Transcatheter Closure of Postinfarction Ventricular Septal Rupture
with the Amplatzer® Occluder

Mechanical complications comprise the second leading cause of in-hospital mortality in patients with ST-segment elevation myocardial infarction (STEMI), especially in the elderly.¹ Among them, ventricular septal rupture (VSR) complicates approximately 0.2% of STEMI cases and is associated with very high mortality.² It usually occurs within 1 week, primarily within the first 24 hours of symptom-onset.
Historically, surgical repair has been the only accepted treatment, but it carries a very high perioperative mortality risk and is therefore applied only to very selected patients.³ In recent years, percutaneous closure of postinfarction VSR has been proposed as an alternative to surgical repair and even to the conservative approach. However, experience in percutaneous closure of postinfarction VSR is very limited and restricted to very selected patients.^4,5 We report the case of a 77-year-old female with postinfarction VSR who was not considered suitable for surgical repair and thus was treated with percutaneous closure using an Amplatzer device.

 
Case Report. A 77-year-old female with a previous history of atrial fibrillation and breast cancer 15 years prior presented to the emergency department 18 hours after the onset of substernal pain and dyspnea. Electrocardiography showed ST-segment elevation at the precordial leads consistent with acute anterolateral STEMI (Figure 1). Cardiopulmonary examination revealed a pansystolic murmur at the left sternal border and bilateral basilar rales. Echocardiography showed akinetic apical and anterior segments, with moderately impaired left ventricular function and a large anterior interventricular septal defect. Cardiac surgeons were contacted, but the patient was considered unsuitable for surgical repair due to her extremely high perioperative risk. Percutaneous closure of the VSR was thus considered as a compassionate therapy for this patient.
At the beginning of the procedure, the patient presented with hypotension and pulmonary edema requiring orotracheal intubation and mechanical ventilation. Also, an intra-aortic balloon pump counterpulsation (IABP) was implanted (left femoral artery), and intravenous inotropes were administered. The procedure was performed under transesophageal echocardiography guidance.

The right femoral artery and right jugular vein were catheterized. A 0.35 inch wire was inserted through the right femoral artery and inserted at the left ventricle. It was advanced through the VSR to the right ventricle, right atrium and right jugular vein (Figure 2A). An interatrial septal defect 35 mm Amplatzer^® device (AGA Medical, Plymouth, Minnesota) was advanced through the 0.35 inch wire to the right ventricle and then to the left ventricle (Figure 2B) (the Amplatzer device which is especially designed for VSR repair was not available at our institution at the time of this procedure). The left side of the device was deployed first at the left ventricle, then the right side at the right ventricle (Figure 2C). After confirming its optimal position in the VSR, the device was finally deployed (Figure 2D). Left ventriculography showed a persistent, moderate leftto- right shunt.
The patient’s hemodynamics improved and remained stable 24 hours after the procedure, but still required the IABP and IV inotropic therapy. Transthoracic echocardiography performed the following day showed the Amplatzer device correctly positioned across the VSR and a minor residual shunt, but with persistence of severe tricuspid regurgitation and moderately impaired biventricular function (Figures 2A and B). Two days after admission to the hospital, the patient suddenly developed cardiogenic shock and cardiac arrest, and died despite advanced resuscitation maneuvers.

Discussion. Early surgical repair is the traditional approach for postinfarction VSR, but due to the significant perioperative risk for these patients, percutaneous closure has been considered an alternative treatment in some, especially for those with a very high surgical risk.^4,5 In some cases, transcatheter closure of postinfarction VSR may provide short-term hemodynamic stabilization allowing elective surgical repair with a more favorable hemodynamic profile and lower surgical risk. However, the aim of percutaneous closure in these patients is to obtain a significant reduction or elimination of the shunt with subsequent hemodynamic stabilization to prevent death.³
Our patient was a very high-risk candidate due to her advanced age and presence of cardiogenic shock with impaired biventricular function. She was thus considered unsuitable for surgical repair, and percutaneous closure was performed as a compassionate procedure. The device was successfully deployed, but the patient continued to experience hemodynamic impairment and died within 48 hours after device implantation.

The case described here illustrates, therefore, that postinfarction VSR is associated with a very high rate of morbidity and mortality, especially when associated with advanced age, cardiogenic shock, inferior MI, morphologically complex septal defects and right ventricular dysfunction. The outcome of most patients with postinfarction VSR and multiple risk factors who are treated with percutaneous closure is very unfavorable, with most dying due to cardiogenic shock.
Experience with percutaneous closure post-MI is limited and primarily based on case reports. One of the few large series of post-MI VSR transcatheter closure procedures was reported by Landzberg and Lock.^6,7 Between 1990 and 1998, they performed percutaneous closure of post-MI VSRs in 18 patients using the clamshell double umbrella, and later on, the CardioSEAL device (NMT Medical, Boston, Massachusetts). Eleven of these patients had undergone prior attempted surgical VSR closure. Of 7 patients treated with primary percutaneous closure, 4 died within 1 week of the procedure, and the only survivors where the 3 with chronic VSRs treated late after the initial infarction at a time when the chance of survival is significantly better than in the acute phase.
Better clinical results were obtained by Holzer et al,³ who prospectively collected data on 18 patients who underwent attempted device closure of postinfarction VSRs between 2000 and 2003. Device deployment across the VSR was initially successful in 16 patients, with a 30-day mortality rate of 28%. However, this population was at a relatively low risk, since only 5 patients were in the acute phase of MI, and only 10% were in cardiogenic shock at the beginning of the procedure.
In a more recent series,⁸ 22 procedures to close postinfarction VSRs were carried out in 19 patients using Amplatzer devices. The procedure was successful in 14 patients, 11 of whom had subacute postinfarction VSRs (between 3, 5 and 12 weeks after the infarction), 1 with a chronic VSR (more than 12 weeks after the infarction), and 2 with postsurgical VSRs. None of the patients with acute VSR who underwent the procedure survived. These results demonstrate that optimal treatment for acute VSR has yet to be determined.⁹
Transcatheter closure of VSRs using an Amplazter septal occluder may be the treatment of choice in patients with subacute VSR. Further trials are required to assess the medium- and long-term efficacy of percutaneous closure of VSRs and to compare the results with those of surgical closure.¹⁰
Acknowledgements. The authors wish to thank Dr. Ángel Sánchez-Recalde, who assisted in performing the procedure, and Drs. Ruíz-Cantador and Filgueiras for their clinical support in this case.

References

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