<?xml version="1.0" encoding="UTF-8"?><!DOCTYPE article  PUBLIC "-//NLM//DTD Journal Publishing DTD v3.0 20080202//EN" "http://dtd.nlm.nih.gov/publishing/3.0/journalpublishing3.dtd"><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" dtd-version="3.0" xml:lang="en" article-type="research article"><front><journal-meta><journal-id journal-id-type="publisher-id">WJCS</journal-id><journal-title-group><journal-title>World Journal of Cardiovascular Surgery</journal-title></journal-title-group><issn pub-type="epub">2164-3202</issn><publisher><publisher-name>Scientific Research Publishing</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.4236/wjcs.2022.129015</article-id><article-id pub-id-type="publisher-id">WJCS-119712</article-id><article-categories><subj-group subj-group-type="heading"><subject>Articles</subject></subj-group><subj-group subj-group-type="Discipline-v2"><subject>Medicine&amp;Healthcare</subject></subj-group></article-categories><title-group><article-title>
 
 
  Recurrent Stroke after Percutaneous Placement of Post-Infarct Septal Occluder Device
 
</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Suguru</surname><given-names>Ohira</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="corresp" rid="cor1"><sup>*</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>B.</surname><given-names>S. Matan Grunfeld</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Amanda</surname><given-names>Hetzel</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Rohinton</surname><given-names>J. Morris</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib></contrib-group><aff id="aff2"><addr-line>Division of Cardiac Surgery, Department of Surgery, Thomas Jefferson University Hospital, Philadelphia, PA, USA</addr-line></aff><aff id="aff1"><addr-line>Division of Cardiothoracic Surgery, Department of Surgery, Westchester Medical Center, New York Medical College, Valhalla, NY, USA</addr-line></aff><pub-date pub-type="epub"><day>07</day><month>09</month><year>2022</year></pub-date><volume>12</volume><issue>09</issue><fpage>191</fpage><lpage>195</lpage><history><date date-type="received"><day>24,</day>	<month>July</month>	<year>2022</year></date><date date-type="rev-recd"><day>5,</day>	<month>September</month>	<year>2022</year>	</date><date date-type="accepted"><day>8,</day>	<month>September</month>	<year>2022</year></date></history><permissions><copyright-statement>&#169; Copyright  2014 by authors and Scientific Research Publishing Inc. </copyright-statement><copyright-year>2014</copyright-year><license><license-p>This work is licensed under the Creative Commons Attribution International License (CC BY). http://creativecommons.org/licenses/by/4.0/</license-p></license></permissions><abstract><p>
 
 
  Surgical intervention for post-infarct ventricular septal defect (VSD) is a challenging procedure due to patients’ complex preoperative conditions. While percutaneous VSD closure can be considered as an alternative to surgical repair, complete closure of the defect remains difficult and is associated with various procedural complications. We report a rare case of a patient with postoperative
   
  residual shunts who experienced recurrent stroke episodes, requiring surgical intervention for repair. The patient, a 71-year-old female, developed acute anterior myocardial infarction and post-infarct VSD. Percutaneous closure with a 14-mm Amplatzer VSD occluder device was performed, yet the closure was incomplete. Following discharge, she developed multiple embolic stroke episodes, likely stemming from the residual VSD, which led to the surgical extraction of the device and VSD repair. Fibrous tissue was found to be solely attached to the core and right ventricle side of the device, whilst no fibrous tissue was observed on the side of the left ventricle. The patient has not experienced new neurological symptoms at an 18-month follow-up. Thus,
   
  it is paramount to keep in mind that an embolic stroke may occur in the setting of percutaneous post-infarct VSD closure. Surgical repair of VSD with device removal should be considered as a treatment option to such a complex case.
 
</p></abstract><kwd-group><kwd>Ischemic Heart Disease</kwd><kwd> Post-Infarct Ventricular Septal Defect</kwd><kwd> Percutaneous Closure</kwd></kwd-group></article-meta></front><body><sec id="s1"><title>1. Introduction</title><p>Post-infarct ventricular septal defect (VSD) is a life-threatening complication following acute myocardial infarction [<xref ref-type="bibr" rid="scirp.119712-ref1">1</xref>] [<xref ref-type="bibr" rid="scirp.119712-ref2">2</xref>] [<xref ref-type="bibr" rid="scirp.119712-ref3">3</xref>] [<xref ref-type="bibr" rid="scirp.119712-ref4">4</xref>]. Early surgical intervention for post-infarct VSD is challenging due to several reasons; first, patients are often in cardiogenic shock with mechanical circulatory support; second, the VSD itself is complex due to surrounding edematous and necrotic tissue, causing an open repair to be challenging; and lastly, its incidence has decreased to less than 1% of acute myocardial infarction cases, with an average number of annual procedures ranging from 0.09 to 3.7 cases/year in the United States [<xref ref-type="bibr" rid="scirp.119712-ref1">1</xref>] [<xref ref-type="bibr" rid="scirp.119712-ref5">5</xref>]. According to the Society of Thoracis Surgeons Database, the overall mortality rate after post-infarct VSD repair was reported to be 42.9% [<xref ref-type="bibr" rid="scirp.119712-ref1">1</xref>]. With the hope of improving early operative outcomes, one of the alternative techniques considered for percutaneous ischemic VSD closure involves using an occluder device [<xref ref-type="bibr" rid="scirp.119712-ref2">2</xref>] [<xref ref-type="bibr" rid="scirp.119712-ref3">3</xref>]. However, there is limited clinical evidence regarding potential complications related to percutaneous ischemic VSD repair that ought to be considered. We report a case of a patient with residual shunts following percutaneous closure of an ischemic VSD in which open surgical repair was required due to post-operative recurrent stroke episodes.</p></sec><sec id="s2"><title>2. Case</title><p>A 71-year-old woman developed acute anterior myocardial infarction which was treated with drug-eluting stenting. The hospital course was subsequently complicated by anterior post-infarct VSD. Percutaneous VSD closure with a 14-mm Amplatzer VSD occluder device (Abbot, Chicago, IL) was performed. However, residual shunts were present causing the Qp/Qs ratio to decrease from 2.9 to 1.9. After discharge with aspirin 81 mg and clopidogrel 75 mg, the patient experienced several syncopal episodes and developed dysarthria, right upper hemiparesis, and transient visual loss within three months of the myocardial infarction. Diagnosis of an embolic stroke in the left corona radiate and temporoparietal region was made with the probable source being the residual VSD and closure device. The patient was placed on warfarin potassium and dual antiplatelet therapy, yet a total of 6 similar episodes were followed. In addition, the clinical course was complicated by melena with supratherapeutic INR requiring blood transfusion. She was then transferred to our hospital for further management.</p><p>Transthoracic echocardiography showed a 14-mm Amplatzer device in place (<xref ref-type="fig" rid="fig1">Figure 1</xref>(A)) with two residual shunt flows around the device (<xref ref-type="fig" rid="fig1">Figure 1</xref>(B)). Fifteen weeks after percutaneous closure of VSD, she proceeded to undergo a surgical extraction of the device and VSD repair. Following aortic cross-clamp, a free wall of the left ventricle (LV) was incised along the left descending coronary artery. No clots were found on the LV side of the Amplatzer device (<xref ref-type="fig" rid="fig2">Figure 2</xref>(A)), yet the device was adhered to a free wall of the right ventricle. Gross inspection of the explanted specimen showed that fibrous tissue was only attached</p><p>to the core and right ventricle side of the device, while no fibrous tissue was attached to the LV side (<xref ref-type="fig" rid="fig2">Figure 2</xref>(B)). After device removal, the VSD was closed with a bovine pericardial patch and LV ventriculotomy was closed using a double-layered closure technique. The patient was discharged with oral aspirin 81 mg. No new neurological symptoms were experienced by the patient at an 18-month follow-up.</p></sec><sec id="s3"><title>3. Discussion</title><p>Outcomes of early surgical repair of post-infarct VSD have remained unchanged throughout the last two decades [<xref ref-type="bibr" rid="scirp.119712-ref1">1</xref>] [<xref ref-type="bibr" rid="scirp.119712-ref5">5</xref>]. Although delayed surgical intervention may seem associated with better survival, unstable hemodynamic conditions in ischemia does not always permit for this delayed approach. In this type of critical setting, percutaneous ischemic VSD closure may potentially be a more attractive alternative to surgical repair due to the reduced invasive nature of the procedure [<xref ref-type="bibr" rid="scirp.119712-ref3">3</xref>] [<xref ref-type="bibr" rid="scirp.119712-ref4">4</xref>]. A large multi-center study from the United Kingdom reported that an immediate complete reduction of the shunt by percutaneous VSD closure technique was attained in only 15% of patients, while a partial reduction of the shunt was seen in 64% of patients [<xref ref-type="bibr" rid="scirp.119712-ref3">3</xref>]. As a result, several complications have been reported to be related to percutaneous ischemic VSD closure, such as a residual shunt, hemolysis, device dislodgement/embolization, infection, atrioventricular block, and LV rupture [<xref ref-type="bibr" rid="scirp.119712-ref4">4</xref>].</p><p>Following an embolic stroke, anticoagulation and/or antiplatelet agents act as standard therapy to prevent a recurrent thromboembolic event. In this present case, after developing an embolic stroke, the patient was treated with dual antiplatelet therapy and warfarin potassium. However, despite these medical interventions, the patient suffered a recurrent stroke following the initial episode. Furthermore, gastrointestinal bleeding had developed as a result of the dual antiplatelet and anticoagulation therapy. Although a revision procedure of VSD percutaneous closure may have been a potential management option, it is technically more challenging. Therefore, surgical repair of the residual VSD and removal of the occluder device was performed.</p><p>In a previous report regarding percutaneous VSD closure, an excised pathological specimen collected during autopsy showed that the nitinol mesh of the VSD occluder device was fully filled with organized tissue, which typically takes a few weeks to form [<xref ref-type="bibr" rid="scirp.119712-ref3">3</xref>]. In the present case, even 3 months following percutaneous VSD closure, the excised specimen showed that there was no organized tissue on the LV side of the Amplatzer device’s surface. Thus, it is difficult to determine whether shunt flow or the presence of the device itself was the cause of embolism. Nevertheless, the patient has not had any new neurological symptoms after the surgical extraction of the Amplatzer device and VSD closure, supporting the feasibility of surgical repair.</p></sec><sec id="s4"><title>4. Conclusion</title><p>In conclusion, we experienced a rare case of a recurrent stroke following percutaneous VSD closure with residual shunts which required an open surgical repair. It is paramount to keep in mind that an embolic stroke may occur after percutaneous post-infarct VSD closure with a residual shunt.</p></sec><sec id="s5"><title>Consent for Publication</title><p>The patient has provided permission to publish this case and the identity of the patient has been protected.</p></sec><sec id="s6"><title>Conflicts of Interest</title><p>The authors declare no conflicts of interest regarding the publication of this paper.</p></sec><sec id="s7"><title>Cite this paper</title><p>Ohira, S., Grunfeld, B.S.M., Hetzel, A. and Morris, R.J. (2022) Recurrent Stroke after Percutaneous Placement of Post-Infarct Septal Occluder Device. World Journal of Cardiovascular Surgery, 12, 191-195. https://doi.org/10.4236/wjcs.2022.129015</p></sec></body><back><ref-list><title>References</title><ref id="scirp.119712-ref1"><label>1</label><mixed-citation publication-type="other" xlink:type="simple">Arnaoutakis, G.J., Zhao, Y., George, T.J., Sciortino, C.M., McCarthy, P.M. and Conte, J.V. (2012) Surgical Repair of Ventricular Septal Defect after Myocardial Infarction: Outcomes from the Society of Thoracic Surgeons National Database. The Annals of Thoracic Surgery, 94, 436-443. https://doi.org/10.1016/j.athoracsur.2012.04.020</mixed-citation></ref><ref id="scirp.119712-ref2"><label>2</label><mixed-citation publication-type="other" xlink:type="simple">Thiele, H., Kaulfersch, C., Daehnert, I., Schoenauer, M., Eitel, I., Borger, M., et al. (2009) Immediate Primary Transcatheter Closure of Postinfarction Ventricular Septal Defects. 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