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Rupture of left ventricular free wall
 
Published on 2014-10-15 by Walid Garzuddine
 
 
History and Findings
 

A 63 year old male was seen in the emergency room because of an attack of severe inter-scapular pain that occurred two days prior to presentation while he was lifting a heavy object which was followed by syncope. After recovering he began to experience increasing dyspnea that ultimately led to his seeking medical help. His blood pressure upon presentation was 100/67 mm. Hg with a heart rate of 117 beats per minute. The electrocardiogram showed ST segment depression V4-V6 with prominent R waves in V1 and V2. The examining physician heard a pericardial friction rub that prompted the request for an echocardiogram. No mention of pulsus paradoxus was made.

Ten years prior to this the patient had undergone aortic valve replacement with a bi-leaflet mechanical valve when he was diagnosed with infective endocarditis and an aortic root abscess. It is noteworthy that the patient, who was from a poor background and living alone with his brother had been off oral anticoagulation for about the last three years.

Echocardiography showed a pericardial effusion with evidence of fluid as well as dense material consistent with thrombus. Along the basal lateral wall there was a clearly visible defect (video 1).  Color flow Doppler showed evidence of  free communication between the left ventricular cavity and the pericardial space (video 2 & 4). Video 3 shows the appearance from the subcostal window. Surprisingly there was no evidence of aortic vale prosthesis dysfunction.

Since the patient was relatively stable a pre-operative coronary angiogram was performed showing total occlusion of the circumflex artery (fig. 1). He subsequently underwent successful surgery with patch closure of the defect.

 
 
 
video 1 | video 2 | video 4 subcostal view | Apical 4 chamber color |
 
 
 
 
 
Discussion
 

Rupture of the free wall of the left ventricle is the second most common mechanical cause of death in acute ST segment elevation MI after cardiogenic shock as a result of pump failure and is usually a fatal event. When FWR occurs, the clinical presentation is dramatic, with the rapid development of hypotension, cardiac tamponade, pulseless electromechanical activity, and death. Unfortunately, the mortality rate is 90%, and few patients can be salvaged by anything other than heroic measures, including emergent pericardiocentesis and surgical repair.

Independent risk factors for the development of a ventricular rupture include first infarction, advanced age, hypertension, and female gender.  In addition, there is a higher incidence in patients without a history of prior angina and with infarcts in the distribution of a single vessel. This complication is more likely to occur in patients with a transmural MI involving the inferolateral wall associated with a left circumflex occlusion or with LAD occlusion.  Intramural hematoma or hemorrhage at the junction of the necrotic and the normal myocardium results in a small endocardial rent which may lead to a catastrophic tamponade or, if a blood clot occurs that can limit the exit of blood into the pericardial space the patient may survive to reach medical attention. Survival beyond the acute episode may allow development of a pseudo-aneurysm after organization of the thrombus/hematoma. It remains a matter of conjecture whether pericardial adhesions from the earlier surgery prevented catastrophic tamponade.

Transthoracic Echocardiography has a high sensitivity for diagnosing rupture. In patients in the coronary care unit the presence of a pericardial effusion post myocardial infarction may be an indicator of possible impending rupture in addition to infarct expansion with significant wall thinning at the infarct site. 

Reperfusion therapy in general is associated with a decrease in the incidence of cardiac rupture by decreasing infarct size however there are reports of a higher incidence of cardiac rupture in patients receiving thrombolytic therapy who were above the age of 70 and especially those who were women. In a study of 1300 patients, the overall incidence of cardiac rupture was lower in those receiving thrombolytic therapy (1.7%) than in those in the conventional therapy group (2.7%) (ref 1).

A study comparing primary percutaneous angioplasty with fibrinolytic therapy showed a significantly lower risk of free wall rupture in patients treated with primary percutaneous coronary angioplasty (ref 2).

Surgical repair is the preferred treatment and was performed successfully in this patient. Percutaneous closure of a pseudo-aneurysm is a potential approach in carefully selected patients.

 

References:

 

1. Richard C. Becker, Judith S. Hochman,  Christopher P. Cannon, et al. Fatal cardiac rupture among patients treated with thrombolytic agents and adjunctive thrombin antagonists observations from the thrombolysis and thrombin inhibition in myocardial Infarction 9 Study. J Am Coll Cardiol 1999;33:479–87.

 

2. Raul Moreno, Jose Lopez, Sendo Eulogio Garcia, et al. Primary angioplasty reduces the risk of left ventricular free wall rupture compared with thrombolysis in patients with acute myocardial infarction. J Am Coll Cardiol 2002;39:598–603.

 
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