CASE 13497 Published on 16.03.2016

Ventricular septal rupture complicating acute myocardial infarction



Case Type

Clinical Cases


Arthur DAVID

Centre Hospitalier de Saint-Nazaire

83 years, male

Area of Interest Cardiac, Veins / Vena cava ; Imaging Technique CT
Clinical History
A 83-year-old male patient was admitted in our institution because of cardiogenic shock and 1-day history of chest pain. Bedside echocardiography was performed by the emergency physician and revealed hyperechoic pericardial effusion.
Imaging Findings
We performed a thoraco-abdominal computed tomography (CT) with the suspicion of aortic dissection. Unenhanced thoracic CT revealed pericardial effusion, with high attenuation (>50 UH) suggesting haemopericardium (Figure 1).
Contrast-enhanced thoracic CT at arterial phase showed a defect in the ventricular septum (Figure 2). Thoracic CT with 70 seconds delay demonstrated hypoenhancement in the inferobasal region of the ventricular septum, where the rupture was seen, consistent with acute myocardial infarction (AMI) (Figure 3).
Contrast-enhanced abdominal CT also showed contrast reflux into hepatic veins suggesting right-ventricular failure (Figure 4).
Ventricular septal rupture (VSR) is a rare but lethal complication of AMI, with an incidence of 0.17 to 0.31% in patients receiving early thrombolytic therapy for AMI [1], which is substantially lower than prethrombolytic era rates of 1-2% [2].
Risk factors for VSR in patients presenting with AMI are older age, female sex, prior stroke, chronic kidney disease and chronic heart failure [2].
Rupture develops after transmural infarction of the ventricular septum, causing necrosis of the myocardium and weakening of the tissues [3]. Subsequent rupture causes a left-to-right shunt from the high-pressure left ventricle (LV) to the lower-pressure right ventricle (RV), resulting in volume overload of the RV with diminished systolic function.
The median time from AMI to VSR is generally 24 hours or less in patients treated with thrombolytic agents and percutaneous coronary intervention, but later onset is still seen [2].
Patients classically present with biventricular failure and severe haemodynamic instability in the setting of recent AMI [2]. Other physical examination findings may include systolic murmum over the precordium as well as a palpable thrill.
When VSR is suspected, the diagnosis is made by a prompt echocardiography with Doppler colour flow imaging, showing defect of the ventricular septum and demonstration of flow across the septum.
CT study is usually not necessary for diagnosis of VSR, but in this case we first suspected aortic dissection. Therefore, only few cases of acute VSR revealed by CT have been reported. CT findings in VSR include: septal defect, signs of right heart failure such as right-ventricular dilatation and contrast reflux into the inferior cave and hepatic veins, haemopericardium.
Medical management of VSR is afterload reduction to increase effective LV stroke volume by reducing the degree of shunt. Intraaortic ballon pump counterpulsation is effective for reducing afterload and increasing cardiac output [4].
Definitive treatment requires surgical repair of the ruptured septum. Current guidelines of the American College of Cardiology–American Heart Association for the treatment of patients with acute myocardial infarction recommend immediate operative intervention in patients with septal rupture, regardless of their clinical status [5].
Differential Diagnosis List
Ventricular septal rupture.
Ventricular free wall rupture
Papillary muscle rupture
Left ventricular aneursym
Acute mitral regurgitation
Aortic dissection
Final Diagnosis
Ventricular septal rupture.
Case information
DOI: 10.1594/EURORAD/CASE.13497
ISSN: 1563-4086