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Peer Review

Peer Reviewed

Clinical Images

Percutaneous Closure of a Large Postinfarct Ventricular Septal Defect With an Atrial Septal Defect Closure Device in a High Surgical Risk Patient

Ashleigh Long, MD, PhD1;  Alex Talreja2;  David Baran, MD1;  Deepak Talreja, MD1 

June 2021
1557-2501
J INVASIVE CARDIOL 2021;33(6):E485-E486. doi:10.25270/jic/20.00547

J INVASIVE CARDIOL 2021;33(6):E485-E486. doi:10.25270/jic/20.00547

Key words: Amplatzer occluder device, percutaneous approach, post-MI VSD, transcatheter closure, ventricular septal defect repair


One of the most dreaded complications following myocardial infarction (MI) involves the rupture of infarcted myocardial tissue, often resulting in devastating structural defects, left-to-right shunting, subsequent biventricular failure, and onset of cardiogenic shock. In the absence of reperfusion therapy, the incidence of post-MI ventricular septal defect (VSD) occurs in approximately 1% of patients with ST-elevation MI and in 0.2%-0.34% of patients who receive fibrinolytic therapy.1 Diagnosis of post-MI VSD typically constitutes a surgical emergency; however, the exact timing of intervention relies on several factors in those patients who are considered surgical candidates.2,3 For those deemed too unstable or medically complex to undergo an invasive approach to repair, early case reports suggest feasibility of transcatheter repair with similar postprocedure outcomes.4,5 As transcatheter strategies for repairing complex structural defects become more widely utilized, more research is needed to assess safety and feasibility of this approach in high surgical risk patients with complicated structural defects. 

We report here the transcatheter closure of a large and complex post-MI VSD involving the papillary muscle, measuring 38 mm in its greatest extent, too large to utilize a VSD occluder device (the largest VSD occluder is 24 mm). This necessitated the novel, off-label use of an atrial septal defect (ASD) occluder instead. Use of an Amplatzer ASD occluder for percutaneous VSD closure has been previously reported once.5 Potential complications with this approach of utilizing an ASD device involve the use of narrower waist width (4 mm) vs the VSD occluder, which is designed for a thicker ventricular septum (waist width of 7 mm on the muscular VSD occluder and 10 mm on the postinfarct VSD device). This could potentially cause incomplete apposition against the ventricular walls or a “bulbing” of the device, although this was not observed in this case. 

Long VSD Figure 1


References

1. Mahajan K, Patel H. Myocardial infarction, post infarct ventricular septal rupture. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Sept 11. Available at https://www.ncbi.nlm.nih.gov/books/NBK534873/. Accessed on May 17, 2021.

2. Arnaoutakis GJ, Zhao Y, George TJ, Sciortino CM, McCarthy PM, Conte JV. Surgical repair of ventricular septal defect after myocardial infarction: outcomes from the Society of Thoracic Surgeons National Database. Ann Thorac Surg. 2012;94:436-443.

3. Faccini A, Butera G. Techniques, timing, and prognosis of transcatheter post myocardial infarction ventricular septal defect repair. Curr Cardiol Rep. 2019;21:59. 

4. Holzer R, Balzer D, Amin Z, et al. Transcatheter closure of postinfarction ventricular septal defects using the new Amplatzer muscular VSD occluder: results of a U.S. registry. Catheter Cardiovasc Interv. 2004;61:196-201.

5. Aggarwal M, Natarajan K, Vijayakumar M, et al. Primary transcatheter closure of post-myocardial infarction ventricular septal rupture using amplatzer atrial septal occlusion device: a study from tertiary care in South India. Indian Heart J. 2018;70:519-527.


From the 1Sentara Heart Hospital, 600 Gresham Drive, Norfolk, Virginia; and 2Ocean Lakes Math Science Academy, Virginia Beach, Virginia. 

Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Baran reports consulting income from Getinge, LivaNova, Abiomed, Abbott, MC3, and Procyrion; speaker income from Novartis and Pfizer. Dr Talreja is a member of the speakers’ bureaus for Merck, Pfizer, AstraZeneca, Janssen, Boehringer Ingelheim, and GSK. The remaining authors report no conflicts of interest regarding the content herein.

Manuscript accepted September 15, 2020.

The authors report that patient consent was provided for publication of the images used herein.

Address for correspondence: Ashleigh Long, MD, PhD, Sentara Heart Hospital, 600 Gresham Drive, Norfolk, VA 23507. Email: Ashleighlong2015@gmail.com


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