European Heart Journal (2014) 35, 2060–2068 REVIEW

doi:10.1093/eurheartj/ehu248

Clinical update

Ventricular septal rupture complicating acute

myocardial infarction: a contemporary review

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Brandon M. Jones 1, Samir R. Kapadia 1, Nicholas G. Smedira2, Michael Robich 2,
E. Murat Tuzcu 1, Venu Menon 1, and Amar Krishnaswamy 1*
1
Department of Cardiovascular Medicine, Cleveland Clinic Foundation, 9500 Euclid Ave, Desk J2-3, Cleveland, OH 44195, USA; and
2
Cardiothoracic Surgery, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195, USA

Received 16 March 2014; revised 17 May 2014; accepted 26 May 2014; online publish-ahead-of-print 26 June 2014

Ventricular septal rupture (VSR) after acute myocardial infarction is increasingly rare in the percutaneous coronary intervention era but mortality
remains high. Prompt diagnosis is key and definitive surgery, though challenging and associated with high mortality, remains the treatment of
choice. Alternatively, delaying surgery in stable patients may provide better results. Prolonged medical management is usually futile, but includes
afterload reduction and intra-aortic balloon pump placement. Using full mechanical support to delay surgery is an attractive option, but data on
success is limited to case reports. Finally, percutaneous VSR closure may be used as a temporizing measure to reduce shunt, or for patients in the
sub-acute to chronic period whose comorbidities preclude surgical repair.
-----------------------------------------------------------------------------------------------------------------------------------------------------------
Keywords VSR † Ventricular septal rupture † Acute myocardial infarction † Percutaneous closure

increasingly rare, complicating between 0.17 and 0.31% of patients

Introduction
Ventricular septal rupture (VSR) is a rare but lethal complication of
acute myocardial infarction (AMI). As acute reperfusion strategies
for AMI have evolved, VSR has become increasingly rare and is iden-
tified earlier in the post-MI course. Despite significant improvements
over the last two decades in overall mortality for patients with AMI,
the outcome of patients who develop VSR remains poor. In this
paper, we will review the incidence and pathophysiology of VSR in
the current era of aggressive reperfusion with dual antiplatelet
therapy and primary percutaneous coronary intervention (PCI),
and provide a current perspective on the surgical and percutaneous
management of VSR.
Epidemiology
The advent of emergent reperfusion strategies for AMI, including
thrombolysis and PCI, has led to a decline in the incidence of VSR
in contemporary series. Restoration of flow in the infarct related
artery leading to myocardial salvage and reduced incidence of trans-
mural infarct may account for this observation. In the pre-
thrombolytic era, VSR was thought to complicate 1– 2% of AMI
presentations.1 More contemporary series, however, show it to be
presenting with AMI (Table 1).2 – 5
It is logical to think that mechanical complications would be less fre-
quent in patients treated with primary PCI when compared with
thrombolysis or medical therapy alone. In contrast to thrombolysis,
optimal PCI results in increased TIMI 3 flow, increased salvage index,
and less haemorrhagic transformation of the infarct zone.6 In the
Global Registry of Acute Coronary Events (GRACE) registry, patients
presenting with ST-elevation MI (STEMI) were evaluated for heart
rupture (VSR or free-wall rupture) based on reperfusion strategy.
Although neither thrombolytic use nor PCI were independent predic-
tors of heart rupture, there was an overall trend favouring patients
treated with PCI (0.7% incidence of heart rupture) vs. those treated
with thrombolytics (1.1%) vs. neither lytic or PCI (1.2%).4 There was
also a significant linear relationship between shorter time to thromb-
olysis infusion and lower incidence of heart rupture (P ¼ 0.02).4 Finally,
it has been shown that the incidence of VSR is lower in patients who
undergo primary PCI compared with those who undergo delayed or
elective PCI after recent AMI.7 Thus, strategies aimed at reducing
door-to-balloon time for STEMI, including pre-hospital electrocardio-
gram and bypass of the emergency department, may contribute to the
observed reduction in heart rupture.8 Unfortunately though, despite a
declining incidence, current mortality among patients with VSR

* Corresponding author. Tel: +1 216 636 2824, Fax: +1 216 445 6153, Email: krishna2@ccf.org
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2014. For permissions please email: journals.permissions@oup.com.
VSR complicating AMI 2061

Table 1 Ventricular septal rupture incidence, time to identification, and resultant mortality in four contemporary clinical
series compared with historical data

Source MI treatment Incidence of VSR, % (n) Time to VSR Mortality, %

(overall cohort) identification
...............................................................................................................................................................................
Historical data Pre-thrombolysis 1 –2 3 –5 days With surgery: 45
Without: 90
MIDAS2 PCI (19%) 0.25– 0.31 (408) Not reported In-hospital:
1990–2007 1990– 92: 41
n ¼ 148 881 patients 2005– 07: 44
with STEMI 1-year:

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1990– 92: 60
2005– 07: 56
GUSTO-13 Thrombolysis (100%) 0.20 (84) 1 day 30-day:
1990–1993 (range 0– 47) with VSR: 73.8
n ¼ 41 021 patients (94% ≤ 1 week) without VSR: 6.8
with STEMI
GRACE4 Primary PCI (15% overall; 0.25 (155) Not reported In-hospital:
2000–2007 38% for STEMI) 41
n ¼ 60 198 patients with ‘ACS’ Lysis (12% overall; 28% for STEMI)
APEX-AMI5 Primary PCI (94%) 0.17 (10) 7.7 h (range 5.5– 23.5) 30-day:
2004–2006 80
n ¼ 5745 patients with STEMI

VSR, ventricular septal rupture; MI, myocardial infarction; PCI, percutaneous coronary intervention.

remains high (41–80% in current series), and appears mostly
unchanged over the last few decades (Table 1).2,3,5
There has been a steady trend toward earlier identification of VSR
after AMI in contemporary trials. While traditionally thought to
occur between days 3–5 after AMI, initial observations from the
SHOCK Registry challenged this paradigm, and the median duration
of VSR presentation among 55 patients was estimated at 16 h.9 These
observations were confirmed in other large clinical series (Table 1).3,5
While these observations may be explained by heightened awareness
of VSR and almost universal access to echocardiography, it could be
postulated that reperfusion injury combined with fibrinolysis has
caused a shift in the underlying pathophysiology, and partially
accounts for this finding.
There are several independent risk factors for VSR in patients pre-
senting with AMI. These include older age, female sex, prior stroke,
chronic kidney disease, and CHF.2,4,9 Patients who develop VSR are
more likely to present with ST segment elevation, initial positive
cardiac biomarkers, cardiogenic shock, cardiac arrest, higher Killip
class, and longer times to first balloon inflation or thrombolytic ad-
ministration.5,7 Interestingly, patients who develop VSR are less
likely to have a history of hypertension, diabetes, prior smoking, or
prior MI. It is possible that these patients have pre-existing coronary
artery disease, leading to the development of protective collateral
circulation, but it is equally possible that these patients develop
cardiogenic shock or fatal rupture, leading to observational bias.
Pathophysiology
Rupture develops after full-thickness (transmural) infarction of the
ventricular septum and can occur at any anatomic location.
Infarctions involving the left-anterior-descending, dominant right-
coronary, or dominant left-circumflex arteries can all involve septal
branches. Ventricular septal rupture seems to occur with similar fre-
quency in anterior and inferior/lateral infarctions.2 Anterior infarc-
tions are more likely to cause apical defects and inferior or lateral
infarctions are more likely to cause basal defects at the junction of
the septum and the posterior wall. Regardless of location, the
newly formed communication results in left to right shunting of oxy-
genated blood from the high-pressure left ventricle (LV) to the
lower-pressure right ventricle (RV). Clinical presentation varies
from complete haemodynamic stability to frank circulatory coll-
apse depending on the size of the defect, presence of RV infarc-
tion, ongoing RV ischaemia, or stunning of the RV from volume
overload. Unpredictable haemodynamic deterioration is the norm
in most patients in the days and weeks following VSR, and reports
of long-term survival independent of corrective surgery are
extremely rare.
The conventional mechanism of septal rupture involves coagula-
tion necrosis of ischaemic tissue with neutrophilic infiltration, even-
tually causing thinning and weakening of the septal myocardium.1
This sub-acute process requires 3–5 days, likely accounting for the
traditional timing reported in the early surgical literature. Rupture oc-
curring within 24-h of presentation is more likely due to dissection of
an intramural haematoma or haemorrhage into ischaemic myocar-
dium. This classically occurs due to physical shear stressors at the
border of an infarct zone, combined with a hypercontractile,
remote myocardial segment. Clinically, it is most commonly seen in
the setting of an inferior infarction with the VSR noted in the basal
inferior septum, abutting the hyperdynamic mid-septum that is
perfused by the LAD. Ventricular septal rupture can also present in
2062 B.M. Jones et al.

concert with other mechanical complications such as ventricular Diagnosis

aneurysm, free wall rupture, or papillary muscle rupture.
Becker and Mantgem10 classified the pathological features of cardiac
free wall rupture (similar in pathophysiology and therefore applicable
to VSR) into three types. Type I rupture shows an abrupt, slit-like tear,
and is associated with acute infarcts ,24 h in age. Type II rupture
demonstrates erosion of the infarcted myocardium, and correlates
clinically with a sub-acute presentation. Type III rupture exhibits con-
comitant aneurysm formation with significant thinning of the septum
and subsequent rupture, a process associated with older infarcts.
Septal ruptures are further classified as simple or complex.1 Simple
It is critical that all patients with AMI have a brief evaluation for mech-
anical complications prior to primary PCI. All patients who develop
haemodynamic compromise during AMI should be rapidly examined
for the characteristic, harsh, systolic murmur over the precordium, as
well as a palpable thrill, both of which may be difficult to detect in
patients with a low output state. Other physical exam findings
result from augmented right-sided flow, and may include a loud pul-
monic component of the second heart sound, left or right S3 gallop,
or tricuspid regurgitation.

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ruptures have a direct connection between the left and right ventricles, Left ventriculography performed in the left-anterior oblique
occurring at the same level in both chambers, while complex ruptures (LAO) projection in a patient with VSR may demonstrate shunting
take a serpigenous course and are more likely to be caused by haem- of contrast from the LV to the RV. If a PA catheter is placed, the diag-
orrhage and irregular tears within the necrotic septum (Figure 1). nosis should be suspected in patients who have acutely rising mixed

Figure 1 Transthoracic echocardiography demonstrating a simple ventricular septal rupture (arrow) in a patient with mid-left-anterior descend-
ing coronary artery infarction in 2D (A) and with colour Doppler (B). Complex ventricular septal rupture in a patient with proximal right coronary
artery infarction in 2D (C) and with colour Doppler (D) showing the ‘serpigenous’ ventricular septal rupture entering the basal left ventricle (arrow)
and exiting at multiple points in the apical RV (arrowheads). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
VSR complicating AMI
venous O2 saturations, which could be reflective of a left-to-right
shunt.
Usually, the diagnosis is made by a prompt transthoracic echocar-
diogram identifying drop-out of the ventricular septum in the 2D
image and demonstration of flow across the septum using colour
Doppler (Figure 1). Evidence of right-ventricular dilation and pulmon-
ary hypertension are also important clues to the diagnosis. The
remaining portions of the left ventricle are often hyperdynamic
unless there is a large territory of infarction, or previous ischaemic
insults have led to compromised function. Colour Doppler evalu-
ation can also be useful to assess the anatomical size of the defect.
When the patient has poor acoustic windows due to mechanical ven-
tilation or body habitus, a TEE should be considered.
When a diagnosis of VSR is made prior to primary PCI, strategies
for prompt restoration of coronary flow must be approached with
consideration towards the competing need for emergent surgery
and the associated risks of surgical bleeding after the administration of
dual-antiplatelet therapy. It remains key to limit the ischaemic burden
in the infarct-related artery, especially if there is right-ventricular in-
volvement, so immediate collaboration between the interventional
cardiologist and cardiac surgeon is critical to develop a case-specific
approach. Ideally, VSR would be diagnosed prior to PCI. Flow may be
restored in the infarct related artery with aspiration thrombectomy
and/or balloon angioplasty, with preparations made for immediate
VSR repair with coronary artery bypass grafting. If surgery is
delayed, consideration should be given to bare-metal stent place-
ment to minimize dual-antiplatelet therapy duration.
Surgical management
Operative management of patients can be complex, and having a sys-
tematic approach is helpful. For an anterior VSR, it is important to
assess the severity of LV dysfunction, presence of coexisting CAD,
suitability of potential revascularization targets, and anatomy of pre-
vious infarctions. For a posterior VSR, an additional understanding of
RV function and the presence of mitral regurgitation is important.
Most patients with acute post-MI VSR are in cardiogenic shock, and
once in the operating room cardiopulmonary bypass with bicaval
cannulation should be initiated expeditiously. Many surgeons prefer
a left ventriculotomy through the infarct (generally 1 cm lateral to
the LAD) to access the VSR as it allows the most direct view of the
defect, and infarctectomy or aneurysmectomy can be more easily
performed if needed.11 There are two common techniques used
for repair of VSR, the Daggett and David procedures (Figure 2). The
Daggett is a single or double patch technique which closes the VSR
by placing a patch over the defect and sewing to the RV and LV.12
In contrast, the David technique is an infarct exclusion procedure
with all sutures placed in the LV.13
In the acute setting, infarcted myocardium is weak and friable, and
holds sutures poorly leading to increased risk of tearing and recurrent
septal defects. Principles of successful repair include debridement of
infarcted tissue back to healthy myocardium (even if it involves enlar-
ging the defect), and avoiding tension on the repair by using an appro-
priately sized patch.14 Large, 1 cm bites of tissue and buttressing of
suture lines with pericardium or felt can improve the strength of
the repair. This is especially important when the infarct is ,24 h
old as it may be difficult to differentiate viable and infarcted
2063
myocardium visually. In a large VSR there may not be enough anterior
septum to allow adequate suturing of the patch. In this case, horizon-
tal mattress sutures can be placed through the right ventricular wall.
Posterior VSRs pose additional technical challenges, as the heart
must be elevated for adequate exposure. Additionally, the PDA
and posteromedial papillary muscle are in close proximity. The tran-
sinfarct ventriculotomy is made 1 cm lateral to the PDA and care is
taken to preserve the mitral subvalvular apparatus. In both anterior
and posterior VSRs, the ventriculotomy is closed primarily or with
a patch (usually Dacron) carefully to avoid post-operative free wall
rupture. If surgical revascularization is planned, the grafts are placed
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prior to addressing the VSR to allow for more complete myocardial
protection and to minimize handling the heart after the defect is
repaired.15 The use of saphenous vein as conduit for all grafts is
common.
Outcomes of surgical ventricular
septal rupture repair
Medical management of VSR is usually futile with rare exception
(Figure 3). Definitive surgery remains the treatment of choice, but
remains a challenging operation associated with high early mortality.
A recently published review of the Society of Thoracic Surgeons
National Database (STS Database) identified 2876 individuals aged
≥18 years who underwent post-MI VSR repair between 1999 and
2010.16 Overall operative mortality was 42.9%, which represented
the highest mortality rate of any cardiac surgery. Patients who did
not survive to 30 days tended to be older, female, had higher
serum creatinine levels, and higher acuity of disease (cardiogenic
shock, reduced LVEF, triple-vessel CAD, or requirement for pre-
operative IABP). Operative mortality was much lower for proce-
dures considered elective (13.2% mortality) vs. emergent (56.0%
mortality) vs. salvage (80.5% mortality).
A smaller study of 68 consecutive patients, 85% of which under-
went surgery ,48 h after VSR diagnosis, investigated determinants
of post-surgical outcomes.17 In this group, residual interventricular
communication was present in 22 of 63 patients (35%) who survived
the initial surgery, and was an independent predictor of post-
operative CHF. It was due to patch dehiscence in all 11 patients
who underwent repeat surgery due to haemodynamic instability
(percutaneous closure for residual VSR is discussed subsequently).
Timing of surgery
Mortality of patients in the STS database varied significantly depend-
ing on timing of surgery. Patients who underwent surgery within 7
days of presentation had a 54.1% mortality compared with 18.4%
mortality if repair was delayed until after 7 days. Mortality was
highest (.60%) in patients who underwent operation in the first
24 h, consistent with other investigators.18
The improved outcome with delayed surgery may be related to
evolution of the infarct and improved stability of the cardiac tissue
allowing a more effective repair, but is also a representation of sur-
vival bias, as early surgery is usually performed on individuals with
marked haemodynamic instability and circulatory compromise.
Ultimately, only 886 of the 2876 patients (30.8%) in the STS database
2064 B.M. Jones et al.

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Figure 2 Daggett vs. David repair of an anterior VSR. The Daggett is a patch technique which closes the VSR by placing a patch directly over the
defect and sewing to the RV and LV (A – C). In contrast, the David technique is an infarct exclusion procedure with all sutures placed in the LV, laying a
patch over the VSR to cover the defect (D). The suture line (used to close the ventriculotomy) is buttressed to prevent the stiches from pulling
through the infarcted left-ventricular tissue (E). A, aorta; LAD, left-anterior descending coronary artery; PA, pulmonary artery; LV, left ventricle;
RV, right ventricle. (Reprinted with permission from Madsen and Daggett.37)

had surgery more than 7 days after presentation, suggesting that a mi-
nority of patients survive until elective repair. Also, the number of
patients turned down for surgery is unreported. Similarly, the
GUSTO-I trial demonstrated a 47% mortality at 30-days among 34
patients who underwent prompt surgical repair (median time 3.5
days, 95% CI, 1 –7) vs. 94% mortality for the 35 patients treated
without surgery (although again, selection bias must be considered).3
Taken together, the evidence demonstrates that although surgical
mortality remains very high, non-surgical mortality is certainly
higher. Thus, the clinician must weigh the known risk of expedient
surgery against the unknown risk of postponing surgery and develop-
ing further clinical deterioration. A simplified version of our own
multidisciplinary strategy for managing these patients is included,
with the caveat that each case requires a tailored approach (Figure 4).
Medical management and
mechanical support
The cornerstone of medical management of VSR is afterload reduc-
tion to increase effective LV stroke volume by reducing left-to-right
shunting. Intravenous afterload-reducing pharmacotherapy such as
sodium nitroprusside has the advantage of being rapidly titrated or
emergently discontinued compared with oral agents. Intra-aortic
balloon counterpulsation (IABP) provides mechanical afterload re-
duction and augmentation of cardiac output, and may be considered
routine care, even in patients who remain haemodynamically stable,
as development of haemodynamic compromise is often unexpected,
rapid, and fatal. Of the 2876 patients in the STS database, 65% had an
IABP placed pre-operatively, and another 8% had an IABP placed
VSR complicating AMI 2065

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Figure 3 Reported 30-day mortality for VSR with immediate surgical management or at various time-points of delayed intervention. Mortality is
reduced as the time between VSR and surgical intervention increases, likely due to a more stable and fibrosed myocardium, but also due to survival
bias. It is unknown what percentage of patients continues to survive as surgery is deferred. In the GUSTO-1 trial, there was 94% mortality at 30 days
without surgery suggesting that conservative management is associated with very high mortality. A strategy of full mechanical support allowing for
planned, delayed surgery at 7 days may both improve survival while surgery is deferred, and allow for better surgical outcomes due to more stable
myocardium, but data are currently limited to case reports.

Figure 4 A multidisciplinary approach for managing acute ventricular septal rupture.

during surgery. IABP utilization was significantly higher in emergent
(84.7%) and salvage (87.9%) cases when compared with elective
cases (18.6%).16
Several case studies in the literature have documented the use of
extracorporeal membrane oxygenation systems to stabilize patients
until surgery can be performed. Other options include placement of a
percutaneous or surgical left-ventricular assist device as a bridge to
surgery or transplant.19,20 The data detailing the success of these
strategies in patients with acute VSR is currently limited to case
reports.21,22
2066
Table 2 Major trials of percutaneous closure of ventricular septal rupture
Author Number of patients
...............................................................................................................................................................................
Assenza,32 2013 30 patients
Primary closure: 12
Residual after surgery: 18
Maltias,34 2009 12 patients
Thiele,30 2009 29 patients
Cardiogenic shock: 16
No shock: 13
Bialkowsk,35 2007 19 patients
Primary closure: 17
Residual after surgery: 2
Demkow,36 2005 11 patients
Holzer,33 2004 18 patients
Primary closure: 8
Residual after surgery: 10
AMI, acute myocardial infarction.
As another strategy, a small series of five patients demonstrated
successful use of the Impella 5.0 L system (Abiomed, Danvers, MA,
USA) for a mean of 14.4 + 6 days as a bridge to surgery with a
30-day mortality of 40%.23 The TandemHeart pVAD system has
been shown to reverse cardiogenic shock in 117 patients, but the
cohort included only five patients with acute STEMI, and an
unknown number of VSRs.24 Finally, a single case report from
Germany documents the use of a total artificial heart followed by a
successful cardiac transplant 14 weeks later.19 In the absence of
large trial data, these reports provide an interesting, albeit limited,
perspective. Short-term mechanical circulatory support as a bridge
to recovery is a IIa (LOE C) recommendation in patients with VSR
and persistent shock according to current ESC guidelines.25
Percutaneous ventricular septal
rupture closure
The past decade has witnessed an exciting evolution in structural
cardiac interventions.26 – 29 As a result, attention has turned to per-
cutaneous options for the closure of VSR in patients with significant
risk for surgical repair, either as a definitive strategy, or as a bridge to
surgery after initial stabilization. Several case series have been pub-
lished documenting single institution experience with both primary
percutaneous VSR closure as well as closure of residual defects
after surgery (Table 2). Similar to the surgical literature, outcomes
improve as patients progress from the acute to chronic phase. The
primary goal is a reduction in residual left-to-right shunting (Qp:Qs),
which in the largest series of primary VSR closure, was reduced from
3.3 (IQR 2.3 –3.8) to less than 1.5:1 in all but four of 29 patients.30
There are several anatomic concerns in selecting patients for a per-
cutaneous repair.31 Most authors suggest that a defect ,15 mm is
optimal, in large part due to the device sizes that are available, as
well as the size of the septum. Inferior/posterior defects are especially
B.M. Jones et al.
Initial procedural Timing of closure 30-day mortality, %
success (days after AMI)
Unspecified 19 (11– 27) 42
54 (22– 173) 11
Unspecified 12.2 42
25/29 65
1 (1 –3) 88
6.5 (4 –16) 38
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14/19 Unspecified 26.3
10/11 2/10 patients: ‘acute’ 100
8/10 patients: 24–392 0
16/18 25 (2–95) 28
challenging as they frequently lack an adequate tissue ‘rim’ to secure
the device. The location of the adjoining tricuspid valve apparatus
(especially the septal leaflet) makes closure of basal defects more dif-
ficult still. Serpigenous defects are not only difficult to cross with a
wire, but can be complicated by significant leakage around the
device since the path between the ventricles is not straight. Finally,
freshly infarcted myocardium may exhibit ongoing necrosis and in-
stability in the days following MI, making peri-device leakage or
even device embolization a concern. Thus, attempting device place-
ment requires a thorough understanding of the defect’s size, shape,
and borders, usually requiring characterization by both surface and
transesophageal echocardiography. Intracardiac echocardiography
is invasive and therefore not often used in the screening phase of man-
agement; however, it may be useful intra-procedurally, especially
when the probe is advanced to the RV.
We favour a retrograde approach across the aortic valve (Figure 5).
A soft wire (i.e. 0.035′′ Wholey wire) is passed across the VSR from
the LV to the RV (along the direction of flow). The wire is then passed
to the pulmonary artery to facilitate snaring. The snare may be
advanced from the internal jugular or femoral venous approach.
While the angle of the SVC to the VSR is more favourable than
that of the IVC, we find that the inherent lack of sterility in operating
from the neck is a limitation to this approach. Once the wire is snared
in the PA, it is externalized. A delivery sheath is then advanced from
the venous side and across the VSR into the LV. The intended device is
then deployed across the septum.
Another novel approach is a combined surgical/percutaneous
hybrid closure. Via a standard thoracotomy, a cannulating needle
and introducer can be inserted directly into the RV or LV. Under
fluoroscopic guidance, the defect is then crossed with a wire and
the procedure conducted through the routine steps. Alternatively,
a septal occlusion device can be placed under direct visualization.
The hybrid approach has the theoretic advantages of easier crossing
of the defect and better visualization than a fully percutaneous
VSR complicating AMI 2067

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Figure 5 Percutaneous closure of an apical ventricular septal rupture (VSR). (A) Left ventriculography in the LAO projection demonstrates the
apical VSR (arrowhead); (B) a balloon-tipped catheter is passed across the interventricular septum (IVS) (arrowhead) and a gooseneck snare is
advanced to the right ventricle (RV, arrow) via the internal jugular (IJ) vein; (C ) a wire is passed through the lumen of the balloon catheter,
snared, and drawn through to the IJ to provide a rail for device delivery (D); (E) the device is deployed across the IVS; (F) left-ventriculography demon-
strates minimal residual shunting of contrast from the LV to the RV.

strategy, and conversely obviates the need for cardiopulmonary
bypass. Furthermore, the surgeon need not suture into freshly
infarcted and structurally poor myocardium. Patients who undergo
percutaneous closure should receive dual anti-platelet therapy for
6 months followed by baby aspirin alone, and should receive appro-
priate antibiotic prophylaxis prior to invasive procedures.
requires substantial critical care, imaging, interventional, and surgical
expertise. It is therefore advisable, when clinically feasible, to transfer
these patients to regional centres with adequate individual experi-
ence in the care of patients with VSR.
Conflict of interest: none declared.

Conclusions
Mortality due to AMI has fallen substantially over the past three
decades. Nevertheless, patients who suffer VSR represent a sub-
group with extraordinarily high mortality. Management of the
patient who is in acute, decompensated cardiogenic shock should
be directed at reducing left-to-right shunt with afterload reducing
agents and IABP placement. There is no clear evidence to guide the
surgical management of patients who are in shock, as all approaches
have shown extremely high mortality. Possible strategies include
emergent surgery, a period of percutaneous mechanical circulatory
support prior to a delayed surgical or percutaneous intervention,
or emergent placement of a percutaneous closure device to
reduce the shunt. Percutaneous closure may also be a viable option
for patients in the sub-acute to chronic period whose comorbidities
preclude surgical repair, and whose septal anatomy is favourable to
device placement. The management of VSR is complicated, and
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