Chapter 30. Left Ventricular Aneurysm

Left ventricular aneurysm has been strictly defined as a distinct area of abnormal left ventricular diastolic contour with systolic dyskinesia or paradoxical bulging (Fig. 30-1).1,2 Yet, a growing number of authors favor defining left ventricular aneurysm more loosely as any large area of left ventricular akinesia or dyskinesia that reduces left ventricular ejection fraction.3–5 This broader definition has been justified by data suggesting that the pathophysiology and treatment may be the same for ventricular akinesia and for ventricular dyskinesia.4,6 However, recent studies suggest that the optimal treatment and outcomes of patients with akinetic segments versus dyskinetic segments might be different.7,8 Intraoperatively, a left ventricular aneurysm may also be identified as an area that collapses upon left ventricular decompression.3,6,9 True left ventricular aneurysms involve bulging of the full thickness of the left ventricular wall, whereas a false aneurysm of the left ventricle is, in fact, a rupture of the left ventricular wall contained by surrounding pericardium.

Left ventricular aneurysms have long been described at autopsy, but left ventricular aneurysm was not recognized to be a consequence of coronary artery disease until 1881.10 The angiographic diagnosis of left ventricular aneurysm was first made in 1951.10 A congenital left ventricular aneurysm was first treated surgically by Weitland in 1912 using aneurysm ligation. In 1944, Beck11 described fasciae latae plication to treat left ventricular aneurysms. Likoff and Bailey12 successfully resected a left ventricular aneurysm through a thoracotomy in 1955 using a special clamp without cardiopulmonary bypass. The modern treatment era began in 1958 when Cooley et al.13 successfully performed a linear repair of a left ventricular aneurysm using cardiopulmonary bypass. More geometric ventricular reconstruction or restoration techniques were subsequently devised by Stoney et al.,14 Daggett et al.,15 Dor et al.,16 Jatene,17 and Cooley et al.18,19

The incidence of left ventricular aneurysm in patients suffering from myocardial infarction has varied between 10 and 35% depending on the definition and the methods used. Of patients undergoing cardiac catheterization in the CASS study, 7.6% had angiographic evidence of left ventricular aneurysms.20 The absolute incidence of left ventricular aneurysms may be declining because of the increased use of thrombolytics and revascularization after myocardial infarction.21,22

More than 95% of true left ventricular aneurysms reported in the English literature result from coronary artery disease and myocardial infarction. True left ventricular aneurysms also may result from trauma,23 Chagas' disease,24 or sarcoidosis.25 A very small number of congenital left ventricular aneurysms also have been reported and have been termed diverticula of the left ventricle.26

False aneurysms of the left ventricle result most commonly from contained rupture of the ventricle 5 to 10 days after myocardial infarction and often occur after circumflex coronary arterial occlusion. False aneurysm of the left ventricle also may result from submitral rupture of the ventricular wall, a dramatic event that generally occurs after mitral valve replacement with resection of the mitral valve apparatus.27 Left ventricular pseudoaneurysm may also result from septic pericarditis28 or any prior operation on the left ventricle, aortic annulus, or mitral annulus.

The development of a true left ventricular aneurysm involves two principal phases: early expansion and late remodeling.

Early Expansion Phase

The early expansion phase begins with the onset of myocardial infarction. Ventriculography can demonstrate left ventricular aneurysm formation within 48 hours of infarction in 50% of patients who develop ventricular aneurysms. The remaining patients have evidence of aneurysm formation by 2 weeks after infarction.29

True aneurysm of the left ventricle generally follows transmural myocardial infarction because of acute occlusion of the left anterior descending or dominant right coronary artery.

Lack of angiographic collaterals is strongly associated with aneurysm formation in patients with acute myocardial infarction and left anterior descending artery occlusion,30 and absence of re-formed collateral circulation is probably a prerequisite for formation of a dyskinetic left ventricular aneurysm (Table 30-1). At least 88% of dyskinetic ventricular aneurysms result from anterior infarction, and the remainder follow inferior infarction.10 Posterior infarctions that produce a distinct dyskinetic left ventricular aneurysm are relatively unusual.

In experimental transmural infarction without collateral circulation, myocyte death begins 19 minutes after coronary occlusion. Infarctions that result in dyskinetic aneurysm formation are almost always transmural and may show gross thinning of the infarct zone within hours of infarction. Within a few days, the endocardial surface of the developing aneurysm becomes smooth with loss of trabeculae and deposition of fibrin and thrombus on the endocardial surface in at least 50% of patients. Because most myocytes within the infarct are necrotic, viable myocytes often remain within the infarct zone. In a minority of patients, extravascular hemorrhage occurs in the infarcted tissue and may further depress systolic and diastolic function of involved myocardium. Inflammatory cells migrate into the infarct zone by 2 to 3 days after infarction and contribute to lysis of necrotic myocytes by 5 to 10 days after infarction. Electron microscopy demonstrates disruption of the native collagen network several days after infarction. Collagen disruption and myocyte necrosis produce a nadir of myocardial tensile strength between 5 and 10 days after infarction, when rupture of the myocardial wall is most common. Left ventricular rupture is relatively rare after the ventricular aneurysmal wall becomes replaced with fibrous tissue.

Loss of systolic contraction in the large infarcted zone and preserved contraction of surrounding myocardium cause systolic bulging and thinning of the infarct. By Laplace's law (T = Pr/2h), at a constant ventricular pressure, P, increased radius of curvature, r, and decreased wall thickness, h, in the infarcted zone both contribute to increased muscle fiber tension, T, and further stretch the infarcted ventricular wall.

Relative to normal myocardium, ischemically injured or infarcted myocardium displays greater plasticity or creep, defined as deformation or stretch over time under a constant load.31 Thus increased systolic and diastolic wall stress in the infarcted zone tends to produce progressive stretch of the infarcted myocardium (termed infarct expansion)32 until healing reduces the plasticity of infarcted myocardium.

Transmural infarction without significant hibernating myocardium within the infarct region is necessary for subsequent development of a true left ventricular aneurysm. Angiographic ventricular aneurysms with evidence of hibernating myocardium (lack of Q waves or presence of uptake on technetium scan; Takotsubo cardiomyopathy, for example) may resolve over days to weeks and thus do not represent true left ventricular aneurysms by strict criteria.33,34

Because of increased diastolic stretch or preload and elevated catecholamines, remaining noninfarcted myocardium may demonstrate increased fiber shortening and, ultimately, myocardial hypertrophy in the presence of a left ventricular aneurysm.35 This increased shortening and increased wall stress increase oxygen demand for noninfarcted myocardium and for the left ventricle as a whole.

In addition to increased regional wall stresses, left ventricular aneurysm can increase ventricular oxygen demand and decrease net forward cardiac output by producing a ventricular volume load because a portion of the stroke volume goes into the aneurysm instead of out the aortic valve. Net mechanical efficiency of the left ventricle (external stroke work minus myocardial oxygen consumption) is decreased by reducing external stroke work (volume times pressure) and increasing myocardial oxygen consumption.

Left ventricular aneurysms can produce both systolic and diastolic ventricular dysfunction. Diastolic dysfunction results from increased stiffness of the distended and fibrotic aneurysmal wall, which impairs diastolic filling and increases left ventricular end-diastolic pressure.

Late Remodeling Phase

The remodeling phase of ventricular aneurysm formation begins 2 to 4 weeks after infarction when highly vascularized granulation tissue appears. This granulation tissue is subsequently replaced by fibrous tissue 6 to 8 weeks after infarction. As myocytes are lost, ventricular wall thickness decreases as the myocardium becomes largely replaced by fibrous tissue. In larger infarcts, the thin scar is often lined with mural thrombus.36

After acute myocardial infarction, animal studies show that ventricular load reduction with 8 weeks of nitrate therapy may reduce expected infarct thinning, decrease infarct stretch, and lessen hypertrophy of noninfarcted myocardium.37 Interestingly, nitrate therapy for only 2 weeks after infarction does not prevent aneurysm formation. This observation emphasizes the importance of late remodeling from 2 to 8 weeks after infarction. Angiotensin converting-enzyme (ACE) inhibitors also reduce infarct expansion and subsequent development of ventricular aneurysm.38 Because animal studies show that ACE inhibitors nonspecifically suppress ventricular hypertrophy, it is not clear whether suppression of the compensatory hypertrophy of surrounding myocardium is ultimately beneficial or harmful. Intravenous administration of atrial natriuretic factor for 4 weeks has improved ventricular function, dimensions, and fibrosis in rats.39

Lack of coronary reperfusion is probably prerequisite for development of left ventricular aneurysm. In humans, reperfusion of the infarct vessel either spontaneously,33 by thrombolysis,40 or by angioplasty41 has been associated with a lower incidence of aneurysm formation. It is speculated that coronary reperfusion as late as 2 weeks after infarction prevents aneurysm formation by improving blood flow and fibroblast migration into the infarcted myocardium. The role of delayed infarct healing in aneurysm development is supported by observations that steroids after myocardial infarction may increase the likelihood of aneurysm formation.42

Arrhythmias such as ventricular tachycardia may occur at any time during the development of ventricular aneurysm, and all these patients have the substrate for reentrant conduction pathways within the heterogeneous ventricular myocardium. These pathways tend to involve border zones surrounding the ventricular aneurysm (see Chapter 57).

The excellent prognosis of asymptomatic patients with dyskinetic ventricular aneurysms who were treated medically was demonstrated in a series of 40 patients followed for a mean of 5 years.2 Of 18 initially asymptomatic patients, 6 developed class II symptoms and 12 remained asymptomatic. Ten-year survival was 90% for these patients but was only 46% at 10 years in patients who presented with symptoms (Fig. 30-2).

Although earlier autopsy series reported relatively poor survival in patients with medically managed left ventricular dyskinetic aneurysms (12% at 5 years), most recent studies report 5-year survival from 47 to 70%.2,20,43–45 Causes of death include arrhythmia in 44%, heart failure in 33%, recurrent myocardial infarction in 11%, and noncardiac causes in 22%.2 The natural history of patients with akinetic rather than dyskinetic left ventricular aneurysms is less well documented.7

Factors that influence survival with medically managed left ventricular dyskinetic aneurysm include age, heart failure score, extent of coronary disease, duration of angina, prior infarction, mitral regurgitation, ventricular arrhythmias, aneurysm size, function of residual ventricle, and left ventricular end-diastolic pressure.2,45 Early development of aneurysm within 48 hours after infarction also diminishes survival.29

In general, the risk of thromboembolism is low for patients with aneurysms (0.35% per patient-year),43 and long-term anticoagulation is not usually recommended. However, in the 50% of patients with mural thrombus visible by echocardiography after myocardial infarction, 19% develop thromboembolism over a mean follow-up of 24 months.46 In these patients, anticoagulation and close echocardiographic follow-up may be indicated. Atrial fibrillation and large aneurysmal size are additional risk factors for thromboembolism.

The natural history of left ventricular pseudoaneurysm is not well documented. Frank rupture of chronic left ventricular pseudoaneurysms is less common than one might expect.47 Rupture of left ventricular pseudoaneurysms may be most likely in the acute phase or in large sized pseudoaneurymsms.48 Left ventricular pseudoaneurysms tend to behave similarly to true aneurysms in that they may present a volume load to the left ventricle or may be a source of embolization or endocarditis. Left ventricular pseudoaneurysms after prior cardiac surgery have also been reported to compress adjacent structures such as the pulmonary artery or esophagus.

Angina is the most frequent symptom in most series of operated patients with left ventricular aneurysm. Given that three-vessel coronary disease is present in 60% or more of these patients, the frequency of angina is not surprising.49

Dyspnea is the second most common symptom of ventricular aneurysm and often develops when 20% or more of the ventricular wall is infarcted. Dyspnea may occur from a combination of decreased systolic function and diastolic dysfunction.

Either atrial or ventricular arrhythmias may produce palpitations, syncope, or sudden death, or aggravate angina and dyspnea in up to one-third of patients.49 Thromboembolism is unusual but may produce symptoms of stroke, myocardial infarction, or limb or visceral ischemia.

The electrocardiogram frequently demonstrates Q waves in the anterior leads along with persistent anterior ST-segment elevation (Fig. 30-3). The chest radiograph may show left ventricular enlargement and cardiomegaly (Fig. 30-4), but the chest radiograph is not usually specific for left ventricular aneurysm.

Left ventriculography is the gold standard for diagnosis of left ventricular aneurysm. The diagnosis is made by demonstrating a large, discrete area of dyskinesia (or akinesia), generally in the anteroseptal-apical walls. Occasionally, left ventriculography also may demonstrate mural thrombus. Quantitative definition of left ventricular aneurysms has been accomplished using a centerline analysis of left ventricular wall motion on left ventriculography in the 30 degree right anterior oblique view.5 Hypocontractile segments contracting more than two standard deviations out of normal range have also been defined as aneurysmal (Fig. 30-5).50 Outward motion is termed dyskinetic, and remaining aneurysmal segments are termed akinetic. The fraction of total left ventricular circumference that is aneurysmal can thus be computed as the value %A.5

Two-dimensional echocardiography is also a sensitive and specific means of diagnosing left ventricular aneurysm (Fig. 30-6). Echocardiography can detect mural thrombus or mitral valve regurgitation, and echocardiography can often distinguish false aneurysm from true aneurysm by demonstrating a defect in the true ventricular wall.

Magnetic resonance imaging (MRI) is the most reliable means of assessing left ventricular volume in the presence of left ventricular aneurysm.51 Magnetic resonance imaging (MRI) can accurately define left ventricular aneurysms and can detect mural thrombus.51 Yet, distinguishing true aneurysms from pseudoaneurysms remains difficult, even with magnetic resonance imaging.52 Gated radionuclide angiography reliably detects left ventricular aneurysms, and thallium scanning or positron emission tomography (PET) can be helpful early after infarction to differentiate true aneurysm from hibernating myocardium with reversible dysfunction.

Because of the relatively good prognosis for asymptomatic left ventricular aneurysm,2 no indications for repairing chronic, asymptomatic aneurysms are established. Yet, in low-risk patients during operation for associated coronary disease, investigators report repairing large, minimally symptomatic aneurysms.10,53 On the other hand, operation is indicated for symptoms of angina, congestive heart failure, or selected ventricular arrhythmias (see Chapter 57) (Table 30-2). For these symptomatic patients, operation offers better outcome than medical therapy.

To be worthy of operation, a dyskinetic or akinetic left ventricular aneurysm should significantly enlarge left ventricular end-systolic volume index (>80 mL/m2) and end-diastolic volume (>120 mL/m2). These volume criteria are, however, poorly defined and limited by technical difficulty measuring left ventricular volume in aneurysmal left ventricles. Because of data suggesting that akinetic versus dyskinetic aneurysms have similar results, Dor and others feel that dyskinesia is not a prerequisite for aneurysm repair.4,5 Nonetheless, the only randomized trial (the STICH trial) has suggested that little benefit is obtained in terms of survival or symptoms in patients who on average have smaller, akinetic aneurysmal segments (end-systolic volume index 82 mL/m2 and 50 to 56% of anterior wall involved).7

Operation is indicated in viable patients with contained cardiac rupture, with or without development of a false aneurysm. Because left ventricular pseudoaneurysms may have a tendency to rupture when acute or of larger size (either with or without symptoms), operation is indicated.47,48,54 Similarly, congenital aneurysms have a presumed risk of rupture and should undergo repair independently of symptoms. Rarely, embolism is an indication for operation in medically treated patients at high risk for repeated thromboembolism. The role of operation in asymptomatic patients with very large aneurysms or documented expansion of aneurysms is uncertain.

Relative contraindications to operation for left ventricular aneurysm include excessive anesthetic risk, impaired function of residual myocardium outside the aneurysm, resting cardiac index less than 2.0 L/min/m2, significant mitral regurgitation, evidence of nontransmural infarction (hibernating myocardium), and lack of a discrete, thin-walled aneurysm with distinct margins. Global ejection fraction may be less useful than ejection fraction of the basal, contractile portion of the heart in determining operability.55

Angioplasty has an uncertain role in the treatment of left ventricular aneurysms but may be indicated in patients with suitable coronary anatomy, one- or two-vessel disease, a contraindication for operation, or asymptomatic status with inducible ischemia.

All patients being considered for operation should undergo right- and left-sided heart catheterization with coronary arteriography and left ventriculography. Patients with at least 2+ mitral regurgitation at cardiac catheterization should have echocardiography to assess the mitral valve and to look for intrinsic mitral valve disease not amenable to annuloplasty. Magnetic resonance imaging can be helpful to assess left ventricular volumes and aid in planning the size and extent of left ventricular reconstruction.51

Preoperative electrophysiologic study is clearly indicated in any patient with preoperative ventricular tachycardia or ventricular fibrillation. The decision to perform an electrophysiologic study in patients without preoperative ventricular arrhythmias is controversial, because the incidence of postoperative ventricular arrhythmias is low and not changed by endocardial resection at the time of operation.10 Electrophysiologic study is frequently not helpful in patients with polymorphic ventricular tachycardia occurring within 6 weeks of myocardial infarction.10

General Operation

Operation for left ventricular aneurysm (aneurysmectomy, aneurysmorrhaphy, ventricular restoration) requires cardiopulmonary bypass and a balanced anesthetic technique, as generally used for coronary bypass grafting. After induction of anesthesia and endotracheal intubation, an electrocardiogram monitor, a Foley catheter, a radial arterial line, and a Swan-Ganz catheter are placed. A median sternotomy is performed, and the patient is given heparin. Saphenous vein or arterial conduits are prepared.

Cardiopulmonary bypass is begun after cannulating the ascending aorta. A single, two-stage cannula is generally adequate to cannulate the right atrium, but dual venous cannulation should be considered if the right ventricle is to be opened. Epicardial mapping is performed if necessary. The left ventricle is inspected to identify an appropriate area of thinned ventricular wall. A linear vertical ventriculotomy, generally on the anterior wall 3 to 4 cm from the left anterior descending coronary artery, is made (Fig. 30-7). The left ventricle is opened (Fig. 30-8), all mural thrombus is carefully removed, and endocardial mapping is performed if necessary. A left ventricular vent is now placed through the right superior pulmonary vein–left atrial junction after mural thrombus is removed. Coronary arteries to be grafted are identified. Endocardial scar, if present, is resected, and afterwards, endocardial mapping is repeated. Body temperature is maintained at 37°C until intraoperative mapping is completed; thereafter, temperature is decreased to 28 to 32°C.

The ascending aorta is clamped, and the heart is arrested with cold anterograde and/or retrograde cardioplegic solution. Alternatively, the aorta is not clamped and the entire procedure is done during hypothermic fibrillation. The left ventricular aneurysm is repaired using one of the techniques described below. The distal coronary anastomoses are performed, followed by releasing the aortic clamp.56 Air is removed by venting the ascending aorta and left ventricle while filling the heart and ventilating the lungs with the patient in the Trendelenberg position. The patient is rewarmed, and proximal coronary anastomoses are performed. Once normothermia is achieved, an electrophysiologic study may be repeated if indicated. Temporary pacing wires are placed on the right atrium and right ventricle, cardiopulmonary bypass is discontinued, and heparin is reversed. The heart is decannulated, and the median sternotomy is closed with mediastinal drains after hemostasis is achieved.

Weaning from cardiopulmonary bypass frequently requires some degree of inotropic support. Typically 5 μg/kg/min of dopamine, nitroglycerin to prevent coronary spasm, and nitroprusside for afterload reduction are used. An intraaortic balloon pump may be needed in patients with borderline ventricular function. Transesophageal echocardiography is useful for assessing left ventricular function and to detect residual intracardiac air.

Additional inotropic support may not increase cardiac output significantly because of abnormal ventricular compliance and may produce arrhythmias and poorly tolerated tachycardia. Hypokalemia and hypomagnesemia are corrected immediately to minimize arrhythmias. Intraoperative and postoperative ventricular ectopy is treated aggressively with intravenous lidocaine. Intravascular volume shifts are poorly tolerated in these patients because of poor ventricular compliance; therefore, rapid transfusions are avoided by meticulous hemostasis before closing. Because the left ventricle is poorly distensible, stroke volume is relatively fixed, and a resting heart rate between 90 and 115 beats per minute is not unusual to maintain a cardiac index of approximately 2.0 L/min/m2.

Growing experience suggests that the ultimate size of the left ventricular cavity at the end of the procedure is critical to patient outcome.

Plication

Plication without opening the aneurysm is reserved for only the smallest aneurysms that do not contain mural thrombus. A two-layer suture line of 0 monofilament is placed across the aneurysm using a strip of Teflon felt on either side. The suture line is oriented to reconstruct a relatively normal left ventricular contour and does not exclude all aneurysmal tissue.

Linear Closure

After removing all mural thrombus, the aneurysmal wall is trimmed, leaving a 3-cm rim of scar to allow reconstruction of the normal left ventricular contour (Fig. 30-9). Care is taken not to resect too much aneurysmal wall and overly reduce ventricular cavity size. A monofilament 2-0 suture may be used to reduce the neck of the aneurysm to the proper size before closure of the ventricular wall.17 Anterior aneurysm defects are closed vertically between two external 1.5-cm strips of Teflon felt, two layers of 0 monofilament horizontal mattress sutures, and finally, two layers of running 2-0 monofilament vertical sutures with large-diameter needles (Fig. 30-10). Similar techniques can be used in less frequent posterior aneurysm resections.57

Circular Patch

Inferior or posterior aneurysms generally require circular patch closure, which also can be applied to anterior aneurysms. After opening the aneurysm (Fig. 30-11) and after debridement of thrombus and aneurysm wall (Fig. 30-12), a Dacron patch is cut to be 2 cm greater in diameter than the ventricular opening. Interrupted, pledgeted 0 monofilament horizontal mattress sutures are placed through the ventriculotomy rim and then through the patch, leaving the pledgets outside the ventricular cavity (Fig. 30-13). Sutures are tied, and additional interrupted sutures or a second layer of running 2-0 monofilament is placed for hemostasis.

Endoventricular Patch

The endoventricular patch technique is suitable for anterior aneurysms but is less suited for inferior or posterior aneurysms, for which the standard (circular) patch technique is used. After debridement of thrombus, a running 2-0 polypropylene suture may be placed at the aneurysm rim to optimize left ventricular size.4,17,50,55 Optimizing patch size and residual left ventricular cavity size can be facilitated with plastic or balloon forms (Chase Medical, Richardson, Texas) chosen to leave a left ventricular end-diastolic volume index of 50 to 60 mL/m2.58 If the remaining ventricular defect is small (<3 cm), then the ventricular wall may be closed linearly.17 More commonly, a patch (bovine pericardium, Dacron cloth, or polytetrafluoroethylene) is cut to size sufficient to restore normal ventricular size and geometry when secured to the aneurysmal rim (Fig. 30-14). The patch is sutured to normal muscle at the aneurysmal circumference using a running 3-0 polypropylene suture that is secured with single sutures at three or four places around the patch circumference. The patch may extend onto the interventricular septum,4,50,55 or aneurysmal septum may be plicated.17 Interrupted 3-0 sutures are placed as needed to ensure good fit. Care is taken not to distort the papillary muscles. The aneurysmal rim is trimmed to allow primary closure of the native aneurysmal wall over the patch using two layers of running 2-0 monofilament suture without pledgets (Fig. 30-15).

Compared with linear and circular patch techniques, the endoventricular patch technique has technical advantages. An endoventricular patch preserves the left anterior descending artery for possible grafting and leaves no external prosthetic material to produce heavy pericardial adhesions. The technique facilitates patching the interventricular septum, and is suitable for acute infarctions when tissues are friable.10,19,58,59

Other Ventricular Remodeling Techniques

In addition to the techniques listed above where left ventricular infarct tissue is excised and/or replaced with patch material, an alternative would be to alter the biological properties of the infarct scar. Remaining infarct scar (whether aneurysmal or not) can then be seeded with myoblasts or stem cells which offer the potential to restore cardiac muscle mass and contraction. This technique has been termed cellular cardiomyoplasty and has been done only on a limited basis in humans.60 In animals, cellular cardiomyoplasty has successfully improved global left ventricular performance and geometry using either myoblasts, stem cells that differentiate into myocytes, fibrocytes, or cells seeded onto a graft matrix.61–63 Cellular cardiomyoplasty could be done by direct injection of cells at the time of coronary revascularization, or even by transcoronary or intramyocardial injection in the cardiac catheterization laboratory. Percutaneous insertion of a parachute-like device into the left ventricular apex has had some early success in humans in Europe (Cardiokinetix, Redwood City, CA).

Coronary Revascularization

Concurrent coronary revascularization is performed as in standard coronary bypass procedures. Because the endoventricular patch technique does not encroach on the left anterior descending coronary, the left internal mammary artery may be used to graft the left anterior descending coronary artery.

Mitral Regurgitation

The severity of mitral regurgitation should be evaluated before cardiopulmonary bypass by intraoperative transesophageal echocardiography. The need for concurrent mitral valve operation increases as the preoperative ejection fraction decreases (Fig 30-16).64 The mitral valve is also inspected from below after opening the aneurysm and beginning repair of the aneurysm. Transventricular mitral valve repair may be done by placing pledgeted polypropylene sutures at both mitral commissures to reduce the circumference of the annulus.57 This technique produces satisfactory short-term results, but long-term results are not known. Usually the mitral valve is repaired via left atriotomy after completion of the distal coronary anastomoses and before releasing the aortic cross-clamp. If mitral regurgitation results from annular dilatation and systolic restriction of leaflet motion (Carpentier type IIIB), an undersized, complete, rigid mitral annuloplasty is generally done.65

Cardiac Transplantation

In symptomatic patients with sufficient depression of global left ventricular function to preclude aneurysm repair, transplantation is a reasonable alternative and may have survival and symptomatic benefit similar to ventricular aneurysm repair at a higher dollar cost.66

Ventricular False Aneurysm

Ventricular false aneurysms are repaired with the same techniques used for true ventricular aneurysms based according to the location and size of the aneurysm. The circular patch technique is particularly useful in that inferior false aneurysms are common and typically have narrow necks. Usually the wall of the false aneurysm is inadequate to close over the defect.

Ventricular Rupture

Any of the techniques described above may be used to manage a contained ventricular rupture. Because infarcted tissue is particularly friable 5 to 10 days after rupture, closure may be difficult. The endoventricular technique is particularly well suited for this uncommon operation because the patch can be sewn to the margins of healthy endocardium, which may be at some distance from the site of rupture. Patient survival also has been reported by gluing a biologic patch to the ventricular epicardium over the site of the rupture.

Hospital Mortality

In a compilation of 3439 operations for left ventricular aneurysm between 1972 and 198721 and in a series of 731 ventricular restoration patients from 2002 to 2004,67 hospital mortality was 9.9 and 9.3% respectively and ranged from 2 to 19%. More recent reports suggest that hospital mortality can be as low as 3 to 7% using either patch10,19,64,68,69 or linear closures.22,53,69 The most common cause of hospital mortality is left ventricular failure, which occurs in 64% of deaths.53

Risk factors for hospital mortality include increased age,21,53,64,67,69 incomplete revascularization,53 increased heart failure class,21,67,69–71 female gender,21,67 emergent operation,21 ejection fraction less than 20 to 30%,64,69,70 concurrent mitral valve replacement,10,21,64,67 preoperative cardiac index < 2.1 L/min/m2,5,67 mean pulmonary artery pressure >33 mmHg,5 serum creatinine >1.8 mg/dl,5 and failure to use the internal mammary artery.71

In-Hospital Complications

The most common in-hospital complications are shown in Table 30-3 and include low cardiac output, ventricular arrhythmias, and respiratory failure.21,22,68,67,69,72 Low cardiac output may be more common in patients undergoing intraoperative mapping because of perioperative cardiac injury.73

Left Ventricular Function

The preponderance of data from the last two decades have shown that left ventricular function improves in most patients undergoing operation for left ventricular aneurysm. Operation improves ejection fraction whether linear repair6,11,74–76 or patch repair16,19,64,77–80 is used (Fig. 30-17). Both techniques decrease end-diastolic and end-systolic volumes64,75,78,80 and improve exercise response19,76 (Fig. 30-18). Aneurysmal repair in general may improve diastolic filling, left ventricular diastolic compliance, left ventricular contractility, effective arterial elastance (Ea), and left ventricular efficiency.35,79–82 However, recent studies have suggested little improvement or even worsening of left ventricular diastolic compliance, particularly in patients with large resections or small ventricular size or without large dyskinetic aneurysms preoperatively.83

Controversy remains strong regarding whether patch techniques provide results superior to those achieved with linear closures. Stoney et al.14,84 noted lower left ventricular end-diastolic pressure when more geometric reconstructions were performed. Hutchins and Brawley85 first noted at autopsy that some patients had severe reduction and distortion of ventricular volume after linear repair. The authors proposed that a more geometric repair might avert these problems. Although no prospective studies compare results from the two procedures, several very experienced groups attribute improved symptoms, less low cardiac output, and greater improvement in ejection fraction to a switch to patch techniques.10,19,86 In other retrospective comparisons, no differences were seen in postoperative symptoms, ejection fraction, echocardiographic ventricular dimensions, or late survival between linear and patch repairs.75,86–89 In an animal model of simulated aneurysm repair, Nicolosi et al.83 found no difference in left ventricular systolic or diastolic function between linear and patch techniques. Two groups reported that switch to patch techniques was associated with increased operative mortality, perhaps because of excessive volume reduction, 90,91 whereas other groups found improved survival when switching from linear to patch techniques.92 One meta-analysis has suggested that the better results with patch techniques are the result of more experience in more recent series.86

The durability of functional benefit from aneurysm repair remains poorly documented. In animals and humans, there is a tendency for the initial improvement in ejection fraction, ventricular volume, and filling pressures to diminish over the next 6 weeks to 12 months,93,94 especially in patients with residual mitral regurgitation.

Although technical differences exist between patch and linear repairs, good functional results are possible with either technique. Suboptimal outcomes result from either technique when left ventricular cavitary volume is overly reduced with resultant decreased stroke volume and impaired diastolic filling.85,94 Excessively small patches reduce stroke volume and impair diastolic filling, but excessively large patches reduce ejection fraction and increase wall stress (Fig. 30-19).

Survival

Survival after operation for left ventricular aneurysm is variable, largely because of differences between patient populations. Five-year survival in recent series varies between 58 and 80%,6,70 10-year overall survival is 34%,70 and 10-year cardiac survival is 57%53 (Fig. 30-20). Cardiac causes are responsible for 57% of late deaths,73 and most cardiac deaths result from new myocardial infarctions. In aneurysm patients randomized to medical or surgical therapy in the CASS study (most of the patients had minimal symptoms), survival was not different between medical or surgical therapy, except for patients with three-vessel disease.45 These patients had better survival with surgery (Fig. 30-21).

Preoperative risk factors for late death include age, heart failure score, ejection fraction less than 35%, cardiomegaly on chest radiograph, left ventricular end-diastolic pressure greater than 20 mm Hg, and mitral regurgitation45,53,73 (Fig. 30-22, Fig. 30-23).

The prospective, randomized STICH trial of 1000 patients with ejection fraction of 35% or less and anatomy amenable to ventricular restoration showed that, on average, left ventricular restoration techniques did not affect survival relative to coronary bypass grafting alone (see Fig 30-20).7 The failure to see benefit in the STICH trial probably resulted from inclusion of relatively few patients with large, classical, dyskinetic aneurysms (mean reduction of end-systolic volume index of 16 mL/m2 versus 48 mL/m2 seen in classical aneurysms).7,8 Although unproven, the net sum of evidence suggests that patients with large, classical, dyskinetic aneurysms probably obtain more benefit from aneurysm repair than do patients with diffuse ventricular dysfunction or small akinetic segments.8

Studies consistently demonstrate improvement in symptoms after operation relative to preoperative symptoms6,74 (Fig. 30-24). In the study of Elefteriades et al.,74 using a linear repair, mean angina class improved from 3.5 to 1.2 and mean CHF class improved from 3.0 to 1.7. In the randomized CASS study, the subset of patients with left ventricular aneurysm achieved a better heart failure class with surgical therapy than with medicine, and rehospitalization for heart failure was less common for the surgical therapy group than for the medicine group.45 At 18 months, 85% of patients are free of rehospitalization for congestive heart failure, with rehospitalization peaking at 2 to 4 months.64 Prucz found in a small, nonrandomized case-control study that ventricular restoration reduced hospitalization rate relative to coronary bypass alone.95 However, the STICH trial found no benefit on average in symptoms or quality of life relative to coronary bypass alone.7,96 (Fig 30-24) The STICH trial found that ventricular restoration significantly increased hospital cost by $14,500 or 26%.96