Chapter 29

Left Ventricular Aneurysm

Donald D. Glower/ James E. Lowe

DEFINITION
HISTORY
INCIDENCE
ETIOLOGY
PATHOPHYSIOLOGY
    Early Expansion Phase
    Late Remodeling Phase
NATURAL HISTORY
CLINICAL PRESENTATION
DIAGNOSIS
INDICATIONS FOR OPERATION
PREPARATION FOR OPERATION
OPERATIVE TECHNIQUES
    General
    Plication
    Linear Closure
    Circular Patch
    Endoventricular Patch
    Other Ventricular Remodeling Techniques
    Mitral Regurgitation
    Ventricular False Aneurysm
    Ventricular Rupture
EARLY RESULTS
    Hospital Mortality
    In-Hospital Complications
    Left Ventricular Function
LATE RESULTS
    Survival
    Symptomatic Improvement
REFERENCES

   DEFINITION
 
Left ventricular aneurysm has been strictly defined as a distinct area of abnormal left ventricular diastolic contour with systolic dyskinesia or paradoxical bulging (Fig. 29-1).1 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.2–4 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.3,5 Intraoperatively, a left ventricular aneurysm may also be defined as an area that collapses upon left ventricular decompression.2,5,6 True left ventricular aneurysms involve bulging of the full thickness of the left ventricular wall, while a false aneurysm of the left ventricle is, in fact, a rupture of the left ventricular wall contained by surrounding pericardium.



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  		FIGURE 29-1 Diagrammatic distinction between aneurysm and other states of the left ventricle. (Reproduced with permission from Grondin P, Kretz JG, Bical O, et al: Natural history of saccular aneurysm of the left ventricle. J Thorac Cardiovasc Surg 1979; 77:57.)

 

   HISTORY
 
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 1881.7 The angiographic diagnosis of left ventricular aneurysm was first made in 1951.7 A congenital left ventricular aneurysm was first treated surgically by Weitland in 1912 using an aneurysm ligation. In 1944, Beck8 described fasciae latae plication to treat left ventricular aneurysms. Likoff and Bailey9 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 al10 successfully performed a linear repair of a left ventricular aneurysm using cardiopulmonary bypass. More geometric ventricular reconstruction techniques were subsequently devised by Stoney et al,11 Daggett et al,12 Dor et al,13 Jatene,14 and Cooley et al.15,16


   INCIDENCE
 
The incidence of left ventricular aneurysm in patients suffering myocardial infarction has varied between 10% and 35% depending on the definition and the methods used. Of patients undergoing cardiac catheterization in the Coronary Artery Surgery Study (CASS), 7.6% had angiographic evidence of left ventricular aneurysms.17 The absolute incidence of left ventricular aneurysms may be declining due to the increased use of thrombolytics and revascularization after myocardial infarction.18,19


   ETIOLOGY
 
Over 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 trauma20 Chagas' disease,21 or sarcoidosis.22 A very small number of congenital left ventricular aneurysms also have been reported and have been termed diverticula of the left ventricle.23

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.24 Left ventricular pseudoaneurysm may also result from septic pericarditis25 or any prior operation on the left ventricle, aortic annulus, or mitral annulus.


   PATHOPHYSIOLOGY
 
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.26

True aneurysm of the left ventricle generally follows transmural myocardial infarction due to 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,27 and absence of reformed collateral circulation is probably a prerequisite for formation of a dyskinetic left ventricular aneurysm (Table 29-1). At least 88% of dyskinetic ventricular aneurysms result from anterior infarction, while the remainder follow inferior infarction.7 Posterior infarctions that produce a distinct dyskinetic left ventricular aneurysm are relatively unusual.


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  		TABLE 29-1 Factors contributing to left ventricular aneurysm formation

 
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. While 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.28 Thus increased systolic and diastolic wall stress in the infarcted zone tends to produce progressive stretch of the infarcted myocardium (termed infarct expansion)29 until healing reduces its plasticity.

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) may resolve over several weeks and thus do not represent true left ventricular aneurysms by strict criteria.30

Due to 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.31 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 through 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.32

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.33 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. 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.

Lack of coronary reperfusion is probably prerequisite for development of left ventricular aneurysm. In humans, reperfusion of the infarct vessel, whether spontaneously,30 by thrombolysis,34 or by angioplasty,35 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.36

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 Ch. 54).


   NATURAL HISTORY
 
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.37 Of 18 initially asymptomatic patients, 6 developed class II symptoms while 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. 29-2).



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  		FIGURE 29-2 Survival in medically treated patients with left ventricular aneurysm based on presence (group B) or absence (group A) of symptoms. (Reproduced with permission from Grondin P, Kretz JG, Bical O, et al: Natural history of saccular aneurysm of the left ventricle. J Thorac Cardiovasc Surg 1979; 77:57.)

 
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%.17,37–39 Causes of death include arrhythmia in 44%, heart failure in 33%, recurrent myocardial infarction in 11%, and noncardiac causes in 22%.37 The natural history of patients with akinetic rather than dyskinetic left ventricular aneurysms is less well documented.

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.37,40 Early development of aneurysm within 48 hours after infarction also diminishes survival.26

In general, the risk of thromboembolism is low for patients with aneurysms (0.35% per patient-year),38 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 period of 24 months.41 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.42 Rupture of left ventricular pseudoaneurysms may be most likely in the acute phase or in large-sized pseudoaneurymsms.43 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.


   CLINICAL PRESENTATION
 
Angina is the most frequent symptom in most series of patients operated upon for 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.44

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.44 Thromboembolism is unusual but may produce symptoms of stroke, myocardial infarction, or limb or visceral ischemia.


   DIAGNOSIS
 
The electrocardiogram frequently demonstrates Q waves in the anterior leads along with persistent anterior ST-segment elevation (Fig. 29-3). The chest radiograph may show left ventricular enlargement and cardiomegaly (Fig. 29-4), but the chest radiograph is not usually specific for left ventricular aneurysm.



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  		FIGURE 29-3 Electrocardiogram showing persistent ST-segment elevation with pathologic Q waves in a 60-year-old woman with left ventricular aneurysm. (Reproduced with permission from Ba'albaki HA, Clements SD Jr: Left ventricular aneurysm: a review. Clin Cardiol 1989; 12:5.)

 


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  		FIGURE 29-4 Posteroanterior chest radiograph in a patient with a calcified left ventricular aneurysm. (Reproduced with permission from Ba'albaki HA, Clements SD Jr: Left ventricular aneurysm: a review. Clin Cardiol 1989; 12:5.)

 
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.4 Hypocontractile segments contracting more than 2 standard deviations out of normal range are defined as aneurysmal (Fig. 29-5).45 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.4



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  		FIGURE 29-5 Examples of preoperative centerline analysis in dyskinetic (A) and akinetic (B) LV aneurysms. Vertical lines indicate the extent of asynergy. E.F., ejection fraction; AB anterobasal; AL anterolateral; AP apical; DI diaphragmatic; IB inferobasal. (Reproduced with permission from Dor V, Sabatier M, DiDonato M: Efficacy of endoventricular patch plasty in large postinfarction akinetic scar and severe left ventricular dysfunction: comparison with a series of large dyskinetic scars. J Thorac Cardiovasc Surg 1998; 116:50.)

 
Two-dimensional echocardiography is also a sensitive and specific means of diagnosing left ventricular aneurysm (Fig. 29-6). Mural thrombus and mitral valve regurgitation are detected most readily by echocardiography. Echocardiography is also useful for distinguishing false aneurysm from true aneurysm by demonstrating a defect in the true ventricular wall. Tomographic three-dimensional echocardiography and magnetic resonance imaging are the most reliable means of assessing left ventricular volume in the presence of left ventricular aneurysm.46 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. Magnetic resonance imaging (MRI) accurately depicts left ventricular aneurysms and is a reliable means for detecting mural thrombus.47



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  		FIGURE 29-6 Four-chamber (4C) and two-chamber (2C) two-dimensional echocardiograms demonstrating a left ventricular aneurysm (AN) during systole (SYST) and diastole (DIAST) (LV, left ventricle; LA, left atrium). (Reproduced with permission from Feigenbaum H: Echocardiography. Philadelphia, Lea & Febiger, 1986; p 484.)

 

   INDICATIONS FOR OPERATION
 
Because of the relatively good prognosis for asymptomatic left ventricular aneurysm,37 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.7,48

On the other hand, operation is indicated for symptoms of angina, congestive heart failure, or selected ventricular arrhythmias (see Ch. 54) (Table 29-2). 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 (over 80 mL/m2) and end-diastolic volume (over 120 mL/m2). These volume criteria are, however, poorly defined and limited by technical difficulty measuring left ventricular volume in aneurysmal left ventricles. Because results are not affected by whether aneurysms are akinetic versus dyskinetic, Dor et al feel that dyskinesia is not a prerequisite for aneurysm repair.3,4


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  		TABLE 29-2 Relative indications for ventricular aneurysm operation

 
Operation is also 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.42,43,49 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.50

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.


   PREPARATION FOR OPERATION
 
All patients being considered for operation should undergo right- and left-sided heart catheterization with coronary arteriography and left ventriculography. Patients with 2+ or greater 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.

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.7 Electrophysiologic study is frequently not helpful in patients with polymorphic ventricular tachycardia occurring within 6 weeks of myocardial infarction.7


   OPERATIVE TECHNIQUES
 
General

Operation for left ventricular aneurysm 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. 29-7). The left ventricle is opened (Fig. 29-8), 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°C to 32°C.



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  		FIGURE 29-7 Technique of exposure for left ventricular aneurysm repair through a median sternotomy. The ascending aorta and right atrium are cannulated. A left ventricular vent is placed through the right superior pulmonary vein. Pericardial adhesions are divided, and the aneurysm is opened.

 


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  		FIGURE 29-8 With the aneurysm wall opened, thrombus is removed, without injury to the papillary muscles.

 
The ascending aorta is clamped, and the heart is arrested with cold antegrade 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 aortic declamping.51 Air is removed by venting the ascending aorta and left ventricle while filling the heart and ventilating the lungs with the patient in the Trendelenburg 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.

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 intra-aortic 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. 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. Using preoperative and postoperative three-dimensional techniques to image the left ventricle, Cherniavsky et al proposed that the aneurysm resection or patch should produce a postoperative left ventricular end-diastolic volume of about 150 mL.52

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 su- ture line is oriented to reconstruct a relatively normal left ve- ntricular 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. 29-9). 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.14 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. 29-10).



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  		FIGURE 29-9 Linear repair. The fibrous aneurysm wall is excised, leaving a 3-cm rim of fibrous aneurysm wall attached to healthy muscle.

 


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  		FIGURE 29-10 Linear repair. The aneurysm walls are closed in a vertical line between two layers of Teflon felt. Two layers of 0 monofilament interrupted horizontal mattress sutures are reinforced with two layers of running 2-0 monofilament sutures.

 
Circular Patch

Inferior or posterior aneurysms generally require circular patch closure, which also can be applied to anterior aneurysms. After opening the aneurysm (Fig. 29-11) and after debridement of thrombus and aneurysm wall (Fig. 29-12), a Dacron (Hemashield) 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. 29-13). Sutures are tied, and additional interrupted sutures or a second layer of running 2-0 monofilament is placed for hemostasis.



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  		FIGURE 29-11 Circular patch repair. The aneurysm wall is incised. An inferior aneurysm is shown.

 


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  		FIGURE 29-12 Circular patch repair. The aneurysmal wall is excised, leaving a 2-cm rim of fibrous aneurysmal wall attached to healthy muscle.

 


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  		FIGURE 29-13 Circular patch repair. The aneurysmal defect is closed with a Dacron patch using interrupted 2-0 monofilament horizontal mattress sutures with reinforcing pledgets.

 
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.3,14,45,50 If the remaining ventricular defect is small (<3 cm), then the ventricular wall may be closed linearly.14 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. 29-14). 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,3,45,50 or the aneurysmal septum may be plicated.14 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. 29-15).



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  		FIGURE 29-14 Endocardial patch. Without excising the aneurysm wall, the ventricular defect is closed with a Teflon felt patch using 3-0 polyproplyene suture secured at three or four points along the suture line. Additional 3-0 pledgeted horizontal mattress sutures may be used to achieve hemostasis.

 


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  		FIGURE 29-15 Endocardial patch. The aneurysm wall is closed over a Teflon patch after resecting excess aneurysm tissue. A double row of running vertical 2-0 polyproplyene suture is used.

 
As 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.7,16,53

Other Ventricular Remodeling Techniques

In addition to the techniques listed above, in which left ventricular infarct tissue is excised and/or replaced with patch material, an alternative is 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.54 In animals, cellular cardiomyoplasty has successfully improved global left ventricular performance and geometry using either myoblasts, stem cells that differentiate into myocytes, or even fibrocytes.55–57 Only myoblasts or stem cells that differentiate into myocytes have improved regional ventricular contractility. 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.

Mitral Regurgitation

The severity of mitral regurgitation should be evaluated by intraoperative transesophageal echocardiography before cardiopulmonary bypass. 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.58 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), Carpentier mitral annuloplasty is done.59

Ventricular False Aneurysm

Ventricular false aneurysms are repaired with the same techniques used for true ventricular aneurysms 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 use to close 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 biological patch to the ventricular epicardium over the site of the rupture.


   EARLY RESULTS
 
Hospital Mortality

In a compilation of 3439 operations for left ventricular aneurysm performed between 1972 and 1987, hospital mortality was 9.9% and ranged from 2% to 19%.18 More recent reports indicate that hospital mortality has fallen to 3% to 7% in the last decade using either patch7,16,60,61 or linear closures.19,48,61 The most common cause of hospital mortality was left ventricular failure, which occurred in 64% of deaths.48

Risk factors for hospital mortality include increased age,18,48,61 incomplete revascularization,48 increased heart failure class,18,61–63 female gender,18 emergent operation,18 ejection fraction less than 20% to 30%,61,62 concurrent mitral valve replacement,7,18 preoperative cardiac index <2.1 L/min/m2,4 mean pulmonary artery pressure >33 mm Hg,4 serum creatinine >1.8 mg/dL,4 and failure to use the internal mammary artery.63

In-Hospital Complications

The most common in-hospital complications are shown in Table 29-3 and include low cardiac output, ventricular arrhythmias, and respiratory failure.18,19,60,61,64 Low cardiac output may be more common in patients undergoing intraoperative mapping due to perioperative cardiac injury.65


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  		TABLE 29-3 In-hospital complications of ventricular aneurysm repair

 
Left Ventricular Function

The preponderance of data from the last two decades has shown that left ventricular function improves in most patients undergoing operation for left ventricular aneurysm. Operation improves ejection fraction whether linear repair5,8,66–68 or patch repair13,16,69–71 is used (Fig. 29-16). Both techniques decrease end-diastolic and end-systolic volumes67,70 and improve exercise response16,68 (Fig. 29-17). Aneurysmal repair in general also improves diastolic filling, left ventricular diastolic compliance, left ventricular contractility, and effective arterial elastance (Ea).31,71,72



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  		FIGURE 29-16 Effects of linear aneurysmectomy on left ventricular end-diastolic volume (LVEDV), ejection fraction (EF), and wall tension. (Reproduced with permission from Kawachi K, Kitamura S, Kawata T, et al: Hemodynamic assessment during exercise after left ventricular aneurysmectomy. J Thorac Cardiovasc Surg 1994; 107:178.)

 


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  		FIGURE 29-17 Relationship between stroke work index and left ventricular end-diastolic pressure. Data are shown at rest and during exercise before (preop) and after (postop) linear aneurysmectomy. Stroke work index increased only with exercise postoperatively. (Reproduced with permission from Kawachi K, Kitamura S, Kawata T, et al: Hemodynamic assessment during exercise after left ventricular aneurysmectomy. J Thorac Cardiovasc Surg 1994; 107:178.)

 
Controversy remains strong regarding whether patch techniques provide results superior to those achieved with linear closures. Stoney et al11,73 noted lower left ventricular end-diastolic pressure when more geometric reconstructions were performed. Hutchins and Brawley74 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.7,16,75–78 In other retrospective comparisons, no differences were seen in postoperative symptoms, ejection fraction, echocardiographic ventricular dimensions, or late survival between linear and patch repairs.67,79,80 In an animal model of simulated aneurysm repair, Nicolosi et al81 found no difference in left ventricular systolic or diastolic function between linear and patch techniques. Two groups reported that a switch to patch techniques was associated with increased operative mortality, perhaps due to excessive volume reduction.82,83

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 6 months.84,85

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.74,77,85 Excessively small patches reduce stroke volume and impair diastolic filling, but excessively large patches reduce ejection fraction and increase wall stress (Fig. 29-18).



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  		FIGURE 29-18 Computer prediction of the effects of patch size on stroke volume (SV), ejection fraction (EF), and wall stress (afterload) at a chamber pressure of 100 mm Hg. Predictions are based on data from an animal model of simulated aneurysm repair, neglecting the effects of afterload on stroke volume. Because increasing afterload in reality decreases muscle shortening, patch reconstruction can increase stroke volume only if contractile reserve is sufficient to overcome the afterload from increased ventricular size. (Reproduced with permission from Nicolosi AC, Weng ZC, Detwiler PW, et al: Simulated left ventricular aneurysm and aneurysm repair in swine. J Thorac Cardiovasc Surg 1990; 100:745.)

 

   LATE RESULTS
 
Survival

Survival after operation for left ventricular aneurysm is variable, largely due to differences between patient populations. Five-year survival in recent series varies between 58% and 80%,5,62 10-year overall survival is 34%,62 and 10-year cardiac survival is 57%48 (Fig. 29-19). Cardiac causes are responsible for 57% of late deaths,65 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.40 These patients had better survival with surgery (Fig. 29-20).



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  		FIGURE 29-19 Survival in 303 patients undergoing left ventricular aneurysmectomy. (Reproduced with permission from Couper GS, Bunton RW, Birjiniuk V, et al: Relative risks of left ventricular aneurysmectomy in patients with akinetic scars versus true dyskinetic aneurysms. Circulation 1990; 82(suppl IV):248.)

 


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  		FIGURE 29-20 Survival in patients with left ventricular aneurysm and three-vessel coronary disease treated with medical or surgical therapy. (Reproduced with permission from Faxon DP, Myers WO, McCabe CH: The influence of surgery on the natural history of angiographically documented left ventricular aneurysm: the Coronary Artery Surgery Study. Circulation 1986; 74:110.)

 
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 regurgitation40,48,65,79 (Fig. 29-21).



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  		FIGURE 29-21 Effects of preoperative NYHA functional class on survival after ventricular aneurysm repair and myocardial revascularization. (Reproduced with permission from Vauthy JN, Berry DW, Snyder DW, et al: Left ventricular aneurysm repair with myocardial revascularization: an analysis of 246 consecutive patients over 15 years. Ann Thorac Surg 1988; 46:29.)

 
Symptomatic Improvement

Studies consistently demonstrate improvement in symptoms after operation relative to preoperative symptoms5,66 (Fig. 29-22). In the study of Elefteriades et al,66 who used 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.40



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  		FIGURE 29-22 Preoperative (Pre-op) and postoperative (Post-op) symptoms of congestive heart failure (NYHA class) in patients undergoing left ventricular aneurysmectomy. (Reproduced with permission from Mickleborough LL, Carson S, Ivanov J: Repair of dyskinetic or akinetic left ventricular aneurysm: results obtained with a modified linear closure. J Thorac Cardiovasc Surg 2001; 121:675.)

 

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