LEFT VENTRICULAR ANEURYSM

Dr MOHIT SHARMA

TIMELINE FACTS COMMENTS

1757

1881

1912

1944

1951

1955

1958

LV ANEURYSM by autopsy

LVA+ CAD

Congenital LVA Rx-surgical ligation

Fasciae latae plication.

First LV ANGIOGRAM

LVA repair without CPB

Cooley et al successfully performed a linear repair of a LVA using CPB.

Geometric ventricular techniques

John Hunter

Weitland

Beck

Likoff and Bailey

Stoney et al, Daggett et al,

Dor et al, Jatene, and Cooley et al.

DEFINITION-

•A post-infarction lt ventricular aneurysm is a well delineated transmural fibrous scar, virtually devoid of muscle, in which the characterstic fine trabecular pattern of the inner surface of the wall has been replaced by smooth fibrous tissue.

•During systole the involved wall segments are akinetic or dyskinetic.

•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.

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.

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.

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.

•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.

CLINICAL FEATURE AND DIAGNOSTIC CRITERIA

•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.

• 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.

Diagnostic modality

EchocardiographyScreening method for detecting LV aneurysmUseful for assessing MV function

Cardiac MRI

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

NATURAL HISTROY

Development of Lt Ventricular aneurysm

•Historically, about 10% to 30% of patients who survived a major MI developed an LV aneurysm.

•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

Patho-physiologic progression of aneurysm

•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

Lt 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.

RV function

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•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.

•Prognosis is adversely affected bydyskinesia rather than akinesia in the aneurysm; the former is usually associated with a low global LV ejection fraction

Factors contributing to LV aneurysm formation

Preserved contractility of surrounding myocardium

Transmural infarction

Lack of collateral circulation

Lack of reperfusion

Elevated wall stress

Hypertension

Ventricular dilatation

Wall thinning

Natural course

Recent 5YRS for medically managed LV

dyskinesia : 47~70%

Cause of death Arrhythmia 44% : Heart failure 33%

Recurrent MI 11% : Non cardiac cause 22%

Factors influencing survival of LV dyskinesiaAge : HF score : Coronary disease severity

Angina duration : Prior infarction : MR

Function of residual ventricle

LV remodeling involves apoptosis of normally perfused peri-infarct tissue

Pathologic condition of postinfarction LV remodeling cause changes

in cellular and biochemical levels

Increased appearance of vacuolated cells in periinfarct zone

indicating apoptotic changes

Upregulation of caspase-3 activity

- key mediator of apoptosis in mammalian cells

Surgical Technique Plication Linear closure

Patch closure – Endoaneurysmorraphy by Cooley

Endoventricular circular patch repair- Dor

Technique for repair of anterior left ventricular aneurysm by linear closure.A, After the aorta is clamped and cardioplegic solution has been infused, an incision is made in the thinnest portion of the aneurysm parallel to the interventricular groove. If pericardial adhesions are dense, the aneurysm can be left attached to the pericardium. The scar is excised (inset). B, After all the scar has been excised, traction sutures are placed at each end of the anticipated line of closure. The defect is closed with No. 1 or 2 double-armed silk or polyester sutures placed horizontally and immediately adjacent to one another. These sutures are placed deep into the ventricular septum to exclude as much septal scar as possible (inset). C, Suture line is reinforced with two continuous No. 0 or 1 polypropylene sutures positioned at each end of the incision, placed in scar tissue superficially to the mattress sutures, and tied to each other.

Technique for repair of anterior left ventricular aneurysm by patch closure.A, After the aorta is clamped and cardioplegic solution has been infused, an incision is made in the thinnest portion of the aneurysm parallel to the interventricular groove (inset). B, A purse-string suture of No. 2-0 polypropylene is placed at the line of demarcation between scar and contractile myocardium on the septum and free wall (inset). Longitudinal and transverse dimensions of the resulting defect are measured. 

Technique for repair of anterior left ventricular aneurysm by patch closure.  C, A patch of gelatin- or collagen-impregnated polyester or of polyester backed with pericardium (inset) is fashioned with slightly larger dimensions (0.5 cm) and is sutured into place, incorporating the purse-string suture, with a continuous No. 3-0 polypropylene suture. D,Remnant of the aneurysmal wall is trimmed and sutured securely over the patch with a continuous No. 2-0 polypropylene suture (inset). Key: LV, Left ventricle; RV, right ventricle.

Replacement of mitral valve through left ventricle (LV). A, An incision is made in the thinnest portion of the aneurysm parallel to the interventricular groove, and the mitral valve is examined. Chordae tendineae are divided at the tips of the papillary muscles. B, Mitral valve leaflets are excised. A small rim of anterior leaflet is left adjacent to aortic valve cusps. C, Valve holder apparatus is removed from mechanical valve or bioprosthesis, and valve is inverted and suspended by two hemostats. Interrupted, pledgeted mattress sutures of No. 2-0 polyester are placed through the mitral anulus, with pledgets on atrial side of anulus. These sutures are then placed through the sewing ring of the prosthesis on the underside of the flanged portion. D, The valve is lowered into the anulus and the sutures tied.

Guilmet procedure

Mickleborough procedure

Circular patch plasty

Endoventricular patch plasty

Dor’s procedureIn the endoventricular circular patch plasty by Dor, the

procedure is carried out under cardioplegia.

The left ventriculotomy is performed in the akinetic or dyskinetic zone (transaneurysmal ventriculotomy), the thrombus is removed .

An endoventricular circular suture (Fontan maneuver) is placed 1 cm distal to the border of healthy muscle in order to prevent its inclusion and allows recreation of the normal shape of LV using continuous 2-0 monofilament polypropylene suture.

Dor’s procedure

Following this, a balloonis placed in LV cavity and inflated to the theoretical diastolic volume of 50—70 ml/m2, and the circular suture is tightened and tied up.

This maneuver makes the definition of the circular patch size easier, which can consist of autologous (endocardium or pericardium) or synthetic tissue.

The patch size is trimmed to match the circular suture circumference after deflation of the balloon.

The patch is fixed by a continuous 2-0 suture inside the LV cavity on the border labeled by the circular suture.

Post Operative ComplicationsLow cardiac output - 22%–39%Ventricular arrhythmias - 9%–19%Respiratory failure - 4%–11%Bleeding - 4%–7%Dialysis-dependent renal failure - 4%Stroke - 3%–4%

Outcomes and prognosis

Low early mortality

2-13%

Acceptable 5 and 10 year mortality

5 year survival 58-80%

10 year survival 30% ( better than medical Tx)

Most patients experience increased LV performance

LVEF Pulm pressure LV volume MV O↑ ↓ ↓ 2 demand ↓ Exercise

tolerance ↑Scientific evidence to be collected through the STICH trial

INDICATIONS OF OPERATION

•A large LV aneurysm in a symptomatic patient, particularly one with angina pectoris but also in one with heart failure, is an indication for operation. Appropriate CABG is indicated at the time of aneurysmectomy.

•Currently, the patch closure technique for remodeling ventriculoplasty is the most widely used for repair of anterolateral aneurysms or areas of akinesis. In view of the high risk of operation in patients with advanced chronic heart failure, operation may not be indicated when the known risk factors are highly unfavorable to survival.

•When the LV aneurysm is small or moderate in size, its presence is not an indication for operation per se. Patients in such situations are advised about operation based on their coronary artery disease and LV function rather than on their aneurysm

SPECIAL SITUATIONSIntractable VT•Although intractable ventricular tachyarrhythmias occur in patients with ischemic heart disease in the absence of areas of LV scarring, they are more common in patients with LV aneurysms or extensive fibrosis. •However, only a small proportion with LV aneurysms develop intractable ventricular tachycardia.•Most patients in whom such an arrhythmia develops have poor global LV function, and it has been suggested that ventricular tachyarrhythmias are particularly likely to occur when the ventricular septum has been involved in the infarction. 

False left Ventricular Aneurysm• A false aneurysm may develop after acute rupture of an infarcted area of LV. Such ruptures are usually fatal, but when the pericardium is sufficiently adherent to the epicardium, rupture may result only in a localized hemopericardium. •Persistent communication of the hemopericardium with the LV cavity results in gradual expansion of the hemo-pericardium into a false aneurysm whose wall is composed of pericardium and adhesions and occasionally of myocardium, and whose mouth is usually narrow.•These aneurysms have a strong tendency to rupture, in contrast to true aneurysms.•Differentiation between true and false aneurysms can be difficult because the imaging characteristics of the two entities are often similar.•However, Doppler color flow imaging and transesophageal echocardiography are useful techniques for demonstrating the presence of a false aneurysm.

Postinfarct ion Left Ventricular Free Wall Rupture•Acute rupture of the free wall of the LV is an infrequent but serious complication of acute MI, occurring in 2% to 4% of patients.•Among 1048 patients with acute infarction and cardiogenic shock evaluated in the SHOCK (SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK?) trial and registry, free wall rupture or tamponade was present in 28 (2.7%).•It is the second most common cause of death following acute infarction (behind acute cardiac failure), accounting for up to 20% of early deaths.•Rupture generally occurs between 1 and 7 days after the infarction.

Congenital Left Ventricular Aneurysm•Congenital LV aneurysm is a rare malformation characterized by thinning of the myocardium, with layers of myocardial cells intermingled with various amounts of fibrous tissue.• It is usually located at the apex of the LV and has a broad neck.This entity differs from a congenital diverticulum of the LV, which is a noncontractile bulging of the LV into the epigastrium.•The latter is characterized by an elongated shape and a narrow connection with the LV cavity. It is also associated with midline thoracic and anterior abdominal defects.

Traumatic Left Ventricular AneurysmRarely, violent nonpenetrating chest trauma produces such a severe contusion of the heart that a localized aneurysm forms.Vascular injury and intramyocardial dissection resulting from blunt trauma may also lead to aneurysm formation

The STICH trial (Surgical Treatment for Ischemic Heart Failure)

Target registry 2800 patients with 90 participating centers

Objectives to seek best treatment for

coronary disease and heart failure

(Inclusive of SVR)

Groups

Medical therapy alone

Medical therapy & CABG

Medical therapy & CABG and SVR

Surgical Treatment for Ischemic Heart Failure (STICH) tr ial( -VE

TRIAL)