This document provides information on left ventricular aneurysms including: - A timeline of important discoveries and advances in LV aneurysm research and treatment from 1757 to 1958. - Definitions, gross pathology, microscopic pathology, location, and natural history of LV aneurysms. - Clinical features and diagnostic criteria for LV aneurysms. - Surgical techniques for repairing LV aneurysms including plication, linear closure, patch closure, and endoventricular circular patch repair.

1. LEFTVENTRICULARANEURYSM
Dr MOHIT SHARMA

2. 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 linearrepair
of a LVA using CPB.
John Hunter
Weitland
Beck
Likoff and Bailey

3. 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trabecular pattern of the inner surface of the wall has been replaced by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.

4. 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.

5. 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.

6. 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.

7. Diagnostic modality
Echocardiography
Screening method for detecting LV aneurysm
Useful 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

8. 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

9. 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.

10. 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

11. 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

12. 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 dyskinesia
Age : HF score : Coronary disease severity
Angina duration : Prior infarction : MR
Function of residual ventricle

13. 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

14. Surgical Technique
Plication
Linear closure

15. Patch closure – Endoaneurysmorraphy
by Cooley
Endoventricular circular patch repair-
Dor

16. 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.

17. 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.

18. 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.

19. 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.

20. Guilmet procedure

21. Mickleborough procedure

22. Circular patch plasty

23. Endoventricular patch plasty

24. Dor’s procedure
In 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.


25. 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.

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

27. 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↑ ↓ ↓ 2demand ↓Exercise
tolerance ↑
Scientific evidence to be collected through the STICH trial

28. 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

29. SPECIAL SITUATIONS
Intractable 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.

30. Postinfarction 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 Aneurysm
Rarely, violent nonpenetrating chest trauma produces such a severe contusion of the
heart that a localized aneurysm forms.Vascular injury and intramyocardial dissection
resulting from blunt trauma may also lead to aneurysm formation

31. 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

32. Surgical Treatment for Ischemic
Heart Failure (STICH) trial(-VE
TRIAL)