in LV performance and symptomatic improvement is not entirely clear. Some patients with symptomatic improvement are without demonstrable improvement in LV function. ^, It is possible that current techniques of studying LV function do not identify the small increases in LV function that allow symptomatic improvement. Although improvement is often noted in indices of LV function after aneurysmectomy without or with CABG, ^{, , , , , , , ,} it does not always occur. Possible mechanisms for failure to improve include:

• •

  Incomplete aneurysm resection leading an insufficient volume reduction (e.g., Froehlich and colleagues found in most of their patients that only 50% of the noncontractile area visualized by left ventriculography was resected );

• •

  Small size of the aneurysm, leading to small changes in function after resection and possible increased diastolic dysfunction ;

• •

  Scar extension in the basal region ;

• •

  Intraoperative damage of the non-aneurysmal portions of the ventricle.

Also, despite improvement in resting LV function, some patients show no improvement in exercise ejection fraction or stroke volume. However, often, the improvement in global and regional ejection fraction during exercise is striking. ^{, ,} Paradoxical movement in the segments in the border zone during isovolumic contraction is usually eliminated by aneurysmectomy. ^, This effect may be the result of more favorable geometry in these segments, a reduction in wall stress related to decreased chamber size, or better coronary perfusion produced by CABG. Wall thickening increases in some but not all uninvolved (remote) segments; in some improved segments, operation fails to increase blood supply. Improvements in LV function are most evident in patients with HF preoperatively.

A reduction in end-diastolic pressure is well correlated with clinical improvement in some patients. In 1969, in three patients with single-system LAD disease and classic aneurysm, Harman and colleagues demonstrated that simple resection without CABG increased LV ejection fraction, stroke volume and stroke work, and cardiac index and reduced LV end-diastolic pressure and volume. Two of the three patients were also relieved of angina pectoris. The data suggest that the resection and resultant decrease in LV volume decreased wall force according to the Laplace law. The decreased tension (afterload) during systole probably increased the rate of fiber shortening, thereby increasing stroke volume, reducing myocardial oxygen consumption, and thereby decreasing angina pectoris.

Although intractable ventricular tachyarrhythmias occur in patients with ischemic heart disease in the absence of areas of LV scarring, they are more common in patients with LV aneurysms or extensive fibrosis. However, only a small proportion with LV aneurysms develop intractable ventricular tachycardia. The majority of patients with such arrhythmias have poor global LV function, and it has been suggested that ventricular tachyarrhythmias occur more frequently when the ventricular septum is involved in the infarction. As a corollary, poor LV function and non-responsiveness to drug therapy for ventricular tachycardia have been identified as risk factors for sudden cardiac death. Management of patients with the combination of LV aneurysm and intractable ventricular tachyarrhythmias is discussed in detail in Chapter 15 .

The aneurysms discussed in this chapter, so-called true aneurysms, are formed by scarring, thinning, and stretching of an infarcted area of LV wall. This process generally produces a wide-mouthed aneurysm. By contrast, a false aneurysm (pseudoaneurysm) may develop after acute rupture of an infarcted area of left ventricle. Such ruptures are usually fatal, but when the pericardium is sufficiently adherent to the epicardium, rupture may result only in a localized hemopericardium. Persistent communication of the hemopericardium with the LV cavity results in the gradual expansion of the hemopericardium into a false aneurysm whose wall is composed of pericardium and adhesions ^, and occasionally of the myocardium, and whose mouth is usually narrow. ^, In contrast to true aneurysms, pseudoaneurysms may rupture. ^, False aneurysms are much more likely than true aneurysms to occur posteriorly (on the diaphragmatic surface of the left ventricle) or laterally. Differentiation between true and false aneurysms can be difficult because the imaging characteristics of the two entities are often similar. However, Doppler color flow imaging and transesophageal echocardiography (TEE) are useful techniques for demonstrating the presence of a false aneurysm. ^,

Previously, surgical repair was advised for most patients with pseudoaneurysms due to the anticipated high risk of rupture. ^{, ,} Recent evidence, however, suggests that the natural history of pseudoaneurysms may be better than previously thought. Moreno and colleagues reported no deaths during follow-up of 9 patients with pseudoaneurysms managed conservatively. Ischemic stroke occurred in one-third of the patients, and the authors recommended chronic anticoagulation. When operation is undertaken, resection may pose formidable problems when the aneurysm sac extends anteriorly beneath the sternum. It is then necessary to begin CPB via cannulae introduced into the femoral artery and vein. If the false aneurysm is very large, the patient is cooled to 20°C before the sternum is opened. As soon as possible, the aorta is clamped, cardioplegia induced (see Chapters 3 and 5 ), and the operation begins. The false sac is entered, and blood from this sac is returned to the circuit using cardiotomy suckers. The aneurysmal wall is resected or left alone, and the left ventricle is reconstructed using techniques described earlier in this chapter (see “ Technique of Operation ”). When indicated, CABG is also performed.

Acute rupture of the free wall of the left ventricle is an infrequent but serious complication after an AMI, occurring in 2% to 4% of patients. ^, Among 1048 patients with acute infarction and cardiogenic shock evaluated in the SHOCK (SHould we emergently revascularize Occluded Coronaries in cardiogenic shock) trial and registry, free wall rupture or tamponade was present in 28 (2.7%). It is the second most common cause of death following acute infarction (behind acute cardiac failure), accounting for up to 20% of early deaths. Rupture generally occurs between 1 and 7 days after the infarction. ^, Occasionally, the rupture is massive, and death quickly results from exsanguination. Cardiac rupture is more often a gradual process, beginning with small areas of endocardial necrosis. These permit formation of hematomas, which gradually dissect through the necrotic myocardium into the pericardium, resulting in tamponade and cardiogenic shock. If rupture is massive (the so-called blowout phenomenon), death occurs suddenly. If it is not, tamponade develops more slowly, allowing time for diagnosis and surgical treatment. Rupture occurs most commonly on the lateral or anteroapical wall of the left ventricle and generally in the middle of the ventricle along the axis from base to apex. ^, Myocardial free wall rupture should be suspected in patients with recent MI who have recurrent or persistent chest pain, hemodynamic instability, syncope, signs of pericardial tamponade, or transient electromechanical dissociation. Diagnosis can be made most expeditiously with echocardiography, which demonstrates a pericardial effusion or pericardial thrombus. Operation is indicated unless the patient is moribund. If the patient is hemodynamically unstable with evidence of tamponade, rapid infusion of fluids and pericardiocentesis may permit stabilization. An intraaortic balloon should be inserted. If the hemodynamic state does not improve, CPB should be established by peripheral cannulation (see “ Cardiopulmonary Bypass Established by Peripheral Cannulation ” under Special Situations and Controversies in Section III of Chapter 2 ). Preoperative coronary angiography is not advisable unless the hemodynamic state is stable. Several techniques have been used for surgical treatment. The traditional approach has involved use of CPB, infarctectomy, and closure of the defect directly with pledgeted sutures or a polyester patch. More recently, sutureless techniques have been used. Patches of polytetrafluoroethylene (PTFE) felt, polyester, or pericardium (autologous or bovine) have been placed over the site of rupture and secured with various glues (gelatin-resorcinol-formaldehyde-glutaraldehyde [GRF], fibrin, cyanoacrylate) with or without suturing the patch to the adjacent noninfarcted myocardium. ^, Synthetic glues, such as cyanoacrylate, are monomers that polymerize when brought into contact with fluid. Padró and coworkers used Histoacryl® to secure a patch of Teflon® onto the myocardium over free wall ruptures and reported 100% survival of 13 patients; 12 of these patients were managed without CPB. This technique appears to be particularly valuable when there is no obvious rupture or “blowout” site. CABG can be added to all these procedures when appropriate.

Operative mortality is significant, and it is related principally to hemodynamic status at the time of operation. Among a group of 66 patients surgically treated by Loisance and colleagues and followed up to 16 years postoperatively, actuarial survival was 44% at 5 years and 26% at 10 years.

Congenital LV aneurysm is a rare malformation characterized by thinning of the myocardium, with layers of myocardial cells intermingled with various amounts of fibrous tissue. ^, It is usually located at the apex of the left ventricle and has a broad neck. This entity differs from a congenital diverticulum of the left ventricle, which is a noncontractile bulging of the left ventricle into the epigastrium. The latter is characterized by an elongated shape and a narrow connection with the left ventricle cavity. It is also associated with midline thoracic and anterior abdominal defects. Both conditions are rare and have been treated surgically with good results.

Rarely, violent, nonpenetrating chest trauma produces such a severe contusion of the heart that a localized aneurysm forms. ^, Vascular injury and intramyocardial dissection resulting from blunt trauma may also lead to aneurysm formation. ^, The aneurysm, which is usually well localized and often thin-walled, may be detected early after the trauma or several years later. Because of the thin wall and propensity for rupture, a posttraumatic LV aneurysm should be resected whenever possible ( Tables 10.1 and 10.2 ).

Because most patients with postinfarction VSD are seriously ill and require operation early after septal rupture, their management before operation is of critical importance. Once the diagnosis of acute postinfarction VSD has been confirmed by echocardiography and a pulmonary artery catheter has been inserted, additional diagnostic studies must be considered before proceeding with operation. (The only exception to this is the occasional patient with essentially no systemic hemodynamic disturbance, as described in “Indications for Operation.”) An intraaortic balloon catheter (IABP) should be inserted urgently because these patients can deteriorate rapidly. In some centers, mechanical circulatory support with extracorporeal membrane oxygenation (ECMO) or an Impella device has been used to bridge patients prior to repair and reverse peripheral organ dysfunction. The benefit of this approach versus proceeding expeditiously with corrective operation and using mechanical support postoperatively is unsettled.

If the patient remains hemodynamically unstable, CPB can be established by peripheral cannulation (see “ Cardiopulmonary Bypass Established by Peripheral Cannulation” under Special Situations and Controversies in Section III of Chapter 2 ). If indicated, the patient is taken immediately to the cardiac catheterization laboratory for special studies (see “ Clinical Features and Diagnostic Criteria ” earlier in this chapter) with the IABP or CPB in place and functioning. When the studies have been completed, or if they are not performed, operation is usually undertaken immediately because permanent improvement is generally not achieved with support devices alone.

After the usual initial preparations in the operating room (see “ General Comments and Strategy ” in Section III of Chapter 2 ), a median sternotomy incision is made. The heart is disturbed as little as possible before CPB is established. While performing the median sternotomy, removal and preparation of saphenous vein is accomplished in the usual manner (see Chapter 9 ). Because of the length and complexity of the operation, the surgical plan must be efficient so that aortic-clamp time is kept to a minimum. CPB is promptly established using two venous cannulae and caval tapes. If CPB is established percutaneously before or immediately after the patient is brought to the operating room, central cannulation should be performed, and CPB established using a pump-oxygenator designed for operating room use. The femoral lines are clamped and removed, and the femoral artery and vein are repaired at the end of the procedure. The aorta is clamped. Myocardial management proceeds as discussed in Chapter 3 and may include warm induction of cardioplegia and controlled aortic root reperfusion. The caval tapes are secured. A left atrial venting catheter may be inserted, but usually is not necessary.

The VSD is usually approached through the left ventricle. When located anteriorly, it is approached through the anterolateral infarction (or aneurysm) that is generally present ( Fig. 10.18 A). The defect in the septum is typically found immediately beneath this area ( Fig. 10.18 B). It is repaired using a collagen- or gelatin-impregnated polyester patch or a patch of autologous or bovine pericardium. The patch is made sufficiently large to cover the adjacent intact but infarcted portion of the septum as well as the VSD. No part of the ventricular septum is resected. The patch is sewn into place on the LV side of the septum, with pledgeted mattress sutures placed away from the edge of the defect into noninfarcted myocardium. The sutures are placed close together, and the pledgets placed on the RV side of the defect ( Fig. 10.18 C). Alternatively, the patch can be sutured into place with a continuous No. 3-0 or 4-0 polypropylene suture, securing the patch to noninfarcted myocardium on the ventricular septum ( Fig. 10.18 D). Infarcted or aneurysmal myocardium on the anterolateral wall of the left ventricle is excised, avoiding the anterolateral papillary muscle. If more than a small amount of tissue is removed from the anterolateral wall, it may be necessary to close the defect in the LV wall with a polyester or pericardial patch. If this is not necessary, the incision in the LV is closed with interrupted heavy (No. 0 or 2-0) silk or polyester sutures placed through strips of PTFE felt and through the patch that has closed the VSD ( Fig. 10.18 E). This suture line is reinforced with a continuous suture of No. 0 or 2-0 polypropylene, which is passed through both strips of PTFE felt, both edges of the myocardium, and the ventricular septal patch ( Fig. 10.18 F).

Repair of anterior postinfarction ventricular septal defect. (A) Incision is made through the anterolateral infarcted myocardium that is usually present or, if some weeks have elapsed, through the scar or aneurysm that has formed. (B) Defect is located immediately beneath the incision. (C) If interrupted sutures are used, the patch is sewn into place on the left ventricular (LV) side of septum, with pledgeted mattress sutures placed away from the edge of the defect into noninfarcted myocardium (dashed line) . Sutures are placed close together, and pledgets are placed on the right ventricular side of the defect. (D) If a continuous suture technique is used, the patch is sutured to noninfarcted myocardium on the ventricular septum adjacent to the area of infarction using a No. 3-0 or 4-0 polypropylene suture. (E) If patch repair of anterolateral wall is not required, the incision in the left ventricle is closed with interrupted heavy silk or polyester sutures placed through strips of PTFE felt, edges of the myocardium, and patch that has closed the ventricular septal defect. (F) Suture line is reinforced with a continuous suture of No. 0 or 2-0 polypropylene, which is passed through both strips of PTFE felt, both edges of the myocardium, and ventricular septal patch. APM, Anterior papillary muscle; LV, left ventricle; RV, right ventricle; VSD, ventricular septal defect.

An alternative technique involves suturing a pericardial patch to the LV endocardium adjacent to the area of the infarction. The left ventricle is opened through an incision in the infarcted anterolateral wall. An oval patch (approximately 4 × 6 cm) of bovine pericardium is sutured to the endocardium of the inferior portion of the noninfarcted endocardium of the ventricular septum with a continuous No. 3-0 polypropylene suture ( Fig. 10.19 A). The suture line is continued into the noninfarcted endocardium of the anterolateral ventricular wall ( Fig. 10.19 B). When placing the continuous suture through the transition zones (superiorly and inferiorly) between the septum and the free wall of the left ventricle, care must be taken to anchor the patch securely to the myocardium to prevent residual communications between the left ventricle and right ventricle. Separate interrupted sutures may be required. Once the patch is completely secured to the LV endocardium, the LV cavity is essentially excluded from the infarcted myocardium ( Fig. 10.19 C). The ventriculotomy is closed using two strips of bovine pericardium or PTFE felt ( Fig. 10.19 D).

Infarct exclusion technique with endocardial patch for repair of anterior postinfarction ventricular septal defect. (A) Left ventricle (LV) is entered through an incision in the infarcted anterolateral wall. An oval patch of bovine pericardium is sutured to the endocardium of the posterior, noninfarcted portion of the ventricular septum with a continuous No. 3-0 polypropylene suture. (B) Suture line is continued into the noninfarcted endocardium of the anterolateral ventricular wall. (C) The LV cavity is thus excluded from the infarcted myocardium. (D) Ventriculotomy is closed using two strips of bovine pericardium or PTFE felt and a continuous polypropylene suture. LV, Left ventricle; RV, right ventricle.

When the VSD is in the apical portion of the septum and is associated with an apical MI, the operation consists of amputating the apex of the ventricle, including the involved portion of the ventricular septum ( Fig. 10.20 A). The left ventricle is opened through the infarcted myocardium, and the septum examined. If the VSD is immediately adjacent to the area of apical infarction, the apex of the heart is excised, including the involved portion of the septum and adjacent right ventricle ( Fig. 10.20 B). Using strips of PTFE felt on each side of the septum and on the edges of the right and LV myocardium, heavy mattress sutures of silk or polyester are placed through these four layers of felt as well as through the right and LV myocardium and the ventricular septum ( Fig. 10.20 C). These sutures are tied, thus excluding the interventricular communication and the openings into both ventricles. The resulting suture line is reinforced with a continuous No. 0 or 2-0 polypropylene suture ( Fig. 10.20 D).

Repair of postinfarction ventricular septal defect in apical portion of septum. (A) Location of infarction at apex of heart. (B) Line of excision through left ventricle, septum, and right ventricle. (C) Closure of apex of heart using strips of PTFE felt on each side of septum and edges of left and right ventricular myocardium. (D) Suture line is reinforced with a continuous No. 0 or 2-0 polypropylene suture. LV, left ventricle; RV, right ventricle.

VSDs located in the posterior septum are more difficult to expose and repair. The heart is lifted out of the pericardium with traction on the LV apex. The defect is approached through a vertical incision in the infarcted LV myocardium ( Fig. 10.21 A). If the VSD is relatively small, the necrotic tissue can be excised, including the infarcted free wall of both the right ventricle and left ventricle, often with the overlying occluded posterior descending coronary artery ( Fig. 10.21 B). The VSD patch (collagen- or gelatin-impregnated polyester or bovine or autologous pericardium) is placed on the LV side of the septum and secured using mattress sutures of No. 2-0 polyester, with pledgets placed on the RV side of the septum ( Fig. 10.21 C). If little or no free wall myocardium has been excised, LV and RV edges are approximated, incorporating the septal patch and two strips of PTFE felt. A large defect in the free wall requires a second patch. The free edge of the septal patch is sutured to the free wall of the left ventricle with interrupted mattress sutures of No. 2-0 polyester using pledgets on the patch and a strip of PTFE felt on the ventricular wall ( Fig. 10.21 D). The patch for closure of the right ventricle is attached to the septal patch already in position and to the free wall of the right ventricle. Pledgets of felt are placed on the inner surface of the right ventricle, and a strip of felt is placed on the outer surface (see Fig. 10.21 D).

Repair of posterior postinfarction VSD. (A) Heart is lifted out of pericardial cavity, and VSD is approached through a vertical incision in infarcted left ventricular myocardium. (B) Infarcted tissue (right ventricle [RV], left ventricle [LV], and septum) is excised. Dashed lines indicate limits of excision. (C) Septal patch is placed on LV side of septum and secured using polyester mattress sutures, with pledgets placed on RV side of septum. (D) If a second patch is required to close the free wall, the free edge of the septal patch is sutured to the free wall of the LV. Patch for closure of RV is attached to septal patch already in position and to RV free wall (see text for details). (E) If extensive infarction is present, no infarcted muscle on the free walls of RV or LV is excised. Septal patch is sutured to RV edge of incision that was made to expose the septum. This suture line incorporates the infarcted but intact LV free wall and a patch of polyester placed over the infarcted muscle (see text for details). (F) Completed repair, with interrupted sutures placed through the myocardium, external patch, and strip of PTFE felt. IVC, inferior vena cava.

Muehrcke and colleagues describe an alternative technique for closure of the free wall when there is extensive infarction. No infarcted muscle on the RV or LV free walls is excised. The septal patch is sutured to the RV edge of the incision that was made to expose the septum. This suture line incorporates the infarcted free wall and a patch of polyester placed over the entire infarcted muscle of the free wall ( Fig. 10.21 E). Pledgeted sutures are placed circumferentially around the area of infarcted muscle and through the polyester patch, then tied over a strip of PTFE felt ( Fig. 10.21 F).

The technique developed by David and colleagues involves an incision in the inferior wall of the left ventricle parallel to the posterior descending coronary artery. Traction sutures are placed on the edges of the ventriculotomy to facilitate exposure ( Fig. 10.22 A). The VSD is identified, and a triangular patch of bovine pericardium approximately 4 × 7 cm is sutured first to the fibrous anulus of the MV using a continuous No. 3-0 polypropylene suture. The medial margin of the patch is sutured to noninfarcted muscle of the septum adjacent to the defect ( Fig. 10.22 B). The lateral edge of the patch is then sutured to the endocardium of the LV free wall adjacent to the posterior papillary muscle ( Fig. 10.22 C). This excludes all infarcted muscle from the LV cavity ( Fig. 10.22 D). The ventriculotomy is closed with two layers of sutures buttressed with strips of bovine pericardium or PTFE felt ( Fig. 10.22 E).

Infarct exclusion technique with endocardial patch for repair of posterior postinfarction ventricular septal defect. (A) Left ventricle (LV) is entered posteriorly through an incision parallel and adjacent to the posterior descending coronary artery. Traction sutures are placed through edges of the myocardium. (B) Triangular-shaped patch of bovine pericardium is first sutured to the fibrous anulus of the mitral valve using a continuous No. 3-0 polypropylene suture. Medial edge of patch is then sutured to noninfarcted muscle of the septum adjacent to the defect. (C) Lateral edge of patch is next sutured to endocardium of the LV free wall adjacent to posterior papillary muscle. (D) This technique excludes all infarcted muscle from LV cavity. (E) LV is closed with two layers of sutures buttressed with strips of bovine pericardium or PTFE felt. IVC, inferior vena cava; RV, right ventricle; VSD, ventricular septal defect.

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