LV aneurysm after acute myocardial infarction

울산의대 서울아산병원 흉부외과

주 석 중

Historical background

• Baily. 1954 년 최초로 좌심실류 절제술에

성공함 .

• Cooley. 1958 년 최초로 심폐기하에서

좌심실류 repair 에 성공 (Plication/

Linear repair)

• Lillehei, Stoney, Daggett, Dor, Jatene,

Cooley 등에 의해서 계속 발전됨 .

Direct correlation between LV volume and survival

Figure 1. Relative risk for death after transmural myocardial Infarction correlates

with end systolic volume. White HD et al. Circulation 1987;76(1):44-

51

ESV more accurately predicts death than low EF

White HD et al. Circulation 1987;76(1):44-51

Long term survivors with low EF have smaller ESV

White HD et al. Circulation 1987;76(1):44-51

LVESVI greater than 60ml/m2 portends poor long term prognosis

Early expansion phase

• 초기 심근 확장은 경색 직후부터 시작

• 경색된 심근 조직은 높은 plasticity 와

creep 를 보임 .

• T=Pr/2h 법칙에 의하여 healing 으로

creep 이 감소 할 때까지 infarct

expansion 이 계속 진행됨 .

Late remodeling phase

• 심근 경색 발생 2-4 주 후 시작하여 grannulation

tissue 가 나타나고 , 6-8 주가 되면 섬유 조직으로 대체됨 .

• Granulation tissue 의 형성은 wound healing

response 의 early phase 로 점차 섬유 세포 및 scar

tissue 로 바뀌는 과정을 밟게 된다 .

• 심근 발생 2 주 이내 재관류가 이루어질 경우 좌심실류의 진행이 어느 정도 예방 또는 억제될 수 있음 .

• Late remodeling phase 동안에 좌심실류의 확장이 이루어지는 기전에 관해서는 아직 확립된 바가 없음 .

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 dyskinesia– Age : HF score : Coronary disease severity

– Angina duration : Prior infarction : MR

– Function of residual ventricle

LV remodelling is a shared pathophysiology of LV aneurysm and

ischemic MR

Grigoni et al circulation 2001;103:1759-1764Diodato MD et al Ann thorac surg 2004;78(3):794-799

Borderzone expansion contributes to post infarction LV remodeling

JACC Vol. 40, No. 6, 2002 September 18, 2002:1160–7

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

Aneurysm repair causes apoptosis down regulation

Group 1 - sham ratsGroup 2 - Aneurysm Group 3 - Anuerysm and repair group

Red : Propidium iodide staining Green : Tunnel staining Ann Thorac Surg 2007;84:1279-87

Diagnostic modality

• Echocardiography

– Screening method for detecting LV aneurysm

– Useful for assessing MV function

• Cardiac MRI

Surgical Technique Plication Linear closure

Guilmet procedure

Mickleborough procedure

Circular patch plasty

Endoventricular patch plasty

Surgical Ventricular Restoration

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 O2

demand ↓ Exercise tolerance ↑

• Scientific evidence to be collected through the STICH trial

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

AMC experience • Duration : 1991 – 2008. 3 월 n=60

• M 52 명 (85%) Mean age : 60.6

Preop NYHA functional class

I 1

II 12

III 35

IV 13

78% of the patients were in functional class III or IV

Associated conditions

3VD 50 (82%)

Preop IABP 4 (7%)

Preoperative echocardiogram

Parameter Value

EF(%) 31.0±10.0

LVIDs (mm) 48.5±10.1

LVIDd (mm) 61.1±8.5

LVESV (ml) 124.3±57.4

LVEDV (ml) 173.5±67.1

Surgical Method

Surgery Value Pication 3Linear repair 28Endoventricular patch 30

Concom. Proced .CABG 59

(96.7) Ring 6 Double orifice 4Pap m. imbrication 3Posterior annuloplasty 5

Postop course

Cumulative survival

Case Case

M/58

LV aneurysm

3 vessel disease

Schema of Surgical Ventricular Restoration

Schema of Surgical Ventricular Restoration

Serial Echo FindingsSerial Echo Findings

EF LV volume

Preop 38 % 133 ml

Immediate 25 % 111 mlpostop

Postop 2 36 % 103 ml

Post op 3 48 % 63 ml(3 years later)

3yrs Later after SVR3yrs Later after SVR

2004-09-3 2007-01-24

P value

EF(%)

Preop. 53.5±12.1 55.0±12.6 NS

Immdiate Postop. 54.1±9.5 56.7±13.2 NS

CT finding

Non-visualization 0(0) 0(0) NS

Faint(%)

LAD 1(2.7) 3(15.0) NS

V1 0(0) 1(5.0) NS

V2 0(0) 0(0) NS

V3 1(7.7) 0(0) NS

LIMA TRA(n=23)SVGseq (n=37)

Prevention of IMR does not prevent LV remodelling after posterolateral MI

J Am Coll Cardiol;43(3):377-83

The key to treating chronic infarction induced heart failure is to treat the underlying cause of the remodeling process

Effects of increasing distal run-off on overall flow