Ventricular septal rupture (VSR) is a rare but lethal complication of myocardial infarction (MI). Bimodal peak Range: few hours  2 weeks Average time to rupture 2-8 days Time course may be accelerated by thrombolysis, possible related to intramyocardial hemorrhage

1. Post MI Ventricular Septal
Defects
Dr. Asma Iqbal
PGR
Services
Hospital,Lahore

2. • Ventricular septal rupture (VSR) is a rare but lethal
complication of myocardial infarction (MI).
• Bimodal peak
• Range: few hours  2 weeks
• Average time to rupture
2-8 days
Time course may be accelerated by thrombolysis,
possible related to intramyocardial hemorrhage

5. PATHOPHYSIOLOGY

6. Ischemia Hyaline degenration
Fragmentation
Enzymatic digestion
Fissure formation
Septal rupture
Pathogenesis

7. Associated Factors
Predictors of VSD
Advanced age,
Anterior location of infarction,
Female sex,
CKD
Thrombolysis after 12 hours also suggested as a
predisposing factor.
Decreased Likelihood
 H/o Smoking
 HTN,
 DM,
 Chronic Angina, previous MI

8. EPIDEMIOLOGY

9. Epidemiology
• uncommon complication of MI.
• Autopsy studies reveal
It occurrs at a rate of
approximately 1-2% without
reperfusion therapy
• 0.2% to 0.34% with
fibrinolytic therapy
• 3.9% among patients with
cardiogenic shock

10. MORTALITY
High mortality despite various
improvements in therapy
30 day mortality- 74%
1 year mortality- 78%
GUSTO analysis, Crenshaw et al,
Circ. 1/2000

11. Relative Improvement in survival due to
Earlier diagnosis
Earlier flow restoration
More aggressive surgical intervention
More aggressive BP control post MI

12. ANATOMICAL SITES AND
CLASSIFICATION

13. Septal blood Supply
The septal blood supply comes from branches of
•the left anterior descending coronary artery,
•the posterior descending branch of the right
coronary artery, or the circumflex artery when it is
dominant

14. There are three types of VSR (the original
classification made by Becker and van Mantgem
was for free-wall rupture):
Type I: there is an abrupt tear in the wall without
thinning,Associated with Acute infarcts
Type II, the infarcted myocardium erodes before
rupture and is covered by a thrombus;
Type III represents the perforation of a previously
formed aneurysm,process associated with older
infarcts
BECKER AND MANTGEM
CLASSIFICATION

15. Anatomical Types of VSR
Two types of VSD (According to site )
Simple: through and through defect usually
located anteriorly, About 60% of VSRs occur
with infarction of the anterior wall,LAD is
Culprit
Complex: serpentiginous dissection tract
remote from the primary septal defect-
most commonly an inferior VSD, 40% with
infarction of the posterior or inferior wall

16. DIAGNOSIS

17. History
Chest Pain
SOB
Hypotension

18. Clinical Findings
Loud S2
S3
Pulmonary edema
RV/LV failure
Loud/harsh pansystolic murmur
Within the first week post AMI
Best heard at Lt. Lower sternal border
Less loud at the apex
Associated with a palpable thrill
Depending on the location, may radiate to the axilla
mimicking MR

19. Diagnosis
Up to 50% of patients experience chest
pain associated with the development
of murmur
CHF and shock often associated with
the development of murmur

20. INVESTIGATIONS
 IMAGING MODALITIES
 ECG
 Catheterization and Pressure Measurement

21. ECG
No electrocardiographic (ECG) features are
diagnostic of postinfarction VSR, though ECG
indeed provides some useful information.
Persistent ST-segment elevation associated with
ventricular aneurysm
may reveal atrioventricular block in one third of
patients.
anatomic location of the septal rupture.

22. RADIOGRAPHS
On plain chest radiography, 82% of patients
with postinfarction ventricular septal
rupture (VSR) demonstrate left ventricular
enlargement,
78% have pulmonary edema,
and 64% have a pleural effusion

23. ECHOCARDIOGRAPHY
Gold standard
RWMA
VSR
L R SHUNT On color
flow Doppler

24. Color Flow
Doppler
100% sensitive and
specific in
differentiating VSR
from acute MR

25. CATHETERIZATION AND PRESSURE
MEASUREMENT
Left-heart catheterization with coronary
angiography is recommended in all stable
patients
An important diagnostic test for differentiating
VSR from mitral valve insufficiency is
catheterization of the right heart with a Swan-
Ganz catheter.
Left- and right-side pressure measurements help
estimate the degree of biventricular failure

26. Need for cardiac catheterization
2/3 of the patients have multivessel
coronary artery disease
Decreased operative mortality and
improved late survival has been shown in
patients with multivessel disease
Cardiogenic shock not a deterrent to Cath
=> Coronary angiography
should be performed

27. TREATMENT MODALITIES
Medical Therapy
Percutaneous Device closure
Surgical Repair

28. Pre-Operative Management
Hemodynamic stabilization so as to
minimize peripheral organ compromise
Reduce Systemic vascular resistance, and
thus, the left-to-right shunt
Maintain or improve coronary artery blood
flow
Maintain cardiac output and arterial
pressure to ensure peripheral organ
perfusion

29. Supportive medical
management
Vasodilators
Vasopressors
The profound level of cardiogenic shock in
some patients precludes vasodilator
treatment, often necessitating vasopressor
support.
Intra-aortic balloon counterpulsation
(IABCP)

30. WHAT IS IABP
COP
L R SHUNT
Perfusion

32. Percutaneous Device Closure

33. Timing of Surgery
Controversial (in the past)
Non-randomized studies showing:
Early repair, 40% - 50% mortality
Late repair (past 3 weeks), 10% mortality
=>
Aggressive Medical management aimed
at delaying surgical intervention

35. Timing of Surgery
Surgery should be performed soon after
diagnosis in most patients
Patients is cardiogenic shock should be
operated on immediately after
anigography
Hemodynamically stable patients
should have surgery on an urgent basis

36. The relative safety of repair 2-3 weeks or
more after perforation has been
established. Because the edges of the
defect have become firmer and fibrotic,
repair is more secure and is easily
accomplished. A successful clinical outcome
is related to the adequacy of the closure of
the VSR;

37. GOALs OF SURGERY
Exclusion or Removal of Infarcted
Myocardium
Elimination of L to R shunt

38. Operative techniques
Resection of Infarcted Myocardium
Double Patch Repair of VSR
3-D Patch Technique

39. Operative Technique
Classical approach to
antero-septal rupture
Infarctectomy, and
Reconstruction of the
ventricular septum with
Dacron patches

40. Operative Technique
Classical approach
to infro-posterior
rupture
Infarctectomy, and
Reconstruction of
infroposterior VSD,
ReconstructionReconstruction free wall
with Dacron patches.

41. Outcome
Six month survival without
surgical intervention stated to be
less than 10%.
Kirklin, Churchill Livingston 1993

42. Outcome
In patients with cardiogenic shock mortality
reported to be the highest
Posterior VSD (IMI) is another factor strongly
associated with poor surgical outcome due to
Difficulty of exposure, and
Frequent concomitant infarction of the postero-
medial papillary muscle

43. THANK YOU