Transcatheter Closures of a Postinfarction Ventricular Septal Defect and Late Ventricular Pseudoaneurysm

J INVASIVE CARDIOL 2010;22:E132–E137

Key words: ventricular septal rupture    Mechanical complications after acute myocardial infarction (MI) such as ventricular septal rupture and ventricular pseudoaneurysm remain a rare but devastating event despite advances in coronary reperfusion.¹ Although immediate operative repair is the treatment of choice for such events,¹ surgery in patients who have previously undergone cardiac surgery is associated with increased morbidity and mortality,^2,3 and operative mortality for mechanical complications of myocardial infarction (MI) in the acute setting remains high, up to 47%.⁴ With superimposed cardiogenic shock, the true operative mortality for repair of mechanical complications after MI (including repeat sternotomy) may be more than additive and is felt by some surgeons to be prohibitive. Such patients are left with minimal therapeutic options. As the population of the United States continues to age, the number of patients returning with recurrent ischemia and MI after coronary artery bypass is likely to increase.⁵    Since the seminal series published by Landzberg and Lock,⁶ transcatheter repair techniques for post-infarction muscular ventricular septal defects (VSD) have emerged as a viable alternative for such patients. Specific devices are now commercially available such as the Amplatzer muscular VSD closure device (AGA Medical, Golden Valley, Minnesota), while others such as the Amplatzer post-MI muscular VSD occluder are undergoing evaluation. A number of case series have now been published using these^7,8 and other similar devices.^9,10 Though rare, another mechanical complication such as ventricular pseudoaneurysm11 can occur after the same infarction event, and transcatheter repair may be required in patients with prohibitive surgical risk. We describe the first use of both an Amplatzer post-infarction muscular VSD occluder after ST segment elevation myocardial infarction (STEMI) and subsequent repair of a ventricular pseudoaneurysm using an Amplatzer Vascular plug II (AGA Medical) in the same patient.    Case Report. An 83-year-old female with a history of coronary artery disease and diabetes presented to an outside hospital with crushing chest pain radiating down her left arm beginning three days earlier. Past medical history was notable for previous coronary artery bypass grafting with a left internal mammary artery (LIMA) graft to the left anterior descending (LAD) artery and radial graft to the ramus intermedius 15 years prior to this presentation. EKG on arrival revealed ST-segment elevations in the anterior lateral leads prompting emergent left heart catheterization.    The LIMA was occluded and an ulcerated plaque in the native mid-LAD was treated with a 3.0 x 13 mm Cypher drug-eluting stent (Cordis, Johnson and Johnson, Miami Lakes, Florida). During this time, the patient became hemodynamically unstable with systolic pressure falling to 50 mmHg. Inotropes and pressors were intiated, and an intraaortic balloon pump inserted. At the close of the case, a left ventriculogram revealed a large ventricular septal defect. A transthoracic echocardiogram (TTE) confirmed this finding (Figure 1A and B). The patient was transferred to our institution for emergent surgical repair.    On arrival, the patient was in persistent cardiogenic shock with evidence of both renal and liver failure. At that time, she was deemed inoperable due to previous cardiac surgery, advanced age, and shock and initially offered comfort care only. However, after consultation with interventional cardiology, the patient was offered transcatheter closure and taken to the catheterization laboratory six days after the initial STEMI.    In the catheterization laboratory, left ventriculogram and transesophageal echocardiography (TEE) revealed two apical ventricular septal defects (Figures 1C and D), the larger of which measured 14–15 mm, the smaller felt not to be clinically significant (≤ 5 mm). The right ventricle (RV) was markedly enlarged and initial hemodynamics revealed a pulmonary artery (PA) pressure of 60/16, mean wedge pressure 19. An oxygen saturation run noted right atrial (RA) oxygen saturation of 58%, PA 83%, and aortic saturation of 98% (Table 1), producing a calculated QP/QS 3:1.    Under fluoroscopic and transesophageal echocardiography (TEE) guidance, a JR4 catheter was positioned in the left ventricle (LV) to allow a Wholey wire to be advanced into the RV and across the tricuspid valve, and into the RA and inferior vena cava (IVC). From the right internal jugular (IJ), a 25 mm Goose Neck Snare (ev3, Inc., Plymouth, Minnesota) was advanced to the IVC, where the Wholey wire was captured and externalized through the right IJ sheath. An Amplatzer 9 Fr delivery sheath was advanced to “kiss” the JR4 catheter and cross the VSD. An 18 mm AGA Amplatzer post-infarction muscular VSD occluder was placed across the septum and appeared well-seated (Figures 1E and F). TEE confirmed placement and occlusion of the larger VSD, with some residual flow remaining through the more apical smaller VSD.    Post-deployment hemodynamics and saturations (Table 1) revealed significant improvement with a PA pressure 34/20, wedge pressure 18, RA oxygen saturation of 71%, PA saturation of 73%, and aortic saturation of 100% and decrease in QP/QS to 1.3:1. She was discharged two weeks later following extubation, weaning of pressors/inotropes, and recovery of renal and hepatic function.    Four months later, the patient presented with recurrent chest pain radiating to the back to an outside hospital. CT angiogram ruled-out pulmonary embolus, but extravasation of contrast from the LV was noted suggesting rupture or pseudoaneurysm. The patient was transferred to our hospital for further evaluation and treatment.    Two-dimensional, contrast-enhanced transthoracic echocardiography (TTE) and repeat CT evaluation confirmed the presence of left ventricular (LV) pseudoaneurysm and demonstrated enlargement when compared to films from the outside hospital (Figure 2). The pseudoaneurysm neck was measured approximately 6–8 mm in length. Although surgical evaluation was requested, the patient did not wish to undergo surgery and was instead offered a second transcatheter procedure, this time to treat the pseudoaneurysm.    In the catheterization laboratory, the stented segment and remaining coronaries were patent. Initial left ventriculography revealed a pseudoaneurysm near the apex of the anterior wall. The pseudoaneurysm was directly cannulated using a JR4 interventional guiding catheter over a Rosen wire. Direct injection of the pseudoaneurysm revealed a segmented structure with an isthmus of 6–8 mm in length and and several partitioned segments (Figure 3A). A 10 mm Amplatzer vascular plug II was introduced into the pseudoaneurysm such that the distal plate deployed in the distal septated portion and the middle plate fell in the more proximal chamber. The proximal plate fortuitously deployed in the isthmus (Figure 3B). Repeat left ventriculography in the RAO position revealed stable positioning of the device with slight penetration of contrast into the isthmus and the pseudoaneurysm effectively occluded (Figure 3C). The previously unclosed ≤ 5 mm distal apical VSD persisted, and the post-MI VSD closure device remained well-seated with near complete occlusion of the larger VSD (Figure 3D).    Repeat cardiac CT the next day showed no further progression of the pseudoaneurysm and stable position of both the vascular occluder and VSD occluder. She was discharged to home in stable condition and on six month follow up was found to have minimal functional limitation. Repeat TTE one year later revealed stable positioning of the closure devices and no residual VSD shunts or pseudoaneurysm with an ejection fraction of 45–50%.    Discussion. Mechanical complications of acute MI remain a rare but devastating event despite advances in coronary reperfusion,^12,13 with ventricular septal rupture occurring at a rate of 0.2–0.34 percent in an analysis of the GUSTO-I trial.⁴ The American College of Cardiology and American Heart Association consensus guidelines recommend immediate surgical repair for post-infarction VSD.¹ However, 30-day mortality despite surgical repair has been reported to be 37%,¹⁴ and in-hospital mortality in the setting of cardiogenic shock as high as 58%.¹⁵ Worse yet, medical management is associated with a one week mortality of nearly 50%13 and 94% mortality at 30 days.⁴ Even patients who initially appear hemodynamically stable may develop sudden clinical deterioration and hemodynamic collapse making delay of definitive treatment a precarious management position.    The case presented raised three major issues: First, the increasing demand for transcatheter repairs for post-MI VSD patients who are not surgical candidates; second, the clinical issues of transcatheter repair of a post-infarction VSD in a critically ill patient; and third, repair of a second related defect, left ventricular pseudoaneurysm, in the same patient. We review the literature for each of these issues.    In this particular case, only transcatheter repair could be offered as the operative risk of cardiac surgery was felt to be prohibitive due to advanced age (83 years old), repeat sternotomy, and advanced cardiogenic shock. Indeed, as the age of the U.S. population continues to increase, the number of Americans older than 65 is expected to double by 2030 with those older than 85 expected to reach 9.6 million.⁵ As such, the number of patients with prior cardiac surgery will also increase. Repeat cardiac surgery increases in-hospital mortality threefold with even higher operative risk in octogenarians.¹⁶ Similarly, cardiogenic shock in the setting of post-infarction VSD is associated with a dismal prognosis when treated with surgical repair (58–81% mortality) or medical therapy (96% mortality).^15,17 Unfortunately, advanced age is associated with higher risk of post-infarction ventricular septal rupture⁴ as is cardiogenic shock.¹⁷ The morbidity and mortality of transcatheter repair of a post-infarction VSD in such a patient, however, is also significant.    Results from the first U.S. registry for the Amplatzer post-infarction muscular VSD device reported a 30-day mortality of 28%, however, 56% of these patients had previously undergone surgical closure, with the median time from presentation was 25 days.⁷ Indeed, timing of repair after rupture, both in open surgical and primary transcatheter approach, has been controversial, with some favoring delay of up to 3 ½ weeks.^8–10 The post-infarction septum is felt to be vulnerable to further necrosis producing expansion of the VSD in the early phase, leading to failure in anchoring the device, residual shunt, continued congestive heart failure, and cardiogenic shock. In contrast, others have advocated early closure1,^18–20 suggesting that extended time from presentation to repair is associated with poorer outcome. Alternatively, ventricular assist devices such as the Tandem Heart (Cardiac Assist, Inc. Pittsburgh, Pennsylvania) have been used as a bridge to delay repair until the myocardium has healed or undergone fibrosis.^21–24 Regardless of timing, patients in refractory or progressive cardiogenic shock must be treated aggressively, as in this case.    During transcatheter closure of a post-MI VSD, ventricular rupture and cardiac tamponade is a catastrophic adverse outcome, whether iatrogenic or as a result of the disease process.^7,9,25 Following pericardial drainage and stabilization, the operator is faced with repair of a second defect, with similarly prohibitive surgical risk. In the present case, while no iatrogenic perforation occurred, a second defect emerged several months later in the form of a ventricular pseudoaneurysm, likely also a result of the inciting MI. This defect was closed using an Amplatzer Vascular Plug. Indeed, experience with transcatheter closure of free wall rupture or ventricular pseudoaneurysm has been far more limited. Eshtehardi et al recently described closure of an iatrogenic left ventricular free wall rupture during an attempt to close a post-infarction VSD. During placement, the device perforated the postero-lateral wall and deployed into the pericardial space. Following emergent pericardiocentesis, the same device was then successfully redeployed to occlude the perforation and closure of the VSD was completed using a second device.²⁵ Other innovative techniques to successfully close ventricular perforation or pseudoaneurysm have included the use of EV3 AXIUM detachable coils (ev3 Endovascular, Inc. Peripheral Vascular, Plymouth, Minnesota),²⁶ an Amplatzer Muscular VSD Occluder (AGA Medical Corp.),^27–29 Amplatzer ASD occluder (AGA Medical Corp.),^30–34 direct injection of fibrin glue (Beriplast, CSL Behring, King of Prussia, Pennsylvania) into the pericardial space,³⁵ and closure of a right ventricular perforation using an Angio-Seal femoral closure device (St. Jude Medical, St. Paul, Minnesota).³⁶ Direct RV puncture and placement of a vascular device has been reported in the context of a hybrid operating room/catheterization lab (Personal Communication, P Loyalka). To the best of our knowledge, the present case is the first report of the use of an Amplatzer post-MI VSD occluder and Vascular Plug to repair a VSD and ventricular pseudoaneurysm in the same patient.    Limitations. A major limitation of the literature regarding transcatheter repair of mechanical complications of acute MI is the low frequency of events. As such, producing a randomized-controlled trial may not be feasible. Nevertheless, the need for transcatheter techniques continues to grow, and future studies regarding optimal techniques will be required. From the Cardiovascular Division, Departments of Medicine and *Pediatrics, Washington University School of Medicine, St Louis, Missouri. Dr. Lin is supported by NIH NRSA 2-T32-HL007081-32. Dr. Balzer is a proctor for AGA Medical. Dr. Lasala is a speaker for AGA Medical. Manuscript submitted December 14, 2009 and accepted January 4, 2010. Address for correspondence: C. Huie Lin, MD, PhD, Washington University School of Medicine, 660 S. Euclid Avenue, Campus Box 8086, St Louis, MO 63110. References

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