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Post-infarct Ventricular Aneurysm

Post-Infarct Left Ventricular Aneursym

1. Definition

A. an area of thin scar devoid of muscle that occurs after myocardial infarction. This area is well-delineated and both walls bulge outward during systole.

2. Morphology

A. The fibrous scar is transmural and delineated from surrounding myocardium
B. Underlying endocardium is smooth and non-trabeculated
C. The aneurysm is thin, devoid of muscle, and often large
D. The walls are akinetic or dyskinetic during systole
E. LVEF is usually depressed to 35% or worse

3. Pathophysiology

A. Fibrous scar tissue develops in about one month after infarct
B. Early aneurysms (7-10 days after infarct) are mostly necrotic muscle and therefore not true aneurysms
C. Overlying pericardium is usually adherent
D. Mural thrombus is present in about 50%, but rarely produces thromboembolism
E. Calcification of thrombus and/or pericardium is common
F. The non-aneurysmal portion of the LV gradually increases in both volume and thickness, resulting in depressed LVEF


Lateralless than 5%
G. 50% of posterior aneurysms are false aneurysms
H. True posterior aneurysms are associated with post-infarct mitral insufficiency

4. Clinical Features

A. Small and moderate sized aneurysms often have no specific associated symptoms
B. Classic presentation is history of previous MI and CHF
C. Ventricular arrhythmias are present in 15-30%, more often when the septum is involved
D. Thromboembolism is infrequent

5. Diagnosis

A. ECG: ST elevation, loss of R wave anteriorly, or evidence of previous infarction
B. CXR: enlarged heart, may show convexity if aneurysm is large and profiled
C. ECHO: demonstrates aneurysm, evaluates LV function and mitral insufficiency
D. Catheterization: look for following features -
1) systolic akinesia or dyskinesia
2) permanent outward bulging
3) thinning of wall
4) loss of trabeculations
5) clear demarcation of aneurysm area
6) concomitant CAD
7) segmental and global LVEF
8) presence of LV thrombus
9) presence and degree of mitral insufficiency

6. Natural History

A. Incidence
1) 10-30% after significant myocardial infarction if untreated
2) The incidence has been reduced by thrombolytic therapy, HTN control, and avoidance of corticosteroids
3) The aneurysm evolves over 6 months and is unlikely to enlarge after 1 year
B. LV function
1) There is global cardiac remodeling and dilitation
2) Systolic efficiency is reduced due to paradoxical movement of the aneurysm
C. Survival (non-operative)
1) Larger size of the aneurysm is a risk factor for premature death
2) With small aneurysms, survival is related to concomitant CAD risk factors rather than the aneurysm
3) The prognosis is poorer with dyskinesia and poor function of the LV
Function5-year survival
Dyskinesia + poor LVEF36%

7. Operative Indications

A. Large aneurysm, with or without symptoms (angina, CHF)
B. Recurrent ventricular tachycardia
C. Risk of late rupture
D. Evidence of thromboembolism
E. A small aneurysm may be a possible indication when undergoing concomitant cardiac procedure
F. Avoid operation with diffuse hypokinesis and no discrete aneurysm
G. Patients with severe LV dysfunction may be candidates for transplant

8. Operative Technique

A. Basic Considerations
1) Avoid clot dislodgement and thoroughly remove all thrombus
2) Remove all LV free wall that has smooth endocardium
3) Excise entire aneurysm, leaving thin rim of scar for closure
B. Methods
1) Incise anterior aneurysm longitudinally and preserve LAD if possible
2) Incise posterior aneurysm along long axis, avoiding papillary muscle
3) Objective is to preserve geometry and maintain LVEF
4) Classic linear closure does cause some distortion and is best used for small or apical aneurysms
5) Remodeling ventriculoplasty (Dor repair) uses patch to recreate wall architecture and is probably the optimum repair
6) Additional procedures as indicated (CAB, arrhythmia surgery)

9. Results

A. Symptoms
1) Symptomatic improvement occurs in most patients
2) Paradoxical wall movement is usually eliminated in the border zones
3) Symptomatic improvement is not always associated with improved LV function
4) Most evident in patients with preoperative CHF
B. Operative Mortality
1) About 5%, most from acute cardiac failure
2) Preoperative risk factors:
a) residual untreated CAD
b) resting LV dysfunction
c) chronic CHF
d) ventricular tachycardia
e) reduced cardiac output
f) elevated LVEDP
g) decreased septal systolic function
h) poor NYHA class
i) poor segmental wall motion
C. Late Mortality
1) 65% 5-year survival; particularly evident in patients with 3-vessel disease
2) One-third die from progressive CHF
3) One-third die from another myocardial infarction
4) Ventricular arrhythmias and sudden death in 15%

10. Special Situations

A. Pseudoaneurysm
1) Develops after acute rupture of contained area
2) Usually fatal, but hemopericardium can be small and contained
3) Small neck distinguishes this from large, wide neck of true aneurysm
4) The wall consists of pericardium and adhesions and gradually expands
5) More often located posteriorly or laterally
6) More likely to rupture than true aneurysm
7) Resection is indicated when the diagnosis is made
B. Post Infarct Free Wall Rupture
1) Occasionally massive with sudden death from exsanguination
2) Usually a more gradual process of dissection through the myocardium
3) Sudden death then occurs from pericardial tamponade
4) Surgical salvage is possible if LV has good function
C. Congenital Left Ventricular Aneurysm
1) Very rare
2) Long, finger-shaped projection projects into epigastrium
3) Rupture is not uncommon; can be excised without CPB

D. Traumatic Left Ventricular Aneurysm Severe localized contusion causes probable pseudoaneurysm Should be resected due to thin wall and propensity to rupture