- Video A: venous and arterial guidewires are visualised—please also note the tip of the previously inserted IABP
- Video B: venous drainage cannula in inferior vena cava is visualised.
A 39-year-old man (BMI 22 kg/m²) with no prior medical history was admitted to a spoke centre with late-presenting anterior ST-segment elevation myocardial infarction (STEMI). He reported chest pain occurring two days earlier and is experiencing dyspnoea. Echocardiography identified a severe biventricular systolic dysfunction with non-restrictive ventricular septal defect (VSD).
Coronary angiography demonstrated single-vessel coronary artery disease with multiple stenoses involving the left anterior descending artery (LAD). Percutaneous coronary intervention (PCI) was performed with deployment of two drug-eluting stents, achieving TIMI 2 flow, and an intra-aortic balloon pump was inserted for haemodynamic support.
Due to progressive deterioration (lactates peaked at 10.4 mmol/L), he was referred to our hub centre for further management. On arrival, patient was intubated due to respiratory distress secondary to pulmonary oedema, intravenous continuous infusions of furosemide and adrenaline at inotropic dose were started. Peripheral venoarterial ECMO was inserted to restore perfusion.
Admitted to cath lab for peripheral venoarterial ECMO insertion:
A. Visualisation of venous (left) and arterial (right) guidewires for ECMO insertion. Tip of intraortic balloon pump is visualised
B. Drainage cannula in inferior vena cava
| Arterial Blood Gas | Laboratory Tests |
|---|---|
| pH: 7.29 | Total bilirubin: 2.1 mg/dL |
| PaO₂: 9.2 kPa (69 mmHg) | AST: 92 U/L |
| PaCO₂: 4.8 kPa (36 mmHg) | ALT: 85 U/L |
| HCO₃⁻: 17 mmol/L | Creatinine: 1.8 mg/dL (159 µmol/L) |
| Base excess: −8 mmol/L | Blood urea nitrogen (BUN): 38 mg/dL (6.3 mmol/L) |
| Lactate: 5.6 mmol/L | White blood cells: 12.4 ×10⁹/L |
| SaO₂: 93 % | Platelets: 210 ×10⁹/L |
| Hemoglobin: 7.8 g/dL |
Conservative medical management in this post-AMI VSD is fatal so prompt surgical opinion was obtained. Surgical indication was confirmed for VSD closure and adviced a 10-day attempt of stabilisation, awaiting frail infarcted tissues to heal. Percutaneous closure was considered but excluded due to unfavorable VSD anatomy and position.
Patient was well offloaded on IABP and VA-ECMO and an acceptable perfusion status was achieved, with good lactate clearance. No inotropic nor vasopressor were required. Successful extubation was also achieved.
At day 10, surgical team performed a median sternotomy for VSD closure using a bovine pericardial patch (patient remained on VA-ECMO throughout the procedure). Peri-operative transoesophageal echocardiography confirmed good, immediate post-operative surgical outcome, with a small residual ventricular shunt observed.
On postoperative day 1, a follow-up transthoracic echocardiogram raised suspicion of a pericardial/pleural effusion compressing the left atrium and partially obstructing pulmonary venous return. Transoesophageal echocardiography was inconclusive, but a CT scan confirmed a haemorrhagic pericardial collection.
The patient was subsequently taken to theatres for a washout procedure.
Left ventricular function improved over the hospital course (up to LVEF 38%). After a successful weaning study, patient was weaned off ECMO, and progressively transitioned to anti-heart failure medical treatment. Patient was discharged home at day 29.
- Ventricular septal defect (VSD) is an uncommon but life-threatening mechanical complication of myocardial infarction with ≈ 50% of patients developing cardiogenic shock.
- Late presentation, persistent ST-segment elevation beyond 72 hours, anterior infarct location, and single-vessel coronary artery disease are well-recognised risk factors.
- Surgical repair remains the preferred treatment. Percutaneous closure techniques are being increasingly adopted, particularly in patients with favourable septal anatomy; however, they are not yet firmly established as a definitive alternative, especially in younger patients.
- The optimal timing for surgery remains uncertain, as early repair is associated with increased mortality due to the fragility of the surrounding fresh necrotic tissue.
- Mechanical circulatory support devices may play an important role in stabilising these patients through several pathophysiological mechanisms, ultimately contributing to right ventricular unloading and haemodynamic support.
- In contrast to congenital defects, post-infarction VSDs are often irregular and serpiginous, which can make complete surgical correction challenging and occasionally leave residual shunting.
Mechanical complications following acute myocardial infarction (AMI) are less common in the contemporary era; however, associated mortality has not declined substantially. Accordingly, systematic screening for mechanical complications primarily related to myocardial tissue rupture should be performed in all patients with AMI, particularly during the first days of hospitalization.
Prompt diagnosis is critical and relies on clinical assessment, hemodynamic evaluation, and appropriate cardiac imaging modalities. Once a mechanical complication is identified, definitive intervention is required. The timing and type of intervention (surgical versus percutaneous), as well as the potential need for mechanical circulatory support as a bridging strategy, should be carefully and promptly evaluated on a case-by-case basis within a multidisciplinary Heart Team.
- Cubeddu RJ, Lorusso R, Ronco D, Matteucci M, Axline MS, Moreno PR. Ventricular Septal Rupture After Myocardial Infarction: JACC Focus Seminar 3/5. J Am Coll Cardiol. 2024;83:1886-1901.
- McDonagh TA, Metra M, Adamo M, et al; ESC Scientific Document Group. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J. 2021;42:3599-3726.
- Roncon-Albuquerque R Jr, Gaião S, Vasques-Nóvoa F, et al. Standardized approach for extubation during extracorporeal membrane oxygenation in severe acute respiratory distress syndrome: a prospective observational study. Ann Intensive Care. 2023;13:86.
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