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Left Ventricular Aneurysm
Definition
A postinfarction left ventricular (LV) aneurysm is a well-delineated transmural fibrous scar, virtually devoid of muscle, in which the characteristic fine trabecular pattern of the inner surface of the wall has been replaced by smooth fibrous tissue. In such areas, the wall is usually thin, and both inner and outer surfaces bulge outward. During systole, the involved wall segments are akinetic (without movement) or dyskinetic (paradoxical movement).
Scars and infarcts are not considered aneurysms. Unlike aneurysms, they are not discrete, the LV wall is not thin, and the scar is interspersed with muscle. The definition of aneurysm and the criteria for separating an aneurysm from other types of LV scars are controversial, and some clinicians have adopted a broader, non-morphologic definition rather than the one given earlier. Johnson and colleagues defined aneurysm as “a large single area of infarction (scar) that causes the LV ejection fraction to be profoundly depressed (to approximately 0.35 or lower).” Although realistically the definition of LV aneurysm is less important to the surgeon than are criteria for and results of surgical excision of LV scars, lack of uniformity of definition complicates almost all discussions of this entity. For example, many reports indicate that most patients with LV aneurysms have single-system left anterior descending coronary artery (LAD) disease, whereas others find that nearly all patients have multiple-system disease. Many patients with multiple-system disease have scars rather than true aneurysms.
Historical Note
Although John Hunter and others recognized that LV aneurysms occurred, it was not until the 1880s that the relationships among stenotic coronary artery disease, myocardial infarction (MI), myocardial fibrosis, and LV aneurysm were recognized. Until about 1950, few cases were diagnosed during life, but thereafter the ability to diagnose LV aneurysms improved. In 1967, Gorlin and colleagues reported that a strong suspicion of aneurysm could be obtained in 75% of patients with this complication of MI based on history, physical examination, and apex cardiographic, electrocardiographic, and radiologic studies. Many clinicians believe the prevalence of LV aneurysms has been decreasing since about 1980. Surgical treatment of postinfarction LV aneurysm probably began in 1944 when Beck reinforced such a lesion with fascia lata in an effort to reduce expansile pulsation and prevent rupture. A closed ventriculoplasty, done with a special side-biting LV clamp, was reported in 1955 by Likoff and Bailey. A few years later, Bailey reported five survivors among six patients treated by this method. In 1959, Cooley and colleagues in Houston reported the first successful open excision of an LV aneurysm using cardiopulmonary bypass (CPB).
Morphology
Gross Pathology
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 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 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, because in an area of MI, myocardial necrosis is rarely homogeneous (see “Myocardial Infarction and Morphologic Sequelae” in Chapter 7 ).
Microscopic Pathology
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 dilatation) 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.
Location
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 LV) 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. Virtually all lateral aneurysms are false aneurysms. True posterior wall postinfarction aneurysms are associated with a high prevalence of postinfarction mitral regurgitation secondary to ischemia or necrosis of the papillary muscle (see Chapter 10 ).
Coronary Arteries
Somewhat less than half of patients undergoing resection of classic LV aneurysms or scars have stenotic coronary artery disease confined to the left anterior descending coronary artery (LAD). More often, multiple-system disease is present. The discrepancy between the reported prevalence of single- and multiple-vessel 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-system disease is more apt to survive an acute infarction and appear in a surgical series than is a patient with multiple-system disease.
Left Ventricle
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 LV 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.
Clinical Features And Diagnostic Criteria
Morphologic diagnosis of postinfarction LV aneurysm can be made with assurance only at operation or autopsy. This is because the akinetic or dyskinetic segmental wall motion of an LV aneurysm can be mimicked by nontransmural scars or early infarcts that are not morphologic aneurysms. Thus, Froehlich and colleagues found no aneurysm at operation in 3 of 18 patients (17%; CL 7%-31%) with a preoperative diagnosis of aneurysm and only a questionable aneurysm, which was plicated, in an additional 4 patients (22%; CL 12%-37%). Small and moderate-sized aneurysms are often associated with no specific symptoms, although the patient may experience angina because of stenoses in other portions of the coronary arterial tree. Patients with large LV aneurysms, however, usually present with dyspnea that often has persisted from the time of infarction. Heart failure requiring medication for control may have appeared by the time of presentation to the physician ( Table 8-1 ). Symptoms related to ventricular tachycardia occur in 15% to 30% of patients and may become intractable to medical treatment and cause death. Although about half of aneurysms contain thrombus, thromboembolism occurs in only a small proportion of patients. On physical examination, palpation over the heart often demonstrates a diffuse, sustained apical systolic thrust and a double impulse. On auscultation, usually a third heart sound and often a fourth (atrial) sound are present. There may be an apical pansystolic murmur if mitral regurgitation is present. Chest radiography and fluoroscopy may show an external bulge or convexity when the aneurysm is large enough and profiled. Methods of LV imaging—namely, left ventriculography, two-dimensional and transesophageal echocardiography, radionuclide cardiac blood pool imaging, computed tomography (CT), and magnetic resonance imaging (MRI)—are all useful diagnostic techniques ( Fig. 8-1 ). However, an incorrect preoperative or premortem diagnosis of aneurysm is still sometimes made. Ventriculography is a sensitive imaging method. When there is akinesia or dyskinesia of the wall segment during systole, a permanent outward bulging or convexity, thinning of the wall and lack of inner wall trabeculation, and clear demarcation of the area from the remaining ventricle, the diagnosis is probably correct. Wall thinning and even bulging of the contrast-medium–lined LV cavity may not be detected when there is extensive smooth mural thrombus, and it is often difficult to define the margins of an area with akinesia. Identification of significant mural thrombus adds to the probability of aneurysm, as does presence of calcification in the wall. Right heart catheterization is useful because it enables measurement of pulmonary artery pressure and calculation of cardiac output. From the left heart study, LV end-diastolic pressure, ejection fraction, and end-diastolic volume are measured or calculated. Coronary angiography is always performed.
Table 8-1
Symptoms in Patients Operated on for Left Ventricular Aneurysm
Modified from Barratt-Boyes and colleagues.
| Symptoms | No. | % of 145 |
|---|---|---|
| Severe angina a alone | 45 | 31 |
| Heart failure alone b | 30 | 21 |
| Heart failure + severe angina | 27 | 19 |
| Ventricular tachycardia c + other symptoms c | 22 | 15 |
| Heart failure + mild angina | 12 | 8 |
| Mild angina d alone | 8 | 5.5 |
| Mild effort dyspnea | 1 | 0.7 |
| T otal | 145 | 100 |
a Severe = Canadian angina class 3 or 4.
b Severe dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fluid retention, hepatomegaly.
c Two or more episodes of documented ventricular tachycardia or ventricular fibrillation despite treatment with antiarrhythmic drugs.
Natural History
Development of Left Ventricular Aneurysm
Historically, about 10% to 30% of patients who survived a major MI developed an LV aneurysm. Today, the prevalence appears to have lessened thanks to improved treatment of patients with acute MI. The most important development may be widespread use of thrombolytic therapy and percutaneous coronary interventions, which have reduced the prevalence of permanently occluded LADs. Other 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.
Pathophysiologic Progression of Aneurysm
Whether large LV aneurysms are large from inception or gradually enlarge once formed is uncertain. The mechanism for increasing symptomatology that characterizes the life 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 nonaneurysmal 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 aggravated by any myocardial ischemia that develops in the nonaneurysmal portion of the ventricular wall.
Left Ventricular Function
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 dilatation. 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.
Function in uninvolved segments of the LV per se (segmental ejection fraction) has been difficult to study because of the complexities of assessing ventricular function in this setting. However, when echocardiographically determined 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. Early in systole, the aneurysm and border zones bulge outward (paradoxical movement) as systolic intraventricular pressure rises to a maximum. Later in systole, after the aortic valve has opened and wall stress is falling, some wall thickening occurs in the border zones, contributing to ejection.
Right Ventricular Function
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 LV within the pericardial cavity.
Survival
The complexities of ischemic heart disease in general and the difficulties in identifying true LV aneurysms have mitigated against 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 remainder of 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), the probability of surviving is dictated primarily by severity and extent of the coronary arterial stenoses and is greater in asymptomatic than in symptomatic patients ( Fig. 8-2 ). Prognosis is adversely affected by dyskinesia rather than akinesia in the aneurysm; the former is usually associated with a low global LV ejection fraction. The functional characteristics of the remainder of the ventricle are also major determinants of survival. In addition, all the usual risk factors for premature death in patients with ischemic heart disease (see Table 7-2 in Chapter 7 ) pertain to patients with LV aneurysm.
Technique Of Operation
Most patients who undergo resection of postinfarction LV aneurysms or other scars also require coronary artery bypass grafting (CABG). The following discussion augments the description of CABG in Chapter 7 .
Preoperative and operating room preparations, removal or preparation of grafts, and median sternotomy are accomplished as described in Chapter 2, Chapter 7 . The pericardial adhesions over the LV are not lysed at this point. If CABG is to be performed, and if the proximal anastomoses are to be placed first, this is done now. If the LAD is to be revascularized, the left internal thoracic artery is prepared. Moderately hypothermic CPB is established using double venous cannulation and caval taping or a single venous cannula. A left atrial or LV vent is not inserted. Dissection of adhesions between the LV and pericardium is deferred until the aorta is clamped, to avoid dislodging and embolizing mural thrombus.
Because patients with large LV aneurysms usually have heart failure and the operation may be prolonged, warm induction of cardioplegia after aortic occlusion and controlled reperfusion with initially hyperkalemic, modified, and enriched blood may be used (see “Cold Cardioplegia, Controlled Aortic Root Reperfusion, and [When Needed] Warm Cardioplegic Induction” in Chapter 3 ). Retrograde cardioplegia (see “Technique of Retrograde Infusion” under Methods of Myocardial Management during Cardiac Surgery in Chapter 3 ) and a “no-touch” technique may be particularly useful. Adhesions, if thin, can be mobilized over the entire aneurysm. If the classic method of repair is anticipated and the aneurysm is densely adherent to the pericardium, the LV can be separated from the aneurysm without disturbing these adhesions. The aneurysm is incised at some convenient point, and loose thrombus is sought and removed. When the aneurysm contains considerable thrombus and debris, a sponge is placed deep inside the ventricle over the aortic and mitral valves to prevent debris from entering the aorta and left atrium. This sponge is removed after the dissection is completed. A small sump sucker is placed through the incision into the ventricle and is positioned so as to maintain a pool of blood within the open ventricle below the level of the ventriculotomy. This prevents air from entering the aorta, coronary ostia, and left atrium. The incision is extended around the entire aneurysm, leaving a thin rim of scar tissue to facilitate closure.
A true aneurysm has a smooth endocardial surface. Additional endocardial tissue may be removed and other procedures done if the patient has a history of life-threatening ventricular arrhythmias (see Section V, “Ventricular Tachycardia and Ventricular Fibrillation in Ischemic Heart Disease,” in Chapter 16 ). When large amounts of thrombus are present, the ventricular cavity is carefully inspected and thoroughly irrigated to remove all debris. If the aneurysm wall is left adherent to the pericardium, thrombotic material is removed from it (this can be done later during rewarming, after the ventricle is closed), and the avascular fibrous tissue is left attached to the pericardium.
Reconstruction of the Left Ventricle
Anterior Aneurysm
When reconstruction is performed with the classic technique (linear closure), a line of closure is selected that will least distort the LV. After opening the ventricle and excising the scar ( Fig. 8-3, A ), a stay suture is placed at each end of the line of closure ( Fig. 8-3, B ). If the aneurysm is small, closure of the LV can be accomplished with two rows of a simple continuous suture using No. 0 or 1 polypropylene on a large curved needle. More often, closure is performed with heavy double-armed sutures (No. 1 or 2 silk or polyester) that are placed horizontally immediately adjacent to one another, incorporating strips of polytetrafluoroethylene (PTFE) felt (see Fig. 8-3, B ). These sutures are placed deep into the ventricular septum (see Fig. 8-3, B [inset]) to exclude as much septal scar as possible. As these sutures are tied, beginning at the basilar portion of the ventricle, volume from the pump-oxygenator is infused, and the lungs are gently inflated to evacuate air from the pulmonary veins and left atrium. Saline can also be infused into the open LV. When this suture line is completed, it is reinforced with two continuous No. 0 or 1 polypropylene sutures that are positioned at each end of the incision, placed through the felt and through the edges of the myocardium superficial to the mattress sutures, and tied to each other ( Fig. 8-3, C ). Incorporation of the distal portion of the LAD into the suture lines should be avoided.
An alternative procedure is patch closure of the defect in the LV ( Fig. 8-4 ). This technique has been termed “endoaneurysmorrhaphy” by Cooley and “endoventricular circular patch plasty repair” by Dor. The rationale for this technique is based in part on the fact that, coexisting with anterior LV aneurysm, scar tissue and akinesis or dyskinesis are present in the anterior portion of the LV septum. When a patch is used for closure, the area of septal scarring can be excluded from the reconstructed LV. This may result in improved LV function. Furthermore, curvature of the left anterior wall may be maintained. Based on echocardiographic measurements in normal hearts, Fontan determined that the patch should be oval and should have a long diameter of 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 too large an end-diastolic LV volume and thus a reduced global ejection fraction. A patch that is too small may reduce LV volume and compliance. A preshaped 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. After opening the LV, the line of demarcation between scar and contractile LV myocardium is identified ( Fig. 8-4, A [inset]). This may be facilitated by palpation if cardioplegia is not used during this portion of the operation. A purse-string suture of No. 2-0 polypropylene is placed at the junction of scar and contractile septal and free wall myocardium ( Fig. 8-4, B ). The longitudinal and transverse dimensions of the resulting defect are measured. A patch of gelatin or collagen-impregnated polyester (that can be lined with autologous pericardium) with slightly larger (0.5 cm) dimensions is fashioned and then sutured into place with a continuous No. 3-0 polypropylene suture ( Fig. 8-4, C ). Before completing the suture line, air is evacuated from the LV 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 No. 2-0 polypropylene suture ( Fig. 8-4, D ).
A second alternative procedure in patients without a calcified aneurysm, and the rare patient with a small LV cavity, is direct LV reconstruction using multiple concentric purse-string sutures without a patch.
Posterior Aneurysm
The techniques described for repairing anterior LV aneurysms are also applicable to posterior aneurysms. However, the defects remaining after excision of the scar or after circular reduction with a suture are generally smaller. Injury to the posterior papillary muscle at the lateral edge of the defect and to the posterior descending coronary artery on the medial edge of the defect must be avoided.
Associated Mitral Regurgitation
Mitral regurgitation of variable degree is often present in patients with LV aneurysm. If repair of the valve is possible, it may be accomplished with standard techniques through a left atrial approach (see Technique of Operation in Chapter 11 ). Alternatively, the “edge-to-edge” repair technique proposed by Alfieri and colleagues can be performed through the ventriculotomy.
If valve replacement is indicated, it can be performed through the opened LV for posterior as well as anterior aneurysms ( Fig. 8-5 ). The ventricle is opened through the aneurysm as previously described, and the mitral valve is examined ( Fig. 8-5, A ). If replacement is indicated, the mitral valve leaflets are excised, and all chordae tendineae are transected. A small remnant of anterior leaflet is left adjacent to the aortic valve cusps ( Fig. 8-5, B ). The valve holder apparatus is removed from the appropriately sized mechanical or bioprosthetic valve, 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 the pledgets positioned on the atrial side ( Fig. 8-5, C ). These sutures are placed through the sewing ring of the prosthesis on the undersurface of the flanged portion (see Fig. 8-5, C ). The valve is then lowered into the anulus and the sutures tied ( Fig. 8-5, D ). 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 LV is then reconstructed using one of the techniques previously described.
Special Features Of Postoperative Care
Postoperative care is the same as that for other patients after intracardiac operations (see Chapter 5 ) and particularly after CABG. The detailed late-postoperative care required for patients undergoing CABG (see Special Features of Postoperative Care in Chapter 49 ) should also be applied to patients whose operation has included resection of a postinfarction LV aneurysm.
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