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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 6  |  Issue : 2  |  Page : 172-175

Device closure of postmyocardial infarction ventricular septal rupture – Winning the battle but losing the war!


Department of Cardiology, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India

Date of Submission18-Jul-2020
Date of Decision18-Jul-2020
Date of Acceptance22-Jul-2020
Date of Web Publication27-Aug-2020

Correspondence Address:
Dr. Dibbendhu Khanra
Department of Cardiology, All India Institute of Medical Sciences, Rishikesh, Uttarakhand
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jpcs.jpcs_29_20

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  Abstract 


Ventricular septal rupture (VSR) after acute myocardial infarction is rare and associated with high mortality despite surgical repair. Percutaneous transcatheter device closure has emerged as an alternative to surgical repair in high-risk patients or as a bridge to delayed surgical repair. Not only the timing but also the morphology of defect matters, and in patients with serpiginous ventricular septal defect, device deployment is challenging. We report a patient with cardiogenic shock due to serpiginous VSR following myocardial infarction who underwent percutaneous transcatheter device closure successfully but expired on the 3rd day following the procedure due to sepsis and multiorgan failure.

Keywords: Cardiogenic shock, multiorgan failure, percutaneous transcatheter device closure, sepsis, ventricular septal rupture


How to cite this article:
Khanra D, Soni S, Duggal B. Device closure of postmyocardial infarction ventricular septal rupture – Winning the battle but losing the war!. J Pract Cardiovasc Sci 2020;6:172-5

How to cite this URL:
Khanra D, Soni S, Duggal B. Device closure of postmyocardial infarction ventricular septal rupture – Winning the battle but losing the war!. J Pract Cardiovasc Sci [serial online] 2020 [cited 2020 Sep 26];6:172-5. Available from: http://www.j-pcs.org/text.asp?2020/6/2/172/293528




  Introduction Top


Ventricular septal rupture (VSR) complicating acute myocardial infarction (AMI) is infrequent in the timely reperfusion era but carries poor prognosis, leading to high mortality.[1] Surgical closure is the mainstay of treatment; however, 30-day mortality still remains high.[2] Transcatheter device closure is an alternative as a bridge to surgical closure or destination therapy where the patient's condition precludes surgical repair.[2] We report a case of a 68-year-old male with VSR following inferior wall myocardial infarction (IWMI), successfully closed by a percutaneous transcatheter device closure technique.


  Case Report Top


A 68-year-old male who underwent an uneventful percutaneous coronary intervention (PCI) to the right coronary artery (RCA) 10 days back, 48 h after an episode of acute IWMI, was admitted to emergency with New York Heart Association Class IV dyspnea for the last 3 days. He had cold and clammy skin, SpO290%, blood pressure 80/50 mmHg, heart rate was 128 beats/min, elevated jugular venous pressure, and bilateral basal rales. Cardiovascular examination revealed a harsh holosystolic murmur maximally at the left lower sternal border suggestive of VSR.

Transthoracic echocardiography revealed mid-septal VSR (peak gradient of 45 mmHg) with hypokinesia of basal inferoseptal, mid-inferior, and basal inferior segments with left ventricular ejection fraction (LVEF) of about 45%. Right ventricular (RV) function was normal as evidenced by tricuspid annular plane systolic excursion of 18 mm. The patient was deteriorating hemodynamically with evidence of altered sensorium and metabolic acidosis, and the patient was put on mechanical ventilation and intra-aortic balloon pump (IABP) and noradrenaline support.

The patient's hematological report showed increased total leukocyte count (17,080 cells/dl) with neutrophilic predominance (91%). Serum creatinine was of 2.78 mg/dl (normal 0.4–1.2 mg/dl). Liver function test revealed serum aspartate aminotransferase level of 184U/L (normal 5–40 U/L), serum alanine aminotransferase level of 764U/L (normal 7–56 U/L), serum alkaline phosphatase (ALP) level of 570.9U/L (normal 45–270 U/L), and total serum bilirubin of 6 mg/dl (normal 0.2–1.2 mg/dl) with model for end-stage liver disease excluding INR (MELD XI) score of 30 (MELD XI = 5.11 × ln [bilirubin] + 11.79 × ln [creatinine] + 9.44). As the patient was hemodynamically unstable and not willing to undergo surgical procedure, we decided to undertake percutaneous device closure of VSR.

VSR was crossed from left ventricular side with J-tip 0.035” Terumo double-length (260 cm) wire and was advanced till left pulmonary artery (LPA) branch [Figure 1]a, [Figure 1]b. The opening systemic pressure on IABP was 74/50/62 mmHg (systolic/diastolic/mean). Cardiac catheterization data showed systolic/diastolic/mean pulmonary artery (PA) pressures of 45/18/27 mmHg (normal < 25/10/15), mean pulmonary capillary wedge pressure (PCWP) was 25 mmHg (normal 10–15 mmHg), and mean right atrial pressure (RAP) was 11 mmHg. Pulmonary artery pulsatility index (PAPi) (calculated as [systolic PA pressure − diastolic PA pressure]/RAP) of 2.45 and ratio of RAP/PCWP of 0.44 (PAPi <1.5, RAP/PCWP >0.8 suggests RV failure).
Figure 1: (a) Retrograde left ventricular angiogram demonstrating ventricular septal rupture (Yellow star, transesophageal echocardiography probe; Blue star, temporary pacemaker lead; Red star, 5-French Pigtail catheter; Red Arrow, ventricular septal rupture) (b) Ventricular septal rupture crossed with 0.035'' Terumo wire (Yellow arrow) and Multipurpose (MPA2) catheter (Blue arrow); (c) Terumo wire exchanged with Ultra-Stiff Amplatz wire (Green arrow), which is placed in left pulmonary artery; (d) 0.035'' Terumo wire placed into left pulmonary artery through femoral venous route (Purple arrow); (e) Ultra-Stiff Amplatz wire snared by Amplatz 20 mm goose-neck snare in left pulmonary artery (White arrow); (f) Arteriovenous loop formed and Ultra-Stiff Amplatz wire externalized through femoral vein; (g) deployment of left disc (Orange arrow) of 36 mm Amplatzer septal occluder device; (h) repeat left ventricular angiogram showing reduction of left-to-right shunt (Red arrow); (i) right disc was not opened properly rendering a snake-like deformity of Amplatz atrial septal occlude device due to serpingeneous shape of ventricular septal rupture.

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The Terumo double-length wire was exchanged with a 145 cm Amplatz Ultra-Stiff wire (Abott) [Figure 1]c. Another Terumo 0.035” double-length wire was introduced to the LPA [Figure 1]d. The Amplatz wire was snared with a 6 French catheter with 120 mm Amplatz goose-neck snare (20 mm diameter loop) [Figure 1]e. An arteriovenous loop was made and was externalized from the right femoral vein [Figure 1]f. A 12-French delivery sheath (with dilator) was placed across the VSR over the Amplatz wire [Figure 1]g. Amplatzer septal occluder (ASO) device of 36 mm was deployed across the VSR under transesophageal echocardiography (TEE) guidance [Figure 2]d. However, the left disc (52 mm) of the device was fully opened in the left ventricle, but right disc (46 mm) took snake-like deformity due to the serpiginous shape of the VSR as the waist (4 mm) could not be fit well [Figure 1]h and i]. LV angiogram showed adequate closure of the VSR [Figure 1]h. TEE confirmed approximately 70% decrease of shunt with a Qp: Qs of 1.4:1 [Figure 2]a, [Figure 2]b, [Figure 2]c, [Figure 2]d, [Figure 2]e and stable positioning of the device [Figure 2]f. The final systemic pressure on IABP was 95/40/76 mmHg (systolic/diastolic/mean). Coronary angiogram showed a patent stent in RCA, and the left coronary system was normal.
Figure 2: Intraprocedure transesophageal echocardiography showing ventricular septal rupture (ventricular septal rupture, red arrow) in the lower part of interventricular septum (a and b) with size of 16 mm (c). Following deployment of the device (yellow arrow), ventricular septal rupture is occluded (d) with a minor residual shunt (e) and good stability in three-dimensional echocardiography (f).

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The patient improved hemodynamically, and mechanical ventilation, noradrenaline, and IABP supports were weaned off. TTE confirmed LVEF of 45% and RV function remained normal. However, 24 h after the procedure, the patient developed a fever and had persistently increased total leukocyte counts of 22,110 cells/dl, with a neutrophilic predominance (92%), but blood culture report was negative. His serum procalcitonin level was also raised to 1.14 ng/ml (Normal 0.024–0.028 in ng/ml). His renal and hepatic function further worsened with a serum creatinine of 4.65 mg/dl and total serum bilirubin of 13.1 mg/dl. However, on the 3rd postprocedure day, the patient died following a cardiac arrest and failed resuscitations.


  Discussion Top


VSR following AMI is increasingly rare in the PCI era but associated with dismal prognosis with 30-day mortality ranging up to 65%.[3],[4],[5] Deferring surgery with after-load reduction by IABP not only stabilizes the patient but also provides better results as compared to immediate surgery.[6],[7] As patients progress from the acute to chronic phase following AMI, surgical outcomes usually improve as seen in most of the case reports.[7] In our case, the patient presented 10 days after AMI, and further delay in VSR closure was not an option as the patient was hemodynamically unstable and was surviving on IABP and ventilator support. The primary goal of VSR device closure is to reduce left-to-right shunt (Qp: Qs), and it was achieved variably in different case series, ranging from 34% to 91%.[2],[7] In our case, postdevice closure Qp: Qs was reduced by 70%. Noradrenaline and IABP supports were weaned off in this patient after the procedure. Defect <15 mm is considered optimal by most authors; however, in our case, it was a large defect of 16 mm and mid-septal in location.[6] Due to a lack of an adequate tissue “rim” to secure the device, inferior/posterior defects are quite challenging and become more difficult due to the adjoining tricuspid valve apparatus (especially the septal leaflet), and most of the case series have evidence of higher mortality in VSR associated with IWMI.[8] In our patient, it was associated with IWMI but had adequate rim size and was lower-septal rather than basal. Sizing of the VSR closure device is important as a device of 1.5–2.2 times the echocardiographic or angiographic size needs to be selected that could fit in the specific anatomic location.[9] In our case, the VSR was 16 mm, and thus we chose a 36 mm Amplatz ASO device. Another challenging aspect of our patient was the serpiginous nature of the defect. In a serpiginous defect, it is difficult to cross wire and carries a high risk of residual shunt around the device.[10] In our case, the right disc was not opened well, and there was “snake-like deformity.” In the absence of evidence of RV failure as evidenced by low PAPi and supporting evidence of leukocytosis with neutrophilic predominance, fever and raised procalcitonin, and inappropriately elevated serum ALP level, all are indicative of sepsis was deemed to be the etiology of liver dysfunction in our case.[10] MELD-XI score higher than 20 was found to be strongly associated with 30-day mortality in patients who underwent postdevice closure of VSR.[9] In our patient, the MELD-XI score was 30, which indicates a higher risk of developing multiorgan system dysfunction in this setting.

Ethical clearance

Ethical clearance was taken.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient's son has given his consent for his images and other clinical information to be reported in the journal. The patient's son understands that the patient's name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Elbadawi A, Elgendy IY, Mahmoud K, Barakat AF, Mentias A, Mohamed AH, et al. Temporal trends and outcomes of mechanical complications in patients with acute myocardial infarction. JACC Cardiovasc Interv 2019;12:1825-36.  Back to cited text no. 1
    
2.
Li H, Zhang S, Yu M, Xu J, Dong C, Yang Y, et al. Profile and outcomes of surgical treatment for ventricular septal rupture in patients with shock. Ann Thorac Surg 2019;108:1127-32.  Back to cited text no. 2
    
3.
Liebelt JJ, Yang Y, DeRose JJ, Taub CC. Ventricular septal rupture complicating acute myocardial infarction in the modern era with mechanical circulatory support: A single center observational study. Am J Cardiovasc Dis 2016;6:10-6.  Back to cited text no. 3
    
4.
Goldsweig AM, Aronow HD. The evolving role of transcatheter repair of ventricular septal rupture. Cardiology 2018;141:233-5.  Back to cited text no. 4
    
5.
Aggarwal M, Natarajan K, Vijayakumar M, Chandrasekhar R, Mathew N, Vijan V, et al. Primary transcatheter closure of post-myocardial infarction ventricular septal rupture using amplatzer atrial septal occlusion device: A study from tertiary care in South India. Indian Heart J 2018;70:519-27.  Back to cited text no. 5
    
6.
Calvert PA, Cockburn J, Wynne D, Ludman P, Rana BS, Northridge D, et al. Percutaneous closure of postinfarction ventricular septal defect: In-hospital outcomes and long-term follow-up of UK experience. Circulation 2014;129:2395-402.  Back to cited text no. 6
    
7.
Lanz J, Wyss D, Räber L, Stortecky S, Hunziker L, Blöchlinger S, et al. Mechanical complications in patients with ST-segment elevation myocardial infarction: A single centre experience. PLoS One 2019;14:e0209502.  Back to cited text no. 7
    
8.
Assenza GE, McElhinney DB, Valente AM, Pearson DD, Volpe M, Martucci G, et al. Transcatheter closure of post-myocardial infarction ventricular septal rupture. Circ Cardiovasc Interv 2013;6:59-67.  Back to cited text no. 8
    
9.
Jones BM, Kapadia SR, Smedira NG, Robich M, Tuzcu EM, Menon V, et al. Ventricular septal rupture complicating acute myocardial infarction: A contemporary review. Eur Heart J 2014;35:2060-8.  Back to cited text no. 9
    
10.
Bernal W. The liver in systemic disease: Sepsis and critical illness. Clin Liver Dis (Hoboken) 2016;7:88-91.  Back to cited text no. 10
    


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  [Figure 1], [Figure 2]



 

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