European Heart Journal (2022) 43, 5033–5036 EDITORIAL

https://doi.org/10.1093/eurheartj/ehac532

Management of post-infarction ventricular

septal defects: are we moving forward?
1 1 2
Fernando Alfonso *, Rio Aguilar , and Guillermo Reyes

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1
Department of Cardiology, Hospital Universitario de La Princesa, Madrid, Spain; and 2Department of Cardiac Surgery, Hospital Universitario de La Princesa, Madrid, Spain

Online publish-ahead-of-print 17 September 2022

This editorial refers to ‘Post-infarction ventricular septal defect: percutaneous or surgical management in the UK national
registry’, by J. P. Giblett et al., https://doi.org/10.1093/eurheartj/ehac511.

Graphical Abstract

Post-Infarction Ventricular Septal Defect (PIVSD)

Key
Key diagnostic issues Heart team discussion
ssio
ion
io n
Clinical features Experience - Expertise?
Age, frailty, comorbidities Surgical team
End-organ failure, futility Interventional team

Haemodynamic status Timing?

Cardiogenic shock, pulmonary oedema Emergent, early (<2 weeks), late
Response to “optimal” medical therapy MCS?
Anatomic and functional characteristics IABP
PIVSD: size, location, morphology, shunt fraction Advanced: Impella, ECMO, both, other
Left and right ventricular function Revascularization?
Other mechanical complication, valvular disease IRA, complete
Extent of coronary artery disease

Surgical repair Percutaneous closure

Diagnosis and management of post-infarction ventricular septal defect (PIVSD). Clinical, anatomical and haemodynamic findings, together with the re­
sponse to aggressive medical management, should be evaluated by the local Heart Team to optimize the time-sensitive decision making process. (?) ,
denotes main issues to be considered and discussed; IRA , infarct-related artery; MCS , mechanical circulatory support; IABP , intra-aortic balloon
pump; ECMO , extracorporeal membrane oxygenation.

The opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.
* Corresponding author. Department of Cardiology, Hospital Universitario de La Princesa, IIS-IP, Universidad Autónoma de Madrid, CIBER-CV, Diego de León 62 Madrid 28006, Spain. Email:
falf@hotmail.com
© The Author(s) 2022. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com
5034
Post-infarction ventricular septal defect (PIVSD) remains a rare yet
dreadful mechanical complication of acute myocardial infarction
(MI).1–6 Due to its dismal prognosis, surgical repair (SR) is considered
the mainstay of treatment although percutaneous closure (PC) is also
being increasingly considered in selected patients.1–6 Remarkably, the
incidence of this devastating complication has been reduced by
10-fold (from ∼2% to ∼0.2%) with the widespread use of early reper­
fusion in MI.2–6 Classical series showed a ∼90% mortality rate in pa­
tients managed conservatively.1 Although SR is recommended by
clinical practice guidelines, early SR remains associated with a very
high mortality (>50%), particularly in patients in cardiogenic shock.1–6
Conversely, a delayed SR (>2 weeks) allows maturation of the friable
necrotic edges of the septal defect, facilitating technical repair with a
lower mortality.1–6 Nevertheless, the better results obtained by delay­
ing SR are drastically confounded by selection and survival bias.1–6
Therefore, the main persisting dilemmas in clinical decision making
are whether, when, and how to intervene on these high-risk patients
(see Graphical Abstract).
Current study
In this issue of the Journal, Giblett et al.7 present a series of 362 patients
with PIVSD treated (416 procedures) with either SR (n = 231) or PC
(n = 131) at 16 UK centres (2010–21). The median elapsed time
from MI to treatment was 9 days, similar between the two strategies.
Patients undergoing SR were more likely to be in cardiogenic shock
(62.8% vs. 51.9%) and require mechanical circulatory support (MCS)
(76.1% vs. 67.2%), and had larger defects (20 mm vs. 18 mm), whereas
those undergoing PC were older (72 vs. 67 years). Immediate proced­
ural success was higher in the SR group (88.3% vs. 79.4%). Although in-
hospital mortality was lower in the SR group (44.2% vs. 55%, P = 0.048),
no differences in mortality were seen after discharge and, eventually,
long-term mortality (primary endpoint) was similar in both groups
(53.7% vs. 61.1%, P = 0.17). Independent predictors of long-term mor­
tality included cardiogenic shock, creatinine, PC, number of vessels, and
early intervention. SR was associated with a higher risk of stroke, pace­
maker and renal replacement therapy, whereas PC was associated with
a higher need of re-interventions. Age, defect size, and centre volume
were independent predictors of PC management.
This large study significantly expands the limited evidence base avail­
able for the management of PIVSD (see Graphical Abstract). Some meth­
odological issues, however, should be discussed.7
First, this represents a highly selected population of patients in whom
repair was attempted in experienced centres. The total number of pa­
tients diagnosed with PIVSD was not reported. The criteria used to se­
lect the intervention, the number of patients rejected for each strategy,
and the outcome of patients managed conservatively, would have been
of value. Notably, the long time elapsed to repair suggests that a survival
bias should be considered.
Second, in this retrospective study, data collection was performed
locally without centralized analysis. Frailty, comorbidities, anatomical
PIVSD characteristics, and associated abnormalities were poorly char­
acterized yet would have been of interest. Likewise, the influence of ad­
juvant management, including inotropic and antithrombotic therapy,
was not elucidated.
Third, technical details of interventions were not provided. Due to
the array of techniques available, additional insights on procedural de­
tails would have been important to assess their potential prognostic in­
fluence. A complete reduction of the defect was only achieved in 66.5%
Editorial
and 19% of patients after SR and PC, respectively. Actually, the defin­
ition of success as ‘at least partial reduction of the leak’, assessed by lo­
cal investigators, might be considered over-optimistic, but reflects what
currently can be expected in this challenging scenario. The implications
of complete closure remained elusive. Importantly, partial reduction of
the defect may allow haemodynamic stabilization and preserve life.
Fourth, these investigators aimed to compare the relative efficacy of
SR and PC. However, the observational nature of the study and the
likelihood of a selection bias underlying the choice of the treatment
strategy, makes this comparative effort likely unrealistic. As nicely ac­
knowledged, some patients too sick/frail for surgery may have been
considered for PC. Alternatively, patients with large defects or unto­
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ward anatomy cannot be amended by currently available PC techni­
ques. Propensity matching was deemed unfeasible, considering the
dataset. Furthermore, 7.8% of SR cases subsequently required PC,
whereas 16.1% of PC cases eventually required SR. This crossover
complicates the comparison between the two strategies but empha­
sizes, first, that complete correction is not always feasible and, second,
that these techniques are complementary and may be used sequentially
to achieve success.
Fifth, PCI to the infarct-related-artery (40% of patients), was asso­
ciated with in-hospital mortality but, paradoxically, predicted survival
after discharge. The futility of this intervention in patients with exten­
sive transmural myocardial necrosis should be considered.
Alternatively, the extent of coronary artery disease was associated
with an adverse prognosis and, therefore, complete revascularization
should be considered to improve prognosis. In this study, half of the pa­
tients undergoing SR had concomitant bypass surgery, but the value of
complete revascularization was not assessed and currently remains
controversial.2–6
Sixth, many interventionists will be disappointed by the unexpected
persistently low number of PC procedures performed during the study.
The Amplatzer post-infarct muscular VSD occluder was selected in
most cases but many ‘off-label’ devices were used. Further technical ad­
vancements and device iterations are eagerly required to expand the
use of this therapy to a growing number of patients aiming to: (i) re­
verse the haemodynamic derangement and provide a bridge to SR;
(ii) treat post-SR residual shunt or patch dehiscence; and (iii) offer a pri­
mary definitive therapy.5
Finally, only two-thirds of patients received intraortic balloon pump
(IABP) and there was a negligible use (<3%) of ‘advanced’ MCS [Impella,
extracorporeal membrane oxygenation (ECMO)]. This is surprising,
considering that most patients had left and right ventricular dysfunction
and were in cardiogenic shock. It seems reasonable to speculate that
clinical outcomes might have been improved had MCS been used
more frequently.8,9
Burning issues in PIVSD
management
Anatomical issues
A high level of clinical suspicion leading to swift echocardiographic
evaluation should allow prompt diagnosis. However, further anatomical
and physiological insights are required for optimal management.2–6 A
comprehensive previous study,10 using computed tomography (CT)
or magnetic resonance imaging, assessed PIVSD morphology in 32 pa­
tients. Most PIVSD were large (26 ± 11 mm), oval, changed during the
cardiac cycle, had thin margins, and rarely were confined to the septum.
Editorial
Posterior PIVSD were large, complex, had serpiginous intramyocardial
dissection tracts reaching the left ventricular free wall, and were asso­
ciated with a poorer prognosis. Importantly, only 50% of the defects
were small enough for the largest available PC device. Previous studies
demonstrated that posterior PIVSD are associated with worse out­
comes due to their untoward morphology, poorer right ventricular
function, and technical difficulties during SR.2–6 3D printing from cardiac
CT images provides a more comprehensive anatomical assessment, fa­
cilitating pre-intervention planning. In the future, this might allow rapid
prototyping and a tailored PC approach.
Strategies
In 1957, Cooley first reported the surgical repair of a PIVSD. The tech­
nique evolved with the David infarct ‘exclusion’ technique and use of
biological glues.3–5 Unfortunately, surgical risk has remained unchanged
in the past three decades.3–5 Alternatively, after the initial report by
Lock et al. in 1988, PC provides an attractive option for selected pa­
tients.5 PC has evolved, from closing residual leaks after SR or stabilizing
critically ill patients, to a definitive primary intervention.5 However,
available series on PC are small and do not provide meaningful data
vs. conservative management or SR.11,12 Technicalities include arterio­
venous loops, oversized devices, valve interferences, and delayed device
endothelization.5 Thiele et al.11 first evaluated the use of early PC in 29
haemodynamically unstable patients with a 30-day survival of 35%.
Calvert et al.11 reported the UK experience with PC in 53 patients
with 58% in-hospital survival. Both SR and PC are demanding proce­
dures requiring expertise but, due to the rarity of the condition, in
most centres experience remains very limited.5,10,11 As transfer of
haemodynamically unstable patients to referral centres is usually un­
feasible, obtaining adequate proctorship should be considered.
Timing
The optimal time to repair remains highly controversial.1–6 During early
SR, trimming and patch exclusion of the friable necrotic myocardium
may be required. Consistently, classical and recent studies reported
better results with delayed SR.2–6 However, allowing tissue recovery
time implies accepting major survival bias. American and European
guidelines have classically diverged in this regard. Whereas in
American guidelines early intervention is recommended for all patients,
European guidelines consider a delayed repair in stable patients under
medical therapy. This policy has been supported by data suggesting that
early surgery is only superior to a delayed strategy in patients in cardio­
genic shock,13 and was advocated by a recent American Heart
Asociation (AHA) scientific statement.6
Circulatory support
The cornerstone of medical management of PIVSD involves decreasing
left ventricular afterload while maintaining systemic pressure. IABP is
the safest and more cost-effective device in this scenario but has a lim­
ited efficacy and, therefore, advanced MCS should be considered.2–6
The Detroit group14 used a computational model to assess the haemo­
dynamic effects of different strategies of MCS. Inotropes and vasopres­
sors worsened left-to-right shunt, whereas vasodilators decreased
shunting although worsened hypotension. All MCS devices increased
aortic flow but none of them normalized pulmonary flow.
Importantly, Impella decreased left-to-right shunt and reduced wedge
pressure. Conversely, ECMO worsened wedge pressure and shunting,
a situation that only could be offset by the concomitant use of Impella.
5035
Advanced MCS is increasingly used nowadays to stabilize the haemo­
dynamic condition and delay the repair. Evidence, however, is limited to
short series with ‘promising’ results. A narrative analysis15 (2440 pa­
tients, mainly case reports) revealed universal adoption of IABP, with
only 5.3% of advanced MCS (mostly ECMO). Mean bridging time was
6 days and in-hospital mortality was 50%, with a lower mortality in pa­
tients receiving ECMO/Impella. However, in other studies, the in­
creased use of advanced MCS has not been associated with a decline
in surgical mortality,13 and some reports have even suggested that ad­
vanced MCS is associated with a higher mortality.4 MCS increases
haemorrhagic and thrombotic complications. Expertise and a multidis­
ciplinary approach with close monitoring is required to optimize the
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interaction of MCS with the PIVSD pathophysiology and the interplay
between concomitant systems to prevent uncoupling.14,15
Conclusions
Authors should be commended for shedding new light on the man­
agement of this devastating complication.7 PIVSD produces a sudden
double haemodynamic insult (a large MI and cardiac shunt), repre­
senting an unmet clinical need as the most lethal cardiac surgical con­
dition. Both SR and PC remain associated with a high mortality, but
are viable and effective options in selected patients, providing dur­
able benefits. Although these strategies appear to be complementary
in nature, further research efforts are required to refine the decision
making process regarding timing of repair, strategy of choice, and use
of MCS, in individual patients presenting with PIVSD (see Graphical
Abstract).
Conflict of interest: None declared.
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