This document discusses post-myocardial infarction ventricular septal rupture (VSR). It notes that VSR incidence has decreased with improved reperfusion therapies. Surgical repair is the definitive treatment but is high risk, while percutaneous closure and mechanical support have improved outcomes. The timing and presentation of VSR depends on its pathophysiology, which can include acute or delayed rupture. Diagnosis is via echocardiography. Management involves surgical closure if stable, while unstable patients may be supported with devices or surgery delayed. Percutaneous closure is an option for inoperable cases.

1. Post-MI Ventricular Septal Rupture
- Dr.Pradeep

2. • Ventricular septal rupture (VSR) remains a devastating complication
following acute myocardial infarction (MI).
• Surgical repair is the definitive treatment, but it is challenging and
associated with high morbidity and mortality.
• The availability of mechanical support and percutaneous closure
has significantly altered the treatment paradigm.

3. How Often Do We See It?
• The incidence of VSR has decreased from 1-3% following
ST-segment elevation MI in the pre-reperfusion era to
0.17-0.31% following primary percutaneous coronary
intervention.
• Optimal reperfusion of the infarct-related artery prevents
development of VSR by salvaging myocardium and
limiting infarct expansion.
• In contrast, late reperfusion remains associated with
increased risk of mechanical complications.

4. •The rarity of clinical presentation results in a lack of medical and
surgical expertise in the identification and management of VSR.

5. Pathophysiology and Timing
• The timing and presentation of VSR is closely related to
the underlying pathophysiology.
• Universally, patients with VSR present with a transmural
infarction, resulting from complete occlusion of any
coronary vessel subtending a portion of the septum.
• The Becker and van Mantgem classification of free wall
rupture usually correlates with clinical presentation.

6. Becker type 1
• Becker type 1 ruptures are slit-like tears through normal
thickness myocardium, occurring abruptly within 24 hours of
an MI, typically related to intramural hematomas dissecting
through tissue planes.
• These typically occur in the setting of a relatively small
inferior MI involving the margins of the posterior descending
artery distribution, likely due to the shear stress generated by
the adjacent hyperkinetic myocardium supplied by the non-
infarct left anterior descending (LAD) artery.
• Such VSRs can be present either at or shortly after clinical
presentation.

7. Becker type 2
•Becker type 2 ruptures typically result sub-
acutely from erosion of infarcted myocardium
and are associated with neutrophilic
infiltration and coagulation necrosis.

8. Becker type 3
• Becker type 3 ruptures result from perforation of thinned
aneurysmal myocardium in the late phase post-MI and occur more
frequently in the absence of reperfusion therapy.
• VSR in these settings occurs sub-acutely or late after the index
infarction.
• As a result, there is a bimodal distribution of time to rupture with
VSR diagnosis occurring within hours or within 3-5 days or even
later of the index MI.

9. Factors associated with increased likelihood of developing post-infarct VSR :
• Older age
• female gender,
• prior stroke,
• ST-segment elevation,
• elevated cardiac markers,
• higher heart rate,
• lower blood pressure,
• higher Killip class, and
• delayed or lack of reperfusion

10. It has been found that patients with VSR are less likely to have :
-History of HTN/DM
-Prior MI
-Prior h/o angina
-Smoking

11. • The LAD and the right coronary arteries are the most common infarct-related
arteries leading to septal rupture (42 and 46%, respectively, of all VSRs in the
SHOCK registry. [Should We Emergently Revascularize Occluded Coronaries
for Cardiogenic Shock] registry).

12. • Anterior and inferior infarctions contribute roughly equally to the VSR
burden.
• Anterior infarctions typically result in apical VSRs.
• These defects are relatively simple, occurring at the same level on both
sides of the septum.
• In contrast, inferior infarctions more commonly result in complex ruptures,
taking serpiginous routes through a hemorrhagic and necrotic basal
inferoposterior septum.

13. • On imaging with computed tomography and magnetic resonance imaging, LAD VSRs
were smaller, had thinner margins, and were more likely surrounded entirely by septum.
• In contrast, right coronary artery VSRs were more likely complex with associated
intramyocardial dissection and involvement of the free wall.

14. Presentation and Diagnosis
• VSR results in left-to-right shunting, right ventricular (RV) volume
and pressure overload, increased pulmonary venous return, and
secondary left-sided volume overload.
• The degree of shunting, or shunt fraction (Qp/Qs), is determined
by the relative vascular resistances in the systemic and pulmonary
beds.
• The left-to-right shunt results in a harsh, systolic murmur heard
throughout the precordium, often loudest at the left sternal
border, associated with a palpable thrill.

15. • Signs of increased right-sided flow may include an accentuated pulmonic component of
the second heart sound, left and/or right S3 gallop, tricuspid regurgitation, and a mid-
diastolic rumble from increased trans-mitral flow.
• Depending on the size of the index infarction, degree of shunting, and RV dysfunction,
patients with VSR may manifest with relative hemodynamic stability or frank
cardiogenic shock.
• In stable patients, the presence of a murmur or findings of routine echocardiography
may be the only clues to the diagnosis.

16. • Patients with cardiogenic shock manifest with hypotension, cold clammy
peripheries, oliguria, and frank pulmonary edema. When the RV is involved,
especially in the setting of an inferior infarction, hepatic dysfunction and
coagulopathy may also be noted.
• Transthoracic and Doppler echocardiography are essential to diagnosing the
presence, size, and hemodynamic impact of VSR and helping establish the
diagnosis while excluding other etiologies of hemodynamic instability.

17. • Transesophageal echocardiography may be necessary if surface images are limited and
is especially useful in inferior MI when percutaneous closure is contemplated.
• On occasion, when faced with unexplained hemodynamic instability in the
catheterization laboratory, left ventriculography will help confirm the presence of VSR.
• Pulmonary artery catheterization will reveal a step-up in oxygen saturation in the RV and
can be used to calculate the Qp/Qs.

18. Management
• Surgical closure is the definitive treatment for post-infarction
VSR.
• Studies reported on surgical outcomes in 2,876 VSR patients
from the Society of Thoracic Surgeons National Database.
• Studies found an overall in-hospital or 30-day mortality of
42.9%, the highest of any cardiac surgeries, with a sharp
decrease in mortality with delay in repair: 54.1% with repair
within 7 days from MI versus 18.4% after 7 days.

19. • Selection and survivorship bias confound the observations of increased survival
with delayed repair. Risk factors for operative mortality include age, female gender,
shock, inferior infarction, pre-operative intra-aortic balloon pump use, pre-
operative dialysis, mitral insufficiency, redo cardiac surgery, emergent surgery, and
timing of repair.

20. Mortality and Timing of Repair

21. • The optimal timing of definitive surgical repair remains elusive. Although the
guidelines recommended emergent surgical repair regardless of hemodynamic
status, the timing of surgery in the setting of VSR remains controversial and should
be individualized.
• In hemodynamically stable patients with preserved end-organ function and favorable
anatomy, early corrective surgery should be considered because sudden and
unpredictable hemodynamic compromise is often noted.
• Delayed surgery in hemodynamically stable patients may be considered when
surgical anatomy is complex and there is concern regarding tissue fragility and the
ability to perform definitive repair.

22. • The perceived benefit of delayed surgery, although fraught with bias, does have a
mechanistic basis.
• Following infarction, metalloproteinase activity and tissue breakdown peak by day 7,
whereas deposition of new collagen begins by days 2-4; necrotic myocytes are entirely
replaced by collagen by 28 days.
• Therefore, delay might facilitate successful repair by allowing friable tissue to organize,
strengthen, and become well-differentiated from surrounding healthy tissue.

23. • In this scenario, close follow-up in the intensive care unit may be considered to enable
tissue healing and promote chances of definitive repair.
• Watchful waiting in this group of patients may also be appropriate in the setting of
significant platelet inhibition from exposure to potent dual antiplatelet therapy.
• In recognition of the possible benefits of delayed repair, the European Society of
Cardiology guidelines promote delayed elective repair in patients initially responding to
aggressive conservative management.

24. VSR Management Algorithm

25. • In stable but inoperable patients, percutaneous device closure may be considered.
• In a review of 13 case series encompassing a total of 273 patients treated with TSC,
Schlotter et al. found an overall procedure success rate of 89% and a 30-day or in-
hospital mortality of 32%.
• The mortality rate in individual studies correlated with the proportion of patients treated
within 14 days of the MI, consistent with the higher mortality seen with early surgical
closure.

26. • Reported procedure complications include arrhythmias, device embolization, ventricular
rupture, device-related hemolysis, blood transfusion, and death.
• In the largest individual series of 53 patients, Calvert et al. found increased mortality
with older age, female gender, larger defect size, lack of revascularization, and higher
acuity disease (cardiogenic shock, inotropic support, and elevated creatinine);
• Prior surgical closure and immediate shunt reduction were associated with survival.

27. • TSC involves obtaining both femoral arterial and femoral or internal jugular venous
access, crossing the defect typically from the left to the right with a soft wire,
landing the wire into the pulmonary artery, and snaring it from the venous
circulation to form an arteriovenous rail.
• The latter is used to advance a device-delivery sheath from the venous side
across the septal defect, through which a septal occluder is deployed with
transesophageal or intracardiac echocardiographic guidance.

28. • The Amplatzer™ (St. Jude Medical; St. Paul, MN) devices are the most commonly
used, designed with two discs that deploy on either side of the septum connected
by a stem that traverses the VSR defect.
• Several factors are considered in patient selection and device sizing, primarily
contingent on VSR morphology and relationship to nearby structures.
• Specifically designed for post-MI VSR repair, the Amplatzer™ PI Muscular VSD
Occluder (St. Jude Medical; St. Paul, MN) is available with a maximum waist size
of 24 mm and disc size of 34 mm.

29. • Using gated computed tomography and magnetic resonance imaging, Hamilton et
al. showed that a 24 mm waist diameter would only occlude 50% of the left side of
VSRs, and a 34 mm disc diameter would reach the margins of 75% of the defects
in both systole and diastole.
• Defects <15 mm are considered optimal for TSC, but successful closure has been
reported with larger defects.

30. • Oversizing the disc may improve procedure success by accounting for defect enlargement
due to tissue necrosis.
• Challenges to TSC include inferior defects due to a lack of a circumferential septal rim,
basal defects due to the proximity to the tricuspid valvular apparatus, serpiginous defects
due to complicated morphology, and closure soon following infarction due to tissue
instability.
• Diligent defect characterization, device selection, and patient selection are perquisites to
successful TSC.
• On occasion, closure devices have also been utilized intra-operatively as an adjunct to
surgical repair. Finally, TSC also has a role as salvage therapy for residual defects
following initial surgical repair.

31. • Surgical outcomes in the setting of cardiogenic shock are dismal. In the setting of the
SHOCK trial, surgical VSR correction was associated with a mortality rate of 87%.
• Survival rates following TSC in this context are equally disappointing. In the series by
Thiele et al., 30-day mortality following TSC was significantly greater in those with shock
versus those without (88 vs. 38%).
• Extensive anatomical destruction of the ventricular septum, hepatic and renal
dysfunction, and RV failure (from infarction, volume and pressure overload, and
consequences of the index infarction) all contribute to prohibitive surgical risk even in the
most experienced centers.

32. • The availability of temporary mechanical circulatory support devices (MCS devices) has
revolutionized treatment strategies in patients with cardiogenic shock.
It is strategy to support such patients with venoarterial extracorporeal membrane
oxygenation, which allows for
1) stabilization of hemodynamics.
2) recovery or prevention of end-organ injury.
3) washout of dual antiplatelet effect.
4)strategy of bridge to decision.

33. • Experienced operators have successfully utilized Tandem Heart (Cardiac Assist, Inc.;
Pittsburgh, PA) in this setting.
• In addition to optimizing hemodynamics and tissue oxygenation, this device
decompresses the left atrium and therefore reduces the degree of left-to-right shunting.
• Kar et al. demonstrated the efficacy of TandemHeart in improving hemodynamic
parameters and end-organ function in 117 patients with cardiogenic shock of various
etiologies.
• Short-term MCS has received a Class IIa recommendation (level of evidence C) as a
bridge in VSR patients.

34. • Patients with severe end-organ failure despite aggressive support may not be
considered for further interventions, and transition to palliative care may be
appropriate.
• Stabilized patients should be considered for eligibility for advanced options.
• Select patients can then be offered corrective surgery with TAH as back-up. In
others with catastrophic cardiac destruction, listing for transplantation and/or TAH
insertion may be the appropriate strategy.

35. • Non-surgical management in this setting is only temporizing and involves afterload
reduction with intravenous nitroprusside and/or intra-aortic balloon counterpulsation
to mitigate shunting.
• Intravenous diuretics may reduce pulmonary congestion. Vasopressors may be
necessary in the setting of circulatory collapse but may result in ischemia,
arrhythmia, and worsened tissue perfusion and acidosis.

36. • Post-infarction VSR is a rare complication with a grim prognosis. Once diagnosed,
management includes any combination of aggressive medical management, surgical
repair, transcatheter closure, novel surgical/percutaneous hybrid procedures, and
palliative care.
• There remains equipoise regarding timing of repair. Use of early MCS in patients with
hemodynamic instability appears to be a promising modality to bridge patients to a
decision of delayed repair, transplantation, or palliative options.
• A multidisciplinary heart team must collaborate at an experienced center to devise a
strategy that is tailored to each patient.

37. THANK YOU