Case of the Week: July 30-August 6, 2009

65-year-old man with nonspecific chest discomfort and a remote myocardial infarction in the left anterior descending vascular territory 6 years ago.

What is the radiographic finding and what is your diagnosis?

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Case Details

PA and lateral chest radiography demonstrates ovoid, curvilinear, laminated rings of calcification located more than 2 mm within the outer confines of the cardiac silhouette delineating the anterior and apical walls of the left ventricle.

Answer

Diagnosis: Left Ventricular Aneurysm

Differential Diagnosis

Myocardial calcifications

  • Atherosclerosis in aorta or coronary arteries.
  • Aortic or mitral valvular or annular calcifications.
  • Mural calcifications post-infarction
  • Calcified thrombus
  • Cardiac fibroma

Pericardial calcifications (calcific pericarditis)

  • Post-traumatic
  • Post-infectious
  • Viral agents
  • Coxsackievirus
  • Influenza A and or B
  • Mycobacterium tuberculosis
  • Histoplasmosis
  • Systemic lupus erythematosus
  • Uremia
  • Rheumatic heart disease

Pericardial cyst

Discussion

Background

Aneurysms of the left ventricle are a potential complication of myocardial infarction. Such aneurysms are classified as either true or false.  True ventricular aneurysm is a chronic complication of myocardial infarction and usually involves the apical or anterolateral wall (85%) and most often follows the left anterior descending coronary artery (LAD) vascular territory. A true aneurysmal sac contains endocardium, epicardium, and thinned fibrous scar tissue that is a remnant of the left ventricular muscle. A true aneurysm contained by diseased myocardium can bulge and may be functionally akinetic or dyskinetic.  A false or pseudoaneurysm of the left ventricle represents pericardium that contains a ruptured left ventricle A false aneurysm usually involves the inferior and/or posterior ventricular wall.  The focal rupture in the myocardial wall creates the neck of the false aneurysm.  Because the clinical differentiation between a true aneurysm and a false aneurysm is critical, further evaluation with various imaging modalities is often necessary.

Etiology

Left ventricular aneurysms most often develop as sequelae of transmural infarction and may present within 48 hours of the infarction.  Past incidence rates of 8-15% following ST-segment elevation myocardial infarcts may be decreasing with current improved revascularization techniques.  Myocardial calcifications may form as early as 6 years post infarction.  Other causes of ventricular aneurysm include congenital (Ravitch syndrome), Chaga's disease, myocarditis, hibernating myocardium, and sarcoidosis.  Trauma is the most common cause of a false aneurysm.

Clinical Findings

A true aneurysm, particularly if small, may cause no symptoms. 50% of true aneurysms develop mural thrombus that can potentially embolize. The bulge in the myocardium subtracts from the stroke volume and the resultant decrease in cardiac output may adversely affect myocardial remodeling. However, rupture of a true aneurysm is an uncommon phenomenon; therefore, surgical resection is only necessary when refractory angina pectoris, heart failure, systemic embolization, or refractory dysrhythmias occur. In contradistinction, false ventricular aneurysms has a high risk of rupture and require repair.

Imaging Findings

Radiography

  • Localized bulge along the left heart border.
  • Shelf-like or squared-off appearance to the mid-lateral margin of the heart border.
  • Rim or laminated rings of calcification confined to one cardiac chamber, more than 2 mm below the cardiac contour (e.g., remote infarction) (Figure 1 and 2).
  • Left ventricular enlargement.
  • Cardiac decompensation.

Cardiac MR

  • Both spin-echo and cine images may reveal a focal out pouching in the left ventricular wall.
  • Delayed hyperenhancement of myocardium consistent with scar (Figure 3)
  • Adjacent myocardium not part of the aneurysm shows no hyperenhancement (Figure 3).
  • Hypokinesis, akinesis, or dyskinesis of affected myocardial wall (Figure 3).
  •  Low signal intensity on single-shot inversion recovery with a long inversion time consistent with thrombus (Figure 3).
  • Signal drop-out from the associated calcification.

Treatment

  • Anticoagulation for systemic embolization prophylaxis.
  • Ablation for dysrhythmias.
  • Aneurysmectomy if medical treatment for dysrhythmias, angina, systemic embolization, or heart failure are unsuccessful.

Prognosis

  • Related to degree of clot burden, dysrhythmias, and/or affect on stroke volume.
  • Rupture rate true aneurysm: 4%

Caveats

  • Myocardial calcifications lie ≥ 2 mm below the external cardiac contour, are linear or laminated, and are limited to the left ventricle.
  • Pericardial calcifications are usually thin, curvilinear and conform to the pericardium, and many times the atrioventricular groove (which can be difficult to differentiate from severe right coronary artery calcifications).
  • More shaggy, thick, and amorphous appearing calcifications are seen with tuberculous pericarditis.

Suggested Readings

  1. Brown SL, Gropler RJ, Harris KM. Distinguishing left ventricular aneurysm from pseudoaneurysm: a review of the literature. Chest 1997;111:1403 -1409
  2. Burgener FA, Kormano M. Predominantly Left Ventricular or Generalized Cardiac Enlargement. In: Differential Diagnosis in Conventional Radiology. Thieme; New York, 2007; 316.
  3. Grizzard JD, Judd R, Kim R. Cardiovascular MRI in Practice: A teaching file Approach   Springer 2008.
  4. Kazerooni EA, Gross BH. Acquired Cardiac Disease. In: The Core Curriculum: Cardiopulmonary Imaging   Lippincott Williams & Wilkins 2003; 570-571.
  5. Webb WR, Higgins CB. Myocardial and Pericardial Disease. In: Thoracic Imaging: Pulmonary and Cardiovascular Radiology   Lippincott Williams & Wilkins 2004; 723.

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    VCU Department of Thoracic Imaging Virginia Commonwealth University VCU Medical Center