Complicated Transcatheter Closure of Postinfarction Ventricular Acute Septal Defect

ABSTRACT: The ventricular septal rupture is an uncommon complication of myocardial infarction (MI) with a reported incidence of 0.2% in the thrombolytic era. The outcome remains extremely poor, and surgical defect closure still remains the only therapeutic option improving survival. There are single reports based on a small series of case reports about transcatheter closure of postinfarction ventricular septal defects (VSD) and experience is limited. We present a case of a 71-year-old man with a posteroinferior MI complicated by a ventricular septal rupture with 24 mm width. Due to the severity of the case, surgical approach was denied; we attempted transcatheter closure of the defect in a lifesaving situation. The VSD was partially closed with a 26 mm Amplatzer^® septal occluder (AGA Medical Corp., Plymouth, Minnesota) without adequate expansion of the right disc, due the complexity of the tract. The patient died one day after the procedure.

J INVASIVE CARDIOL 2011;23(10):E244–E246

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Introduction

Ventricular septal rupture incidence decreased to about 0.2% in the thrombolytic era¹, but despite improvements in medical and surgical therapies, this uncommon complication is still associated with a high mortality. Although there is still limited experience, the transcatheter closure of postinfarction ventricular septal defects (VSD) provides new potentials and options for the treatment of this complication.

Case Report. A 71-year-old male presented with a history of dyslipidemia, hypertension and cerebrovascular disease, partly autonomous. He was initially admitted for acute non-ST elevation myocardial infarction (N-STEMI) secondary to anemia of unknown etiology. On the first day of admission he had an episode of posteroinferior MI with ST-elevation. Urgent catheterization was performed, which revealed 90% stenosis of the proximal left circumflex coronary artery and total occlusion of the right coronary artery (RCA) in the middle third, with unsuccessful angioplasty of this artery by the inability to cross the lesion. The patient was hospitalized in a cardiac intensive care unit, where he underwent an echocardiogram that showed no dilated heart chambers, apparently intact septum, inferior wall akinesis, hypokinesis of septal and posterior wall, mild depression of global systolic function (GSF) of the left ventricle (LV), with right ventricle (RV) preserved GSF. During hospitalization, the patient had an episode of pericarditis and extension of the infarction to the RV, which conditioned severe depression of the RV GSF. He showed good clinical response to anti-inflammatory treatment and plasma expanders. On the sixth day post-infarction, he had an episode of severe dyspnea and hypotension with the onset of a holosystolic murmur on left sternal border. The echocardiogram revealed a ventricular septal rupture (Figure 1), measuring 24 mm in the middle third of the posterior interventricular septum (IVS) with left-to-right shunt and a maximum gradient LV/RV of 60 mmHg, severe pulmonary hypertension, and deterioration of LV systolic function.

We started inotropic support with dobutamine and norepinephrine. The Center of Thoracic Surgery was contacted but due to the high probability of intraoperative mortality, a surgical approach was declined. 

Given the clinical deterioration, the patient was transferred on the same day to a hemodynamic center for transcatheter percutaneous closure. A 24 mm defect was measured by transthoracic echocardiography and balloon sizing. Standard right and left heart catheterization was performed to assess the degree of left-to-right shunt (Qp/Qs 2.80) and to measure pulmonary artery pressure and pulmonary vascular resistance. During VSD occlusion, transthoracic echocardiography and fluoroscopic control was performed for device guidance and VSD visualization and assessment.

The femoral artery was punctured and an 8 mm sheath was inserted. The VSD was then crossed from the LV using a diagnostic multipurpose catheter and a hydrophilic long guidewire, which was advanced into the pulmonary artery. The guidewire was then snared and exteriorized out of the right internal jugular vein, thereby establishing an arterial-venous circuit.

A right internal jugular venous access is usually needed for defects located in the mild apical or posterior septum.² The delivery sheath was advanced through the jugular vein into the LV (Figure 2) where the tip of the sheath was placed. After removing the delivery sheath dilator and wire, the loaded flexible Amplatzer^® device (AGA Medical Corp.) was advanced through the delivery sheath across the septal rupture into the LV. The device was pushed partially out of its catheter sheath until release of the first disk. A 24 mm Amplatzer^® muscular VSD occluder was implanted (AGA Medical Corp.), but pulled through into the right ventricle before the detachment. A 26 mm Amplatzer^® septal occluder (AGA Medical Corp.) was then implanted without adequate expansion of the right disk (Figures 3 and 4) due to the long and tortuous tract with residual persistent shunting.

During the procedure, the patient had hemodynamic deterioration and 3rd degree AV block requiring an intra-aortic balloon and temporary pacemaker. Given the reduction of the shunt, we kept the Amplatzer, since we expected that the reduction of the shunt would lead to clinical improvement and better operating conditions for further surgical repair. Unfortunately, the patient died one day after implantation due to multi-organ failure.

Discussion. Ventricular septal defect complicating acute MI is uncommon with a reported incidence of 0.2–0.34% in the interventional era, but there is a lack of research available on the incidence of VSD occurrence.³ It typically occurs in the first week after infarction, with a mean time from symptom onset of 3 to 5 days. Advanced age, anterior infarction location, female sex, no current smoking, hypertension, extensive coronary artery disease, and no previous MI or angina were found to be important predictors of VSD.^1,4,5 A poor prognostic factor in patients with VSD includes development of cardiogenic shock, right ventricular dysfunction, and inferior infarct location.^1,6 The outcome remains extremely poor and 94% of patients treated medically die within 30 days. Surgical defect closure still remains the best therapeutic option for survival, but mortality rates remain high at 20–87% in current cases.³ Current guidelines recommend immediate surgical closure but in some cases transcatheter approach might allow for immediate complete VSD closure or initial hemodynamic stabilization.

The Amplatzer^® devices (AGA Medical Corp.) provide new potentials and options for transcatheter treatment of this complication. The Amplatzer device is a self-expandable, double disk device made from nitinol wire mesh, with dacron polyester patches sewn into each disk and the connecting waist to increase the thrombogenicity of the device.² The self-expanding properties of the device are useful in cases of defect enlargement. The discs extend the waist by 5 to 7 mm. The size of the occluder is determined by the diameter of the waist, which is made to fit the defect. The device selected should be the same size or 1-2 mm larger than the VSD.⁷

Since Lock et al introduced interventional VSD closure, several case reports and some smaller series have been reported on transcatheter closure of postinfarction VSD. However most of the patients underwent VSD closure in the chronic/subacute phase. Consequently, these published cases have an inherent selection bias. In the acute period, patients are often hemodynamically unstable and the defect evolves with fragile margins and ongoing necrosis unlike the chronic phase (3-4 weeks) when the septum becomes fibrotic and the scar develops. This partly explains the high incidence of procedure failure and the observed elevated mortality rate in this stage.

In our case, available VSD occluder device size was not sufficient to fully close the VSD. In consequence, an atrial septal defect (ASD) occluder was used, which led to suboptimal device deployment of the RV disc due to the length of the waist with persistent shunting.

Healing of the infarcted myocardium over time may increase the size of the VSD leading to ASD dislodgement and embolization.³ Other complications of transcatheter approach seem to arise mainly in the acute phase of the procedure and have been described in a small number of patients. They include aortic and tricuspid regurgitation, complete heart block, transient left-bundle-branch block, hemolysis, and perforation.²   

The transcatheter closure of postinfarction VSD might be suitable rather than immediate surgery in patients with simple defects that are < 15 mm.⁸ Complex septal ruptures with irregular, serpiginous tracts as those associated with inferior infarcts tend to have a poor outcome and are not the best candidates for transcatheter closure.⁷

Attempting percutaneous closure in this case was a difficult decision, but given the lifesaving situation we thought this technique might allow initial hemodynamic stabilization and thus gain time for further surgical intervention.

Conclusion. There is still no data indicating that early closure of post-MI VSD can improve survival. Primary percutaneous closure may offer an alternative or an adjunctive treatment to surgery but future multicenter studies and development in devices and delivery techniques are still needed.

References

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2. Moodie DS. Technology Insight: Transcatheter closure of ventricular septal defects. Nat Clin Pract Cardiovasc Med. 2005 Nov; 2(11):592-596.
3. Holger T,  Kaulfersch C, Daehnert I, et al. Immediate primary transcatheter closure of postinfarction ventricular septal defect. European Heart Journal. 2009; 30, 81-88.
4. Feneley MP, Chang VP, O’Rourke MF. Myocardial rupture after acute myocardial infarction: Ten year review. Br Heart J. 1983;49:550-556.
5. Skehan JD, Carey C, Norrell MS, et al. Patterns of coronary artery disease in post-infarction ventricular septal rupture. Br Heart J. 1989;62:268-272.
6. Moore CA, Nygaard TW, Kaiser DL, et al. Postinfarction ventricular septal rupture: The importance of location of infarction and right ventricular function in determining survival. Circulation. 1986;74:45–55.
7. Demkow M, Ruzyllo W, Kepka C, et al. Primary transcatheter closure of postinfarction ventricular septal defects with the Amplatzer septal occluder- immediate results and up-to 5 years follow-up. EuroIntervention. 2005 May;1(1):43-47.
8. Rizwan A. Blauth C. Which patients might be suitable for a septal occluder device closure of postinfarction ventricular septal rupture rather than immediate surgery? Interact Cardiovasc Thorac Surg. 2010;11:626-629.

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From the ¹Department of Cardiology of Tâmega e Sousa Hospital Center E.P.E, Penafiel, Portugal, and ²Department of Cardiology of  São João Hospital E.P.E, Porto, Portugal.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted February 25, 2011, provisional acceptance given March 7, 2011, final version accepted April 20, 2011.
Address for correspondence: Nuno Fernando Morais Moreno,  Rua de Francos nº393 3.1, 4250 – Porto, Portugal E-mail: numoreno@yahoo.com