Ventricular septal rupture (VSR) is a rare but serious complication of myocardial infarction where a tear forms in the ventricular septum, creating a left-to-right shunt. It typically occurs 2-8 days after MI. Diagnosis is made through echocardiography which demonstrates the shunt. Urgent surgical repair is the treatment of choice to close the defect before hemodynamic deterioration, though supportive medical management may be used to stabilize the patient pre-operatively. Surgical techniques involve infarct removal and patch reconstruction of the septum. Prognosis depends on factors like presence of cardiogenic shock, with posterior defects associated with higher mortality.
Percutaneous Balloon Mitral Valvuloplasty (PBMV) is a procedure to dilated the mitral valve in the setting of rheumatic mitral valve stenosis. A catheter is inserted into the femoral vein, advanced to the right atrium and across the interatrial septum. Then the mitral valve is crossed with a balloon and it is inflated to relieve the fusion of the mitral valve commissures effectively acting to increase the mitral valve area and reduce the degree of mitral stenosis. Mitral regurgitation is a potential complication and thus PBMV is contraindicated if moderate or severe regurgitation is present. The Wilkins score examines mitral valve morphology and is determined via echocardiography to assess the likelihood of using PBMV based on certain echocardiographic criteria.
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
Percutaneous Balloon Mitral Valvuloplasty (PBMV) is a procedure to dilated the mitral valve in the setting of rheumatic mitral valve stenosis. A catheter is inserted into the femoral vein, advanced to the right atrium and across the interatrial septum. Then the mitral valve is crossed with a balloon and it is inflated to relieve the fusion of the mitral valve commissures effectively acting to increase the mitral valve area and reduce the degree of mitral stenosis. Mitral regurgitation is a potential complication and thus PBMV is contraindicated if moderate or severe regurgitation is present. The Wilkins score examines mitral valve morphology and is determined via echocardiography to assess the likelihood of using PBMV based on certain echocardiographic criteria.
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
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1. Post MI Ventricular Septal
Rupture
Dr. Asma Iqbal
Dr. Nadish
Dr. Aneera
Dr.Nimra
2. Ventricular septal rupture (VSR): Tear or Laceration in the
Interventricular septum creating a Left to Right Shunt.
• It 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
INTRODUCTION
8. Epidemiology
• Uncommon complication of MI.
• Autopsy studies reveal
• It occurs 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
9. Relative Improvement in survival due to
Earlier diagnosis
Earlier flow restoration
More aggressive surgical intervention
More aggressive BP control post MI
10. 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
11. ANATOMY OF VSR
Two types of post MI VSR
Simple: through and through single large defect usually
located anteriorly
Complex: serpentiginous dissection tract remote from the
primary septal defect- most commonly an inferior VSD
Apical VSR with anterior MI(due to LAD occlusion)
Basal VSR with inferior MI (due to RCA/LCX occlusion)
12. CLINICAL PRESENTATION
Patient may remain relatively comfortable early in the disease
course.
Recurrence of angina, pulmonary edema, hypotension, and
shock may develop abruptly later in the course.
Abrupt onset of hemodynamic compromise characterized by
hypotension, biventricular failure, and a new murmur may be
the initial manifestation.
13. PHYSICAL FINDINGS
The diagnosis should be suspected when a new pansystolic
murmur develops, especially in the setting of worsening
hemodynamics
16. 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.
17. 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
18. ECHOCARDIOGRAPHY
Transthoracic echocardiography is the test of choice for the
diagnosis of VSR
Basal VSR is best visualized in the parasternal long axis with
medial angulation, the apical long axis, and the subcostal long
axis.
Apical VSR is best visualized in the apical four- chamber view.
It determines the size of the defect and the magnitude of the
left-to-right shunt
An assessment of RV and LV function is key to prognostication
and management
21. 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
22.
23. 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
25. MANAGEMENT
Priority of therapy. Urgent surgical closure is the treatment
of choice (Class I recommendation), especially when the
patient’s condition is stable because hemodynamic
deterioration in this setting is unpredictable
The mortality rate for patients with VSR treated medically is
24% at 72 hours and
75% at 3 weeks.
26. 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
27. Supportive medical management
Vasodilators can decrease left-to-right shunt
and increase systemic flow by means of
reducing systemic vascular resistance (SVR).
Vasopressors
The profound level of cardiogenic shock in
some patients precludes vasodilator treatment,
often necessitating vasopressor support.
Intra-aortic balloon counterpulsation (IABP)
29. 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
32. Operative Technique
Classical approach
to infro-posterior
rupture
Infarctectomy, and
Reconstruction of
infroposterior VSD,
Reconstruction free wall
with Dacron patches.
33. Outcome
In patients with cardiogenic shock mortality
reported to be the highest
Posterior VSR (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
35. SCANERIO :
A 55 Year old Hypertensive male, diagnosed with
extensive anterior wall MI and managed with
SK,unremarkable general and systemic examination
On 4 th Day He became suddenly Dyspenic with B.P=
80/60, rales heard at lower half of lungs B/L,Cardiac
examination revealed New pansystolic murmur at left
lower parasternal border. Ionotropic support started but
vitals did not improve, so IABP inserted…
36. WHAT IS YOUR PROVISIONAL DIAGNOSIS?
HOW Will you proceed ?