Acute ventricular septal rupture - ventricular septal defect (VSD) following acute myocardial
infarction remains a critical condition. We present an 80 year-old patient with an acute VSD
following an acute inferior myocardial infarction. Percutaneous VSD closure with an
Amplatzer ventricular septal occluder (AVSO) was performed successfully, two days after
initial admission. In-hospital follow-up was uneventful.
We speculate that percutaneous VSD closure with an AVSO can be an alternative to surgical
correction for these patients. Despite the impressive result, this innovative approach needs
further investigation and refinements before it can be recommended as the treatment of choice
for acute ischemic VSD. (Cardiol J 2007; 14: 411-414

Bilodeau, Luc

Ibrahim, Reda

Waciński, Piotr

English

Via Medica Journals

411www.cardiologyjournal.orgCASE REPORTCardiology Journal2007, Vol. 14, No. 4, pp. 411–414Copyright © 2007 Via MedicaISSN 1897–5593Address for correspondence: Piotr Waciński, MDDepartment of Cardiology, Lublin Medical UniversityJaczewskiego 8, 20–950 Lublin, PolandTel: +48 81 724 42 56; e-mail: piotr.wacinski@onet.plReceived: 19.12.2006 Accepted: 28.04.2007Successful early percutaneous closureof acute ventricular septal rupture complicatingacute myocardial infarction withAmplatzer ventricular septal occluderPiotr Waciński1, Luc Bilodeau2 and Reda Ibrahim21Department of Cardiology, Lublin Medical University, Lublin, Poland2Montreal Heart Institute, 5000 Belanger East, Montreal H1T1C8, Quebec, CanadaAbstractAcute ventricular septal rupture — ventricular septal defect (VSD) following acute myocardialinfarction remains a critical condition. We present an 80 year-old patient with an acute VSDfollowing an acute inferior myocardial infarction. Percutaneous VSD closure with anAmplatzer ventricular septal occluder (AVSO) was performed successfully, two days afterinitial admission. In-hospital follow-up was uneventful.We speculate that percutaneous VSD closure with an AVSO can be an alternative to surgicalcorrection for these patients. Despite the impressive result, this innovative approach needsfurther investigation and refinements before it can be recommended as the treatment of choicefor acute ischemic VSD. (Cardiol J 2007; 14: 411–414)Key words: myocardial infarction, acute ventricular septal defect, Amplatzerventricular septal occluderIntroductionDespite substantial improvements in surgicaland interventional cardiology techniques for thetreatment of acute myocardial infarction (AMI),acute ventricular septal rupture — ventricular sep-tal defect (VSD) remains a challenging clinical con-dition associated with high mortality and morbidi-ty. There is acute ischemic insult and loss of thestructural integrity of the interventricular septumthat is, as is very well documented, essential for par-titioning and providing mechanical support for bothventricles in the setting of AMI [1]. The interven-tricular septum also actively participates in theintracardiac conduction system [2, 3]. The conse-quences of an acute VSD include right ventricularfailure, atrioventricular block, biventricular failureand, ultimately, cardiogenic shock. Two types ofacute VSD are presently recognised, namely a sim-ple direct perforation or a complex multifocal com-munication with a serpiginous course [4].The Amplatzer ventricular septal occluder(AVSO), a self-expandable, self-centring wire-meshdouble disc with a connecting central stent part(AGA Medical Corporation, Golden Valley, Minne-sota, USA), has been shown to be effective in thetreatment of congenital VSD, muscular VSD andsome membranous VSD from 4 to 20 mm [5–7]. Thedevice is now available in sizes of 6–24 mm that aredelivered through 6 to 9 French sheaths [5–7].Despite its success in congenital VSD, AVSO implan-tation faces a challenge in acute ischemic VSD inview of the location of the rupture, the underlyingtissue quality (ischemic and/or necrotic) and, quitecommonly, an already failing right ventricle.412Cardiology Journal 2007, Vol. 14, No. 4www.cardiologyjournal.orgCase descriptionWe present an 80 year-old patient with a histo-ry of hypertension but without previous cardiac prob-lems. He was admitted for an acute inferior wallmyocardial infarction 6 hours after the onset of chestpain. Initial troponine T serum level was noted at 0.35mg/l (N < 0.03 mg/l). On physical examination a loudholosystolic murmur was heard at the lower left ster-num border. Following this finding, initial echocar-diography was performed and a muscular VSD witha gradient of 55 mm Hg was described. Ejection frac-tion (EF) was calculated at 60% with akinetic inferi-or wall and right ventricle dilatation of up to 49 mm.The day after this the patient was referred to ourinstitution for coronary angiography and VSD treat-ment. The coronary angiogram demonstrated a nor-mal left main artery, non-significant atherosclerot-ic changes in the left anterior descending and verydistal left circumflex  80% stenosis. The dominantright coronary artery was normal. The left ven-triculography presented a VSD in the inferior sep-tum with an estimated EF of 55% (Fig. 1). Cardiacoutput was calculated at 3.19 l/min with a cardiac in-dex of 1.92 l/min/m2. Qp/Qs was estimated at 1.67.The VSD diameter was estimated to reach 13–14 mmwith a definite left-to-right shunt (Qp/Qs = 1.8) andright ventricular dilatation.After discussion with the patient and our car-diac surgeons and in consideration of the respec-tive interventional and surgical risks of VSD clo-sure it was decided to proceed with percutaneousclosure.  Before the procedure the patient received80 mg of Gentamycine IV and 2 g of Cefazoline IVfor endocarditis prophylaxis as well as 8000 U ofUFH. Then, general anesthesia was initiated withFentanyl IV and 8 F right femoral vein and 5 F rightfemoral artery introducer sheaths were inserted.A 5 F Pigtail 155° catheter was advanced into theleft ventricle. The VSD was measured before theprocedure with transesophageal echocardiography(TEE) in the LAX view (VSD of 13–14 mm of dia-meter) for AVSO device size selection. An ExtraStiff 260 cm guidewire was inserted via the rightfemoral artery across the aortic valve, the VSD andthe pulmonic valve, landing in the pulmonary artery.This wire was exteriorised from the right intimaljugular vein using a Microvena snare wire.A 20 mm AVSO was inserted via the right jug-ular vein and advanced in the VSD and deployedunder TEE guidance. Control left ventriculographyshowed a successful deployment with only minimalnon-significant residual shunting (Fig. 2). This resultwas also confirmed by TEE (Fig. 3). Subsequently leftand right ventricular pressures dropped from 110/0–20to 99/0–20 mm Hg and from 50 mm Hg/19 mm Hgto 34 mm Hg/13 mm Hg respectively. Cardiac out-put and index rose to 7.9 l/min and 4.62 l/min/m2respectively. Post-procedural and hospital follow-upwas uneventful. Six days later the patient was dis-charged. Endocardial prophylaxis was maintainedfor one year. Clopidogrel was prescribed for6 months and acetylsalicylic acid indefinitely.Figure 1. Left ventriculogram with ventricular septal de-fect (arrow).Figure 2. Amplatzer ventricular septal occluder in place.No para-device leak. Transesophageal echocardiogra-phy probe above.413Piotr Waciński et al., Successful early percutaneous closure of acute ventricular septal rupturewww.cardiologyjournal.orgDiscussionPatients with post-AMI VSD may benefit froma relatively quick and simple closure which mayallow hemodynamic stabilisation and survival. Thisprocedure can be performed as the definitive ther-apy, as in the patient discussed here, or as a bridgeto future surgical correction in optimal conditions.There are few reports on the efficacy of acute VSDtreatment. Thielle et al. [8] describe a series of23 patients with acute VSD who were surgicallytreated with prior insertion of an intra-aortic bal-loon pump (IABP). The mean age of the patientswas 72 ± 10 years (ranging from 46 to 89) and theinterval from the onset of AMI to the detection ofVSD was 4 ± 4 days (ranging from 1 to 14). At thetime of enrolment 12 patients were in cardiogenicshock (52%). The mean duration of IABP supportwas 10.8 ± 9.5 days (ranging from 1 to 25) and20 patients (87%) underwent surgical closure of theVSD [8]. In the work of Thielle et al. [5] early sur-gical closure because of cardiogenic shock result-ed in an ominously high mortality rate of 83%. Themortality rate in a hemodynamically stable groupwith IABP with delayed surgery was at 29%.  Over-all, perioperative mortality was 45%. Crenshawet al. [9], in the largest study of VSD, describedthe outcomes of patients with VSD complicatingAMI in the GUSTO 1 trial. Mortality with this com-plication remains extremely high despite improve-ments in medical therapy. Patients who underwentsurgical repair had a lower mortality at 30 days andone year then the patients who were treated med-ically: 47% vs. 94% at 30 days (p < 0.001) and 53%vs. 97% at 1 year (p < 0.001). Mortality rates for allpatients with VSDs were similar at 30 days and oneyear (74% and 78%). These data suggest that if thepatient survives the initial treatment, the long-termprognosis is relatively good [9]. Similarly, Landz-berg and Lock [10] reported that, despite improve-ments in the surgical management of ventricularseptal rupture after AMI, perioperative risk may beexcessive for some patients. They suggested thatoptimal management of patients with post-MI ven-tricular septal rupture requires surgical-medical col-laboration and treatment selection based on individu-al patients. In a registry in the USA, of 18 patients withtranscatheter closure of post-infarction VSD with anAmplatzer muscular VSD occluder, the 28 day-mor-tality was 28%. Five patients underwent the closurein the acute phase within 6 days of infarct; the re-maining patients underwent closure at any time from14 to 95 days after diagnosis [11].ConclusionsIn the current American College of Cardiolo-gy/American Heart Association guidelines urgentsurgery is recommended for acute ventricular sep-tal defect regardless of hemodynamic status [12].Despite an inherent high mortality risk, surgicalventricular septal defect correction remains a life-saving procedure that cannot be deferred [13, 14].Acute ventricular septal defect closure with theAmplatzer ventricular septal occluder may, however,represent a viable alternative for these patients.Nevertheless, long-term safety studies are requiredbefore this technique becomes widely used in rou-tine clinical practice. The obvious heterogeneity oflocation and anatomy of ischemic ventricular sep-tal defect calls for refinements in the technique andocclusive devices.Despite the very encouraging result of this in-novative approach, further data, namely larger seriesand long-term follow-up, need to be collected beforewe may change our current treatment options.References1. Banka VS, Agraval JB, Bodenheimer MM et al. In-terventricular septal motion; biventricular angio-graphic assessment of this relative contribution toleft and right ventricular contraction. Circulation,1981; 64: 992–996.Figure 3. Final result. Amplatzer ventricular septal occlu-der in place. Transesophageal echocardiography probeabove.414Cardiology Journal 2007, Vol. 14, No. 4www.cardiologyjournal.org2. Vlodaver Z, Edwards JE. Rupture of ventricular sep-tum or papillary muscle complicating myocardial in-farction. Circulation, 1977; 55: 815–822.3. Topaz O, DiSciascio G, Vetrovec GW. Septal perfo-rator arteries: from angiographic-morphologic char-acteristics to related revascularisation options. AmHeart J, 1992; 124: 810–815.4. Topaz O, Mallon SM, Chahine RA et al. Acute ven-tricular septal rupture: angiographic features andclinical assessment. Chest, 1989; 95: 292–298.5. Tofeig M, Patel RG, Walsh KP. Transcatheter clo-sure of a mid-muscular ventricular septal defect withan Amplatzer VSD occlusion device. Heart, 1999;81: 438–440.6. Thanopoulos BD, Tsaousis GS, Konstadopoulou GNet al. Transcatheter closure of muscular ventricularseptal defects with the Amplatzer ventricular septaldefect occluder: Initial clinical applications in chil-dren. J Am Coll Cardiol, 1999; 33: 1395–1399.7. Hijazi ZM, Hakim F, Al-Fadley F, et al. Transcatheterclosure of single muscular ventricular septal defectsusing the Amplatzer muscular ventricular septal de-fect occluder: Initial results and technical considera-tions. Cathet Cardiovasc Interv, 2000; 49: 167–172.8. Thiele H, Lauer B, Hembrecht R et al. Short- andlong-term hemodynamic effects of intraaortic balloonsupport in ventricular septal defect complicating acutemyocardial infarction. Am J Cardiol, 2003; 92: 450–454.9. Crenshaw BS, Granger CB, Birnbaum Y et al. Forthe GUSTO-I (Global Utilization of Streptokinaseand TPA for Occluded Coronary Arteries) Trial In-vestigators. Risk factors, angiographic patterns, andoutcomes in patients with ventricular septal defectcomplicating acute myocardial infarction. Circulation,2000; 101: 27–32.10. Landzberg MJ, Lock JE. Transcatheter management ofventricular septal rupture after myocardial infarction.Semin Thorac Cardiovasc Surg, 1998; 10: 128–132.11. Holzer R, Balzer D, Amin Z et al. Transcatheter clo-sure of postinfarction ventricular septal defects us-ing the new Amplatzer muscular VSD occluder: re-sults of a U.S. registry. Catheter Cardiovasc Interv,2004; 61: 196–201.12. Ryan TM, Antman EM, Brooks NH. ACC/AHAguidelines for the management of patients with acutemyocardial infarction: A report of the American Col-lege of Cardiology/American Heart Association TaskForce on Practice Guidelines (Committee on theManagement of Acute Myocardial Infarction). J AmColl Cardiol, 199; 34: 890–911.13. Boden WE. Is it time to reassess the optimal timingof coronary artery bypass graft surgery following acutemyocardial infarction? Am J Cardiol, 2002; 90: 35–38.14. Topaz O. The enigma of optimal treatment of acuteventricular septal rupture. Am J Cardiol, 2003; 92:419–420.

Successful early percutaneous closure of acute ventricular septal rupture complicating acute myocardial infarction with Amplatzer ventricular septal occluder

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Successful early percutaneous closure of acute ventricular septal rupture complicating acute myocardial infarction with Amplatzer ventricular septal occluder

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