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\begin{document}

\title{Ventricular Septal Defect Complicating Myocardial Infarction: A Case of
Delayed Percutaneous Transcatheter Closure}



\author[1]{Qianhang Xia}%
\author[1]{Meihong Chen}%
\author[2]{Qingxian Tu}%
\author[2]{Min Xu}%
\author[1]{Qianfeng Jiang}%
\affil[1]{Zunyi Medical University}%
\affil[2]{The Third Affiliated Hospital of Zunyi Medical University（The First People’s Hospital of Zunyi） Zunyi 563000 China}%


\vspace{-1em}



  
  \date{May 27, 2024}


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\selectlanguage{english}
\begin{abstract}
A 57-year-old man suffered chest pain during the COVID-19 pandemic, but
he delayed medical treatment due to fear of infection. Four months
later, symptoms chest tightness and shortness of breath appeared.
Electrocardiogram (ECG) revealed old myocardial infarction; color
sonography and myocardial CT revealed apical myocardial defect. He
refused surgery and percutaneous transcatheter closure, and follow-up
observation. After 22 months, the symptoms of chest tightness and
shortness of breath aggravated. He recovered after percutaneous
transcatheter closure, and was discharged. This case shows delayed
closure is one of the possible options for the patients without severe
organ dysfunction or hemodynamic disturbance.%
\end{abstract}%



\sloppy


Ventricular Septal Defect Complicating Myocardial Infarction: A Case of
Delayed Percutaneous Transcatheter Closure

Qianhang Xia\textsuperscript{1}, Meihong Chen\textsuperscript{2}
,Qingxian Tu\textsuperscript{3}, Min Xu\textsuperscript{4},Qianfeng
Jiang\textsuperscript{*(correspondence author; E-mail:
jiangqianfeng2005@126.com)}

1,2,* Faculty of clinical medicine, Zunyi Medical University, Zunyi
563000, China

3,4 The Third Affiliated Hospital of Zunyi Medical University(The First
People's Hospital of Zunyi), Zunyi 563000, China

\textbf{Abstract}

A 57-year-old man suffered chest pain during the COVID-19 pandemic, but
he delayed medical treatment due to fear of infection. Four months
later, symptoms chest tightness and shortness of breath appeared.
Electrocardiogram (ECG) revealed old myocardial infarction; color
sonography and myocardial CT revealed apical myocardial defect. He
refused surgery and percutaneous transcatheter closure, and follow-up
observation. After 22 months, the symptoms of chest tightness and
shortness of breath aggravated. He recovered after percutaneous
transcatheter closure, and was discharged. This case shows delayed
closure is one of the possible options for the patients without severe
organ dysfunction or hemodynamic disturbance.

\textbf{Key Words} : Acute myocardial infarction, Complication,
Ventricular assist device, Radial percutaneous coronary intervention,
Covid-19, Case report

\textbf{Ethics approval statement regarding}

This case report was approved by the ethics committee of The Third
Affiliated Hospital of Zunyi Medical University. We certify that the
case report was performed in accordance with the 1964 declaration of
HELSINKI and later amendments.

\textbf{Informed consent statement regarding}

Written informed consent was obtained from all the participants prior to
the enrollment of this case report.

\textbf{Introduction}

Post-AMI VSD is a rare complication of AMI, with various clinical
manifestations, including hemodynamic instability, cardiac dysfunction
and cardiogenic shock. Its incidence is about
0.17\%-0.34\%\textsuperscript{{[}1{]}}, but the in-hospital mortality
can reach 41-80\%\textsuperscript{{[}2{]}}.

At present, the development of interventional therapy has opened up a
new idea for the treatment of post-AMI VSD. Percutaneous transcatheter
closure therapy which has the advantages of less trauma and no need for
general anesthesia, provides a new treatment idea for the patients with
post-AMI VSD who cannot undergo early surgical treatment.

We reported a patient with post-AMI VSD who underwent delayed
percutaneous transcatheter closure.

\textbf{Case Report:}

A 57-year-old man suffered sudden chest pains, mainly in the middle and
lower sternum, accompanied by sweating, while he rested at home 4 months
ago. He chose to delay medical care because of the COVID-19 epidemic.
Three months later, he developed chest tightness, shortness of breath
and other discomfort. The symptoms of depression and shortness of breath
aggravated significantly after a little activity, complicating systemic
edema, especially in the extremities. Physical examination after
admission revealed heart rate of 98 beats/min, blood pressure of
131/103mnHg, no rales in both lungs, intermittent rales in the third and
fourth ribs and systolic ejection murmur on the left sternal border.
Besides, Troponin was 0.01\selectlanguage{greek}μ\selectlanguage{english}g/L; CK-MB was 12.8U/L; BNP was 880.6pg/ml.
Electrocardiogram indicated myocardial infarction of anterior interwall
and anterior wall (Figure 1 A). Color echocardiography revealed abnormal
movement of the anterior and interanterior walls of the left ventricle
with septal perforation (Figure2 A). Myocardial CT showed myocardial
defects at the apex of the ventricular septum, being consistent with
myocardial perforation (Figure 3). Coronary angiography revealed a
three-vessel lesion.( (Figure4 A)(174)

The patient improved slightly after the treatment of vasodilating,
diuresis and heart strengthening. For ventricular septal defect, there
was high risk of surgery according to the cardiac surgery consultation.
His family members gave up surgical treatment and interventional
plugging treatment. The patient was treated with anti heart failure
drugs after risk assessment. The patient was followed up in our hospital
every 3 months. During the period, his chest tightness, shortness of
breath and other symptoms did not worsen. Color echocardiography reveals
there was no ventricular septal defect enlargement and cardiac function
decline. The patient developed chest tightness, and increased shortness
of breath, with significant restrict~of~activity after 22 months.
Physical examination revealed heart rate of 98 beats/min, blood pressure
of 131/103mnHg, no rales in both lungs, intermittent rales in the third
and fourth ribs and systolic ejection murmur on the left sternal border.
Supplementary examination revealed that Troponin and CK-MB were within
normal limits. Electrocardiogram indicated old myocardial infarction
(Figure1 B). Color echocardiography showed no enlarged perforation
(Figure 2 B).

Percutaneous transcatheter closure was chosen after communication with
family members (Figure4 B). Postoperative echocardiography showed
changes after ventricular septal closure (Figure2 C). After treatment
with anti-heart failure and symptomatic support, the patient's symptoms
of chest tightness and shortness of breath were relieved. And he was
discharged from the hospital upon recovery.

\textbf{Discussion}

In our report, the patient did not seek medical treatment. Studies have
shown that most VSD occurs 3-5 days after AMI\textsuperscript{{[}3{]}}.
The patients receiving drug therapy alone have a median survival time of
5 days; more than 75\% of patients die within 12 days after the onset of
VSD symptoms, with 93.6\% of 30-day mortality rate, and 96.2\% of
long-term mortality rate\textsuperscript{{[}4{]}}. Therefore, based on
the experience, the patient's onset of VSD might be approximately 4
weeks before the first visit. The patient had no discomfort such as
chest pain and no obvious hemodynamic disorder at the first visit. Based
on the above-mentioned factors, we dared to make the clinical decision
of agreeing to the patient's temporary refusal of closure and choosing
follow-up observation. Regular follow-up is a vital guarantee for
delayed ventricular septal closure. For patients who need to perform
delayed closure, it is crucial to closely monitor whether patients have
organ dysfunction and hemodynamic disorder.

Closure of ventricular septal perforation is the key to the treatment of
post-AMI VSD. Current guidelines still recommend surgical treatment for
post-AMI VSD\textsuperscript{{[}5{]}}. According to the STS database
report on the results of VSD surgery after infarction, however, only
2,876 patients received surgery in 666 participating
institutions\textsuperscript{{[}6{]}}, and most surgeons operated on no
more than 1 patient per year. Moreover, patients were often complicated
with complications such as shock and high surgical trauma. The patients
undergoing surgical treatment still face the mortality rate of
40\%\textsuperscript{{[}7{]}}. For the patients with severe hemodynamic
disorders, it is particularly important to close ventricular septal
defects as early as possible\textsuperscript{{[}8{]}}. Such patients,
however, often cannot be treated surgically immediately. Transcatheter
closure of the ventricular septum may be a more feasible option for
these patients. In addition, increasing number of evidences show that
percutaneous transcatheter closure of post-AMI VSD is an effective
treatment. It can immediately reduce shunt and thus prevent hemodynamic
deterioration\textsuperscript{{[}9{]}}. Besides, it does not require
general anesthesia and has little trauma and is tolerable for vast
majority of patients.

At present, the optimal intervention time for post-AMI VSD remains
controversial. Guidelines recommend early ventricular septal closure for
the patients with severe hemodynamic disorders. However, current studies
have shown that using supportive treatments including cardiopulmonary
bypass, stable hemodynamics and delay closure can also benefit
patients\textsuperscript{{[}10{]}} and reduce the mortality of
patients\textsuperscript{{[}11{]}}.In this case, the patient underwent
the occlusion 22 months after the onset of VSD, much later than the
recommended time in the guidelines. It could provide clinical evidence
for delayed closure of patients with post-AMI VSD. This case shows that
it is necessary to reevaluate whether early ventricular septal closure
is needed for all patients with post-AMI VSD.

The patient reported in this case delayed medical care due to COVID-19,
which is a common phenomenon during the epidemic. According to related
data, during the epidemic period, the number of emergency visits has
been reduced by nearly 50\%, and the out-of-hospital mortality has
increased accordingly because of patients' fear of coronavirus infection
and other factors\textsuperscript{{[}12{]}}. Evidence has shown that the
incidence of mechanical complications of AMI is significantly higher
than that in previous years due to patients' delayed medical treatment
during COVID-19\textsuperscript{{[}13{]}}. Enough attention should be
paid to the consequences of delayed medical care during the COVID-19
pandemic. Besides, the impact of the COVID-19 epidemic on patients'
long-term health-seeking habits still needs to be observed in the longer
term.

\textbf{Conclusion}

Percutaneous transcatheter closure has become an alternative treatment
strategy for patients with post-AMI VSD. Delayed closure is one of the
feasible options for patients without severe organ dysfunction or
hemodynamic disturbance. The optimal time to perform percutaneous septal
closure still needs further study and evaluation.

\textbf{References}

{[}1{]} Mahtta D, Mohammed I, Elgendy I Y. Overview of prevalence,
trends, and outcomes of post myocardial infarction mechanical
complications{[}J{]}. Ann Cardiothorac Surg, 2022, 11(3): 322-324.

{[}2{]} Flynn C D, Morris P, Manuel L, et al. Systematic review and
meta-analysis of the mechanical complications of ischemic heart disease:
papillary muscle rupture, left ventricle rupture and post-infarct
ventricular septal defect{[}J{]}. Ann Cardiothorac Surg, 2022, 11(3):
195-209.

{[}3{]} David T E. Post-infarction ventricular septal rupture{[}J{]}.
Ann Cardiothorac Surg, 2022, 11(3): 261-267.

{[}4{]} Sanmart\selectlanguage{ngerman}ín-Fernández M, Raposeiras-Roubin S, Anguita-Sánchez M,
et al. In-hospital outcomes of mechanical complications in acute
myocardial infarction: Analysis from a nationwide Spanish
database{[}J{]}. Cardiol J, 2021, 28(4): 589-597.

{[}5{]} Lawton J S, Tamis-Holland J E, Bangalore S, et al. 2021
ACC/AHA/SCAI Guideline for Coronary Artery Revascularization: Executive
Summary: A Report of the American College of Cardiology/American Heart
Association Joint~Committee~on~Clinical Practice Guidelines{[}J{]}. J Am
Coll Cardiol, 2022, 79(2): 197-215.

{[}6{]} Arnaoutakis G J, Zhao Y, George T J, et al. Surgical repair of
ventricular septal defect after myocardial infarction: outcomes from the
Society of Thoracic Surgeons National Database{[}J{]}. Ann Thorac Surg,
2012, 94(2): 436-43; discussion 443-4.

{[}7{]} Ronco D, Matteucci M, Kowalewski M, et al. Surgical Treatment of
Postinfarction Ventricular Septal Rupture{[}J{]}. JAMA Netw Open, 2021,
4(10): e2128309.

{[}8{]} Jaswaney R, Arora S, Khwaja T, et al. Timing of Repair in
Postinfarction Ventricular Septal Defect{[}J{]}. Am J Cardiol, 2022,
175: 44-51.

{[}9{]} Giblett J P, Jenkins D P, Calvert P A. Transcatheter treatment
of postinfarct ventricular septal defects{[}J{]}. Heart, 2020, 106(12):
878-884.

{[}10{]} Ronco D, Matteucci M, Ravaux J M, et al. Mechanical Circulatory
Support as a Bridge to Definitive Treatment in Post-Infarction
Ventricular Septal Rupture{[}J{]}. JACC Cardiovasc Interv, 2021, 14(10):
1053-1066.

{[}11{]} Matteucci M, Ronco D, Corazzari C, et al. Surgical Repair of
Postinfarction Ventricular Septal Rupture: Systematic Review and
Meta-Analysis{[}J{]}. Ann Thorac Surg, 2021, 112(1): 326-337.

{[}12{]} Walker L E, Heaton H A, Monroe R J, et al. Impact of the
SARS-CoV-2 Pandemic on Emergency Department Presentations in an
Integrated Health System{[}J{]}. Mayo Clin Proc, 2020, 95(11):
2395-2407.

{[}13{]} Primessnig U, Pieske B M, Sherif M. Increased mortality and
worse cardiac outcome of acute myocardial infarction during the early
COVID-19 pandemic{[}J{]}. ESC Heart Fail, 2021, 8(1): 333-343.

\textbf{Figure legends}

Figure1: A)V1-V5 shows QS pattern, and V1-V6 arch elevates
0.05-0.5Mv\selectlanguage{english};B) V2-V4 shows QS pattern, and V2-V4 arch elevates
0.05-0.15mv.

Figure 2 A) Echo-interruption in the left ventricular septum near the
apex was observed by color echocardiography, with a range of about
18.5mm and EF: 51\%; B) Echo interruption at the apex of the ventricular
septum, and the shunt layer at the ventricular septum stump was
dissected. The echo interruption in the left ventricular plane and the
right ventricular plane was 19mm, and 12mm, respectively; C) The
enhanced echo of the occluder can be seen at the ventricular septum near
the apex of the heart, and a small gap can be seen below the occluder
with a width of about 1.9mm.

Figure 3: Myocardial CT reveals myocardium defect of 2.2x2.1cm in
maximum cross-section at the apex of the ventricular septum.

Figure4: A) Coronary angiography (CAG) shows that the LAD is subtotal
occlusion in the middle and distal segments, with blood flow TIMI2: 60\%
stenosis in the middle segment of LCX; TIMI3: diffuse 50-70\% stenosis
in the proximal segment of RCA; 60\% stenosis in the proximal segment of
posterior descending branch, with blood flow TIMI3; B) Angiography
confirms ventricular septal perforation after apical myocardial
infarction, with the defect of about 17mm in diameter. A right heart
catheter was placed through the femoral vein under fluoroscopy. The
right ventricular and pulmonary artery pressures were measured as
RVP53/13mmHg (26mmHg) and PAP52/12 MMHG (24mmHg), respectively. A 260cm
guide wire was successfully inserted into the right ventricle through
the ventricular septal defect, and then sent into the pulmonary artery.
The guide wire snare was inserted through transvenous sheath and pulled
out through transvenous sheath pipe. The 28mm(14g) interventricular
septum wall packer was sent to left ventricular lateral through14F
transmit sheath pipe after successfully establishing the track. Next,
the packer left tray umbrella was released and the sheath tube retreated
at the same time. The right tray umbrella was released after completely
blocking the ventricular septal defect. The left ventricular angiography
confirmed there was no shunt in local part. Moreover, the auscultation
noise was obviously reduced, and X-ray images showed that the occluder
was in good shape, thus, the occluder was completely released. The
postoperative left ventricular pressure was 114/6(41)mmHg.\selectlanguage{english}
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