Ann Thorac Surg 2005;80:1907-1909
© 2005 The Society of Thoracic Surgeons
Case report
Transcatheter Repair of Recurrent Postinfarct Ventricular Septal Defects
Nirav R. Shah, BA
a
,
Jeffrey A. Goldstein, MD
b
,
David T. Balzer, MD
b
,
John M. Lasala, MD, PhD
b
,
Nader Moazami, MD
a
,
*
a Division of Cardiothoracic Surgery, Washington University School of Medicine, St. Louis, Missouri, USA
b Division of Cardiology, Washington University School of Medicine, St. Louis, Missouri, USA
Accepted for publication June 4, 2004.
* Address correspondence to Dr Moazami, Washington University School of Medicine, Division of Cardiothoracic Surgery, Queeny Tower, Suite 3108, One Barnes-Jewish Hospital Plaza, St. Louis, MO63110 (Email: moazamin{at}msnotes.wustl.edu).
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Abstract
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Surgical repair of recurrent postmyocardial infarction septal defect is associated with a high mortality rate. We present 2 patients whose recurrent defects were closed percutaneously using an Amplatzer device.
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Introduction
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A ventricular septal defect (VSD) occurs in 1% to 2% of acute cases of myocardial infarction (MI) [1]. Emergent cardiac surgery continues to provide the best option for long-term survival; however, large residual or recurrent VSDs occur in 10% to 20% of patients who survive the initial surgery. Reoperation for repair confers an additional mortality of 13% to 31% [2–4]. A transcatheter approach for repair of a recurrent VSD offers an alternative option for management of these patients. Devices originally designed for closure of patent foramen ovale and atrial septal defects have been modified for closure of muscular VSDs. We present 2 patients who underwent repair of recurrent post–MI VSD with an Amplatzer device.
A 63-year-old man presented to an outside hospital with an acute inferior posterior MI and was treated with thrombolytics. Sixteen hours later, respiratory distress developed. Transthoracic echocardiogram (TTE) confirmed the presence of a VSD in the midseptal location with a calculated Qp/Qs of 5.3. The VSD was repaired through a left ventricular approach with a two-patch technique. Intraoperatively, there was significant bleeding from the ventriculotomy site requiring placement of additional pledgetted mattress sutures, reinforcement with topical glue, and packing with Surgicel (Ethicon Inc, Somerville, NJ). The initial postoperative course was uneventful, and the patient was extubated. Twelve days later, he had respiratory distress necessitating reintubation. A TTE demonstrated a recurrent VSD with a Qp/Qs of 2.54. The patient was transferred to our institution for reoperation. Given the difficulty of the initial surgery, it was decided to proceed with percutaneous closure of the VSD. A balloon-tipped end-hole catheter was placed in the left ventricle from the right femoral artery and directed through the VSD into the right ventricle. A 0.035-inch guidewire was advanced through this catheter into the pulmonary artery. An Amplatz Goose Neck Snare (Microvena, White Bear Lake, MN) was then advanced from the right femoral vein (RFV). The guidewire was snared and externalized through the RFV. After the balloon-stretched diameter of the VSD was determined (Fig 1), a 22-mm Amplatzer postinfarction device was successfully delivered through a 12F sheath in the RFV. The next day, it was possible to wean the patient from the ventilator and dobutamine therapy. He was discharged 1 week later and at 1 month follow-up was in New York Heart Association (NYHA) functional class II. Repeat TTE demonstrated mildly decreased biventricular function. The Amplatzer device was in appropriate position (Fig 2). Peridevice flow was barely detectable with Doppler color flow imaging.
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Fig 2. Follow-up transthoracic echocardiogram demonstrating appropriately positioned ventricular septal defect device (arrow).
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The second patient, a 62-year-old man, presented to an outside hospital with an acute inferoposterior MI complicated by a VSD and cardiogenic shock. He underwent emergent surgical repair of the VSD by David's infarct exclusion technique. He gradually improved and was discharged home 2 weeks later with no evidence of residual VSD by TTE. One month after his infarct, he was readmitted with hypotension and congestive heart failure. An echocardiogram demonstrated recurrent VSD with a Qp/Qs of 2.2. His VSD was closed using a 10F Amplatzer delivery sheath with a 20-mm Amplatzer postinfarction VSD device. At 1 month follow-up he had been discharged home and had NYHA class II symptoms. Color Doppler imaging demonstrated small peridevice shunt flow.
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Comment
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Early surgical repair of post–MI VSDs provides the best prognosis for patients; however, 5% to 11% of cases are complicated by a recurrence of the VSD [5]. That may largely be due to infarct extension, which may compromise the integrity of the surgical repair and lead to patch dehiscence, or create a new VSD beyond the margins of the surgically repaired area.
Recurrence of a VSD may result in an abrupt decline in the patient's clinical status with the onset of congestive heart failure and cardiogenic shock. Most of these patients are early in their postoperative course and still have a varying degree of ventricular dysfunction that puts them at a high risk for reoperation. Given the poor clinical status of patients and the high morbidity and mortality of reoperation, an effective percutaneous approach would be ideal.
Outcomes of percutaneous closure methods have been mixed. Early closure of post–MI VSDs has generally been associated with poor outcomes, likely related to continued tissue necrosis and extension of the primary defect, resulting in incomplete closure [6]. The application of percutaneous methods to defects that have been previously repaired surgically has been more promising [7, 8]. This may likely be due to the maturation of the margin between viable and necrotic tissue, allowing for better closure of the VSD. In addition, the patch may provide a better anchor for the device.
This study reports our initial experience with the Amplatzer postinfarction device in the treatment of 2 patients who presented with a residual post–MI VSD after initial surgical correction. The successful delivery and deployment of the device allowed closure in both cases. Consistent with previous reports, there was persistent echocardiographic evidence of shunting in both patients, likely reflecting the complex anatomy of recurrent septal defects as well as deficiencies in the current generation of devices to achieve complete closure of these defects. Nonetheless, both patients had dramatic improvement in their clinical status and were discharged home.
In summary, percutaneous closure of post–MI VSDs initially corrected by surgical repair is a promising alternative to surgery in clinically debilitated patients. Improved understanding of mechanisms and anatomy of recurrent VSDs will likely lead to better devices and improved ability to achieve complete closure and decrease peridevice leak. An ongoing evaluation of this approach is needed to establish the safety and long-term effectiveness of these devices. Known pitfalls include incomplete closure, embolization, perforation, and bleeding at the access site. Contraindications include endocarditis, nickel allergy, or end-organ damage making recovery unlikely. In the interim, in view of the high mortality rate associated with reoperation for recurrent VSDs, the percutaneous method seems to be a viable option if the anatomy of the defect is favorable.
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References
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- Skillington PD, Davies RH, Luff AJ, et al. Surgical treatment for infarct-related ventricular septal defectsimproved early results combined with analysis of late functional status. J Thorac Cardiovasc Surg 1990;99:798-808.[Abstract]
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Abstract
Introduction
