74 year-old male with past medical history significant for an anterolateral myocardial infarction.

Figure 1: Sagittal image demonstrating left ventricular apical out pouching.

Figure 2: Same left ventricular apical out pouching in the coronal plane.

Movies 1 and 2: There is a 3 cm thin-walled out pouching at the apex of the left ventricle, demonstrating paradoxical movement relative to the left ventricular contraction. This area of out pouching arises from the LV contour with a smooth angle. The LV myocardium tapers gradually in thickness up to the margin of the out pouching. There appears to be trabeculations in the out pouching as well. There is no evidence of thrombosis within the out pouching. Mild mitral regurgitation is noted. The right ventricle demonstrates normal wall motion.

True aneurysm of the left ventricular apex.

A left ventricular (LV) aneurysm is a segment of the left ventricular wall that protrudes from the expected outline of the ventricular chamber and displays either akinetic or dyskinetic motion. LV aneurysms occur in approximately 12-15% of patients after myocardial infarction. Weakening of the myocardial wall at the infarction site permits the development of a local bulge. Pathologically there is a large thin-walled sac bulging from the lumen and the external surface of the heart, usually clearly demarcated from normal myocardium.

Many patients with small left ventricular aneurysms are asymptomatic. As the size of the aneurysm increases, patients can present with angina refractory to medical treatment, congestive heart failure, arrhythmias, and systemic emboli. Complications of left ventricular aneurysms include mitral incompetence (via aneurysm of the posterior left ventricle which supports the papillary muscle and chordae tendinae of the mitral valve), cardiac failure, and mural rupture leading to tamponade and/or cardiogenic shock.
Plain radiographic findings can be normal, but the aneurysm can be seen on a chest x-ray as a bulge in the contour of the left heart border. Curvilinear peripheral calcification is an infrequent but important sign that occurs only after several years.

True ventricular aneurysms are broad necked, thin-walled, localized out-pouchings which have an intact fibrous myocardial wall with adherent overlying pericardium. True aneurysms most commonly occur after a transmural myocardial infarction from severe left anterior descending (LAD) coronary artery disease. Less common causes include congenital, Chagas disease, and myocarditis. These aneurysms are most commonly located in the anterolateral, apical, and septal walls. True aneurysms have a neck that is greater than or equal to the maximal diameter of the aneurysm. They are either akinetic or dyskinetic and do not contract during systole. The left ventricle is usually dilated and the remaining wall is hyperkinetic in order to maintain cardiac output. These aneurysms may contain thrombus and have a very low risk of rupture.

False ventricular aneurysms, or pseudoaneurysms, are contained myocardial ruptures consisting of a localized hematoma surrounded by adherent pericardium. These aneurysms develop when the free wall of the left ventricle ruptures into the pericardial space after a myocardial infarction. Other causes include penetrating trauma, abscess from bacterial endocarditis, and surgical ventriculotomy. False aneurysms are most commonly located in the posterolateral and retrocardiac areas of the left ventricle. They have a neck size that is less than the maximal diameter of the aneurysm. Imaging studies may demonstrate contrast material oscillating in and out of the neck of the aneurysm because of the narrow communication with the left ventricular chamber. False aneurysms almost always contain thrombus and have a high risk for rupture.

References:

1. Brant, W.E. and Helms, C.A. Fundamentals of Diagnostic Radiology, 2nd Edition. Philadelphia: Lippencott Williams & Wilkins, c1999. pp.552-553.
2. Pohost, G.M. and O’Rourke, R.A. (eds). Principles and Practice of Cardiovascular Imaging. Boston: Little, Brown & Co., c1991. pp. 93-394.