Mechanical complications Post Acute myocardiac infarction and the role of CABG

1. Mechanical complications Post
AMI and the role of CABG
Nora Albogami
PGY-3

2. AMI mechanical complications:
Ventricular Septal Rupture
Left Ventricular Free Wall Rupture
Papillary Muscle Rupture

3. Introduction
• Although mechanical complications occur with only a small fraction of acute myocardial infarctions (AMI),
these types of complications are some of the most lethal and catastrophic complications of AMI
• With medical management only, each of these complications carries mortality between 80% and 100%
within 2 months of onset.
• Even with well-timed surgical intervention, mortality from each of these complications remains high.

4. Ventricular Septal Rupture
• Incidence 0.17% and 0.34%.
• Despite the relatively low incidence of this complication, its mortality remains extraordinarily high, with
medical management only almost uniformly fatal.
• Even with optimal treatment including surgical correction, mortality from this complication remains as high
as 19% to 54%.

5. Pathophysiology of Ventricular Septal Rupture
• If infarcted myocardium remains ischemic following an AMI, coagulation necrosis ensues within the
infarcted area.
• Neutrophils are the primary mediators of this inflammatory response to infarction, and as they enter the
necrotic area, they undergo apoptosis within 3 to 5 days of the insult and release lytic enzymes.
• It is these enzymes that digest the necrotic tissue, thus leading to erosion of the septum and formation of a
VSD.
• In contrast, septal ruptures that occur only 1 to 2 days following an AMI are usually the result of an infarct-
associated intramural hematoma that dissects within the septal wall and then ruptures

7. Anterior VSR vs Posterior VSR?

8. Septal rupture locations:
• Septal ruptures tend to occur in 1 of 2 places, either anterior, which is associated with occlusion of the left
anterior descending (LAD) coronary artery, or inferoposterior, which is associated with occlusion of the right
coronary artery or much less frequently with the circumflex artery.
• Ruptures that occur posteriorly tend to be more complex, with septal defects occurring through serpiginous
tracts, wherein the septal entry point in the left ventricle is not directly across from the corresponding defect
in the right ventricular septal wall.
• This is in contrast to anterior septal infarctions, which tend to be apical and simple, that is, a discrete defect
with a direct communication through the septum.

9. Studies show…
“ The location of the rupture is significant because multiple studies have
demonstrated a significantly increased mortality with ruptures in the posterior
portion of the septum. This increased mortality appears to be associated with right
ventricular infarction and subsequent right heart failure”

10. • A left-to-right shunt is created
with a VSR, which rapidly
produce right ventricular
volume overload and failure.
• This, in turn, leads to increased
blood flow through the
pulmonary circulation, with
subsequent secondary volume
overload of the left heart.
• As the left heart begins to fail,
systemic vascular resistance
increases to maintain afterload,
which then increases the
magnitude of the left-to-right
shunt until the left heart fails to
the point that it cannot maintain
systolic pressure, and left-to-
right shunting declines.

11. Risk Factors to developing VSR
• Female gender
• Advanced age
• Chronic kidney disease
• Congestive heart failure
• Presentation in cardiogenic shock
• Incomplete coronary revascularization and absence of prior myocardial infarction (MI),
• lack of collateralization of coronary blood flow

12. Based on observational studies:
• Diabetes
• Hypertension
• Tobacco use
“Although these findings could be attributed solely to observational bias, another
theory is that these patients have a history of coronary atherosclerotic disease
from these various comorbidities, thus making them more likely to develop
coronary collateralization”

13. Diagnosis
• Most patients who sustain a VSR present in profound cardiogenic shock, with common presenting symptoms
including chest pain, shortness of breath, and signs of low cardiac output.
• Findings on physical exam can include an S3 gallop, palpable parasternal thrill, and a harsh holosystolic
murmur centered at the lower left sternal border with radiation throughout the precordium
• As congestive heart failure ensues, however, flow across the septal defect will be reduced, leading to a
quieter murmur and absence of a palpable parasternal thrill.

14. • CAG to confirm CAD and specify culpurit vessels
• Definitive diagnosis of a VSD is easily made with transthoracic echocardiography
(TTE).
• Color Doppler imaging will demonstrate flow across the septum and a drop-out
of signal in 2-dimensional imaging of the septum in a 4-chamber view
• The left ventricle may be hyperdynamic, provided it does not already have
significant areas of infarcted tissue.

16. Medical Management:
• Goal: hemodynamic stabilization and medical optimization to limit the development of cardiogenic shock.
• Mechanical circulatory support, especially placement of an intraaortic balloon pump (IABP) for afterload
reduction, can be rapidly implemented to aid left ventricular function.
• Pharmacologic afterload reduction is also essential to reduce the extent of left-to-right shunting.
• Diuretics and inotropic support are necessary to temporize left ventricular volume overload and decreased
contractility; yet, increasing contractility can increase left-to-right shunting, therefore propagating the
hemodynamic derangement

17. Surgical Repair
• surgical repair of postinfarction VSD remains an essential means of limiting mortality in these patients. As
previously mentioned, rushing these patients to the operating room after discovery of the VSR is associated
with higher operative mortality.
• Stabilization of patients’ hemodynamics and limiting the extent of cardiogenic shock is associated with
improved outcomes following surgical repair of the ruptured septum, and most studies support waiting
before proceeding to the operating room.
“ the septal tissue surrounding the defect tends to become increasingly fibrotic as the
inflammatory response progresses and unable to hold sutures”

18. Methods of VSR repair:
A. Daggett technique
 repair essentially via infarctectomy and closure.
 A wide excision of the infarcted myocardium, and
closure of the septal defect with or without a prosthetic
patch and with pledgets and/or Teflon felt strips to
prevent suture tearing through the myocardium.
 +/- apical amputation if limited to the apex.
 Other variations on this technique include a single-
patch technique, in which the septal defect and the
ventriculotomy are closed with a single prosthetic
patch, or a multiple-patch technique for more extensive
defects.

19. B. David technique
 The predominant method of repair
 exclusion of the infarcted myocardium.
 bovine pericardium is used to make a
wide patch to cover the entire infarcted
area.
 The patch is sutured to healthy
endocardium, and the VSD and infarcted
myocardium are excluded from the left
ventricle

20. • Short- and long-term complications are indicated for each repair technique, most commonly residual
shunting, uncontrolled hemorrhage, and low cardiac output syndrome.
• Despite the Daggett procedure being less technically demanding and having a shorter cross-clamp time with
a smaller patch and shorter suture line; however, the David technique has demonstrated superior short- and
long-term survival.
• Retrospective comparison of the techniques demonstrated five-year survival of 67% with the David
technique and 48% with the Daggett technique.

21. • Left ventricular approaches are preferred to right ventricular approaches, as the trabeculations within the
right ventricle make visualization and accurate repairs of the defect more challenging.

22. Role of CABG in VSR?
• Contraversal, some studies have demonstrated no benefit to either short- or long-term outcomes with the
addition of revascularization to VSR repair.
• All of these studies, however, are only observational studies, and a randomized controlled trial is needed to
adequately address this question and the impact of CABG on survival in patients after VSR.

23. Percutaneous closure of the VSD
• Series of percutaneous VSR closure demonstrated successful reduction of shunting; yet, not all patients are
adequate candidates for primary percutaneous device closure of VSD because of specific anatomic features.
 A defect < 15 mm at its largest diameter
 not eccentrically located within the septum,
 Has enough surrounding tissue against which the device can be deployed and remain seated.
 Distal to the TV and its septal leaflet
• Furthermore, myocardial necrosis and contraction occurs after the rupture, and this remodeling can
continue after placement of the device, eventually leading to leakage around the device and possibly even
device embolization.
With this multitude of complicating factors, outcomes with Amplatzer devices have remained poor.

24. • Although mortality from VSR following an AMI remains high, it has decreased considerably over the past few
decades.
• While clear, singular guidelines for optimal surgical management of these patients do not exist, initial
resuscitative efforts should be focused on reducing afterload, including placement of an IABP, and
decreasing left-to-right shunting across the VSD, as this hemodynamic stabilization can improve outcomes
following surgical repair of the VSR

25. https://mmcts.org/tutorial/1702

26. Left Ventricular Free Wall Rupture
• A rare mechanical complication of AMI, LVFWR does not always present with catastrophic hemodynamic
decompensation as its name would imply.
• Although a dramatic presentation and precipitous course usually accompanies patients who sustain LVFWR,
some patients present with subacute rupture or even chronic rupture sealed with a left ventricular
pseudoaneurysm.
• Despite being relatively rare, with its incidence ranging from 6% to 12%,[53],[54] LVFWR is the second most
common cause of in-hospital mortality following an AMI and has been estimated to occur 5 to 10 times
more often than other mechanical complications of AMI.

27. Pathophysiology
• LVFWR usually occurs in the anterior wall of the left ventricle, with associated acute obstruction of the LAD
coronary artery.
• There also tend to be endocardial tears near the insertion sites of the papillary muscles, believed to be due
to the arrangement of myocardial muscle fibers and wall stress.
• Left ventricular pseudoanuerysms constitute another pathophysiologic subset of LVFWRs. These patients
tend to present following inferior and posterior MIs, as blood tends to accumulate in these areas; thus,
ruptures in these territories are more likely to coalesce into a pseudoaneurysm, with the pericardium
forming the wall of the pseudoaneurysm.[57] Weakening of the myocardium following infarction is likely
promoted through matrix metalloproteinases, and it is this thinned myocardium that forms the
pseudoaneurysm neck

28. Risk Factors
Patient characteristics known to increase the likelihood of free wall rupture include:
1. female gender
2. hypertension without left ventricular hypertrophy,
3. lack of a prior MI or anginal symptoms,
4. advanced age (greater than 60 years),
5. use of steroids or nonsteroidal anti-inflammatory drugs during the acute phase of myocardial remodeling
(days 1-7) after an MI
6. A longer time to reperfusion following an MI

29. Diagnosis
• Most patients with an anterior free wall rupture present in acute cardiogenic shock, with complete
hemodynamic decompensation and cardiac tamponade rapidly leading to electromechanical dissociation
and death; in fact, the diagnosis is rarely established before death. Individual clinical courses, however,
depend on the rate of hemorrhage from the ventricle and pericardial compliance
• Electrocardiographic (ECG) findings are consistent with a transmural infarction of the myocardium, and
ostensibly, patients with persistent ECG changes and arterial hypertension in the days following the MI are
more likely to experience free wall rupture.[60] Rupture is also typically accompanied by chest pain similar
to that of an MI, and ECG changes, including re-elevation of the ST segment or negative T waves becoming
positive, can also occur. Although the significance of this chest pain and the ECG changes are unclear, they
are believed to reflect extension of the infarct or even rupture of the necrotic myocardial wall.

30. • Free wall ruptures typically occur within 2 time frames: early rupture occurs within 48 hours of an AMI, and
late rupture occurs more than 48 hours after an AMI.[61] Although there are believed to be a similar
incidence of each presentation, the number of patients with early LVFWR is likely underestimated because of
the number of patients who die from LVFWR before they reach the hospital.

31. • Patients who sustain LVFWR early after an AMI have little to no thinning of the myocardium and appear to
experience the complication with sustained arterial hypertension, whereas those with late rupture typically
have thinned infarcted tissue that is more susceptible to rupture.[60],[61] Patients with late rupture are also
more likely to present following unduly strenuous physical activities or actions such as persistent vomiting or
coughing.

32. • Patients with acute free wall rupture typically present in a dramatic and easily identified fashion, with
hemodynamic decompensation and electromechanical dissociation secondary to acute cardiac tamponade.
Patients can also present in a subacute fashion, a description reserved for those patients who present with
signs of moderate to severe tamponade, some degree of hypotension, and a rhythm disturbance, usually
sinus bradycardia or a junctional rhythm.[61] Classic signs of cardiac tamponade, including pulsus paradoxus
and jugular venous distention, are usually absent.[49],[52] Although LVFWR is the most common cause of
hemopericardium after an AMI, definitive diagnosis can only be obtained with a thoracotomy or sternotomy,
though a rupture may be demonstrated on echocardiography or with blood leaking into the pericardium on
angiography.[61] In the setting of an AMI with clinical signs, symptoms, and echocardiographic evidence of
cardiac tamponade, the patient should be considered to have sustained a LVFWR until proven otherwise.

33. Medical Management
• Once LVFWR is suspected, initial therapeutic stabilization should include rapid fluid administration, inotropic
support, and possible pericardiocentesis. Although IABP support is widely utilized for patients with VSR
following an AMI, the role of IABP for treating LVFWR is less well defined; most, however, believe that
placement of an IABP can significantly reduce afterload and wall tension until the patient reaches the
operating room.[15],[64] There are some isolated reports of patients surviving LVFWR without surgical
intervention; however, the natural history of the pathology is not favorable

34. Surgical Repair
• Because almost all literature regarding LVFWR consists of case reports and small observational studies, there
are no evidence-based or even well-established methods of surgical repair of this devastating complication.
These patients generally present in cardiogenic shock; thus, emergency surgery is the most viable option for
improving survival in this otherwise moribund population.
• There are essentially 3 methods of repair of LVFWR that have emerged over the past several decades.
• The oldest and least successful method of repair involved placement of Teflon-reinforced sutures for direct
closure of the pericardium. This method, however, is not recommended because sutures are placed in
necrotic myocardium, thus predisposing to a secondary tear.
• A second method of repair involves initial infarctectomy with direct closure of the defect, a technique that
is useful when there is an associated VSR to be repaired.

35. • The most successful method of repair involves epicardial patch repair of the defect with the patch securing
using epicardial sutures and/or bioprosthetic glue
• In this method, the heart is accessed through a standard median sternotomy and pericardiotomy.
• Epicardial patches with or without fibrin glue or several layers of fibrin glue sheets are applied to the area of
infarction over the ruptured myocardium.
• The patch is then manually compressed for several minutes until hemostasis is achieved.
• If sutures are used, they are placed into healthy, nonischemic myocardium around the edges of the patch.

36. • More modern series report more successful outcomes with placement and securing of the patch with only a
bioprosthetic glue.[32],[71],[72],[73],[74] This method has the advantage of avoiding cardiopulmonary
bypass in patients who exhibit relative hemodynamic stability.[50],[75] Patch materials have also evolved
over time from polytetrafluoroethylene (PTFE) and pericardium to TachoComb (CSL Behring, Tokyo, Japan)
and TachoSil (Baxter Healthcare, Deerfield, IL, USA),[73],[76] materials that do not require epicardial sutures.
•
• With any of these repair methods, it is important to have the aorta cross-clamped, and cardioplegia given
before lifting of the heart, as the left ventricular wall is fragile and prone to further deterioration.

37. • Thirty-day mortality with surgical repair of LVFWR remains relatively high, with modern series reporting
mortality as high as 24% to 36%[68],[71] This is in contrast, though, to the abysmal outcomes in patients
with diagnosed LVFWR who receive medical management.[57] Multiple organ failure is the most common
cause of death in patients who die shortly after LVFWR.
•

38. • Pseudoaneurysms are also a known complication following patch repair of a LVFWR, and that pathology
should be expected in any postinfarction patient presenting with new onset heart failure.[77],[78] Because
there is a high risk of rupture with these pseudoaneurysms, these patients should undergo expeditious
surgical repair; however, operative repair carries its own elevated risk because of these patients’ underlying
ischemic cardiomyopathy.[77] Although repairs can vary, depending on the exact location, size, and extent of
the pseudoaneurysm, most are repaired through a median sternotomy and with a patch using epicardial
sutures placed through peripheral healthy myocardium and then through PTFE felt strips. The wall of the
pseudoaneurysm is generally left intact to lay over the patch and provide additional reinforcement of the
patch.[77]

39. • LVFWR is one of the most feared mechanical complications of an AMI, largely because most patients with
this complication present in decompensated cardiogenic shock and cardiac tamponade leading to
electromechanical dissociation and arrest before they even reach the hospital. Those who do receive timely
medical intervention should receive expeditious fluid resuscitation and inotropic support with afterload
reduction, usually with an IABP. These patients should also undergo the least complex surgical intervention
possible, preferably without the assistance of cardiopulmonary bypass, to reduce morbidity and mortality of
the pathology and concomitant surgical intervention.

40. Papillary Muscle Rupture
• Another rare, but very often catastrophic complication of an AMI, PMR is implicated in approximately 5% of
early deaths following an MI.[79] Although there is a spectrum of pathologic severity, PMR commonly results
in acute mitral regurgitation, pulmonary edema, and decompensated cardiogenic shock. Left untreated,
survival is less than 20% at 1 week following AMI.

41. Pathophysiology
• The anterolateral and posteromedial papillary muscles are an integral part of the mitral valve apparatus.
These heads of muscle within the left ventricle contract and relax with the left ventricle to move the
anterolateral and posteromedial leaflets of the mitral valve via the attached chordae tendinae. Through their
coordinated action, the papillary muscles’ action on the mitral valve leaflets control blood flow through the
left side of the heart.
•
• Because of their relative distance from the epicardial coronary arteries and because they receive most of
their blood from small penetrating arteries rather than large, dedicated coronary branches, the papillary
muscles are at increased risk of ischemia.[81] The posteromedial papillary muscle is estimated to rupture
following an AMI 6 to 12 times more frequently than the anterior papillary muscle because the blood supply
of the posterior papillary muscle is derived only from the posterior descending artery, whereas the
anterolateral papillary muscle is supplied by both the left circumflex and LAD arteries

42. • Rupture of the muscle may be partial or complete, and it may occur at the muscle head supporting a few
chordae tendinae or within the muscle trunk and affect many chordae tendinae attached to both valve
leaflets.[82] Most patients who sustain a PMR after AMI have not had a prior MI, and the infarcted tissue
usually does not significantly affect the mitral valve annulus. PMR usually occurs after inferoposterior or
posterolateral transmural or subendocardial MIs, and it is thought that PMR occurs because of increased
shear forces on the papillary muscles when the infarct size is small and systolic function is relatively
preserved.[81]
•
• Acute mitral regurgitation (MR) complicates 1% to 3% of all AMIs, but only a small fraction of those patients
has AMR from a ruptured papillary muscle.[83] Small changes in the geometry of the LV caused by regional
wall motion abnormalities can lead to impaired leaflet coaptation, changes in the annular geometry, or
impaired papillary muscle motion, all of which lead to MR without a ruptured papillary muscle.

43. Diagnosis
• PMR most commonly occurs 4 to 7 days following an AMI, and patients usually present in cardiogenic shock
with acute pulmonary edema. A systolic murmur, usually without a thrill, is variably present. An absent
murmur may indicate pressure equalization between the left atrium and left ventricle, thus a functionally
absent mitral valve; therefore, the absence of a murmur does not rule out PMR.[81] ECG changes are usually
consistent with an inferior or posterior MI, but ischemic changes may be absent with small infarcts that
could still cause PMR.[81]
•
• Two-dimensional echocardiography is the gold standard for diagnosing PMR, and Doppler with color flow
imaging is useful for assessing the severity of MR. Indications of PMR on echo include an abnormal
demarcation of the papillary muscle, a mobile mass attached to the chordae tendinae, mitral leaflet
prolapse, or flail mitral leaflet.[84],[85],[86] Difficulties such as patient body habitus or a lack of adequate
echocardiographic windows from inferences such as mechanical ventilation can make TTE less than optimal
for diagnosing PMR; transesophageal echocardiography (TEE), however, allows much better visualization of
the mitral valve to diagnose PMR.[81], Reported sensitivity for diagnosing PMR with TTE is 45%, whereas the
sensitivity of TEE for diagnosing is reported to be greater than 92%

44. Medical Management
• Once PMR is diagnosed with echocardiography, the patient’s hemodynamics should be supported with
vasodilators and the insertion of an IABP. These methods of afterload reduction help to reduce the
regurgitant volume and the amount of fluid backing up into the lungs. Ideally, these interventions should
help to stabilize the patient in order to undergo cardiac catheterization before surgical intervention.[81] A
cardiac catheterization is indicated before taking the patient to the operating room to correct the PMR
because patients who do not undergo concomitant CABG with their mitral valve intervention have higher
mortality

45. Surgical Repair
• Much like VSR and LVFWR, there are no evidence-based guidelines to direct surgeons on the absolute best
methods of repairing these catastrophic pathologies.[89] Historically, most patients with PMR underwent
emergent mitral valve replacement. Replacement of the valve is usually pursued if there is evidence of
papillary muscle necrosis or suspicion of ongoing myocardial ischemia.[90],[91] The subvalvular apparatus
should be left intact,[92] and the valve is replaced in standard fashion. One rare but documented
complication of mitral valve replacement in the setting of PMR is subsequent LVFWR.

46. • Mitral valve repair is possible in limited circumstances following PMR, usually when a
single papillary muscle head is infarcted and the myocardium is not
necrosed.[94],[95],[96],[97] Then, the head of the papillary muscle can be sutured in
place with pledgeted sutures. Repair may also necessarily include chordal transfer or
chordal replacement to correct for flail leaflets.[95],[97] Although mitral valve repair for
PMR has been successful, there is not enough evidence to definitively recommend mitral
valve repair over replacement for patients with PMR.[98] There is, however, a relatively
high rate of PMR recurrence following repair, and replacement of the mitral valve is
generally preferred following primary papillary muscle rupture.
•
• Myocardial revascularization has variably affected perioperative mortality for
PMR[83],[99],[100]; however, there is definitive evidence that myocardial
revascularization improves long-term outcomes when performed with mitral valve
surgery[88],[101]; thus, current recommendations advise performing CABG when
operating for PMR.[91],[98]
•

47. • Modern series report a perioperative mortality of 21% to 39% for patients presenting after PMR and
undergoing emergent surgery.[91],[99],[102],[103], Complete PMR, preoperative renal failure, or
preoperative IABP use or ECMO have been shown to be independent predictors of in-hospital
mortality,[99],[104] whereas preoperative inotropic support and mitral valve replacement without
preservation of the subvalvular apparatus were independent predictors of lower overall long-term
survival.[92]
•
• Patients who develop acute muscle rupture (MR) but have preserved LV systolic function following their first
MI, especially inferior or posterior, should be suspected to have PMR. Although patients can present with
acute MR following an MI without sustaining a PMR, this complication represents the most serious cause of
MR after an AMI. Stabilizing patients’ hemodynamics and minimizing the development of pulmonary edema
with afterload reduction are the first steps in treating patients with acute PMR. Despite having a high
mortality, emergent surgical intervention with a mitral valve replacement, possibly including a mitral valve
repair, and myocardial revascularization is the best option for treating PMR.

48. Conclusion
• Any of these mechanical complications following an AMI represent a cardiac surgical emergency,
necessitating rapid diagnosis and intervention to limit further hemodynamic deterioration. Without any
reliable or effective medical interventions, emergent surgical repair is the mainstay of treatment for these
critically ill patients.
•