Myocardium, Pericardium, and Cardiac Tumor

Anatomy

The pericardium can be thought of as two layers of a deflated balloon, which is wrapped around the heart. One side of that balloon becomes the inner layer (visceral layer), which is wrapped around and closely adheres to the heart and the overlying epicardial fat and coronary arteries. The outer layer (the parietal layer) of the balloon is embedded into the surrounding structures, namely the pericardial fat in the mediastinum.

Instead of air, there is a small amount of fluid (25-50 mL) within the balloon. The small amount of fluid between the two layers allows for nearly friction-free motion between the visceral layers of the pericardium (which moves with the beating heart) and the outer parietal portion, which is relatively stationary, fixed to the mediastinum. Like the pleura and peritoneum, the normal pericardium may not be seen along its entire course; it becomes more visible when diseased and thickened or when pericardial effusion is present.

The inner visceral layer of the pericardium, also called serous pericardium or epicardium, is directly attached to the heart and gives a glistening appearance to the heart. The parietal pericardium is attached to the surrounding mediastinum, anteriorly to the superior pericardial sternal ligament, inferiorly to the central tendon of the diaphragm, and posteriorly to the esophagus and descending thoracic aorta. The fat outside the parietal pericardium is called pericardial fat. The fat inside the visceral pericardium is called epicardial fat, and it is directly attached to the cardiac chambers. The coronary arteries run within the epicardial fat. The visceral pericardium covers both coronary arteries and epicardial fat. The pericardium does not cover only the heart but also extends about 3 cm into the root of the aorta and pulmonary artery where the visceral and parietal pericardium come together to form the pericardial reflection ( Figure 6-1 ).

There are a few spaces inside the pericardial cavity in which fluid tends to accumulate and through which surgeons could stick their fingers or pull bypasses if they choose to do so—and sometimes they do ( Figure 6-2 ). The transverse sinus and oblique sinuses are the two major sinuses. The transverse sinus is located inferior and posterior to the aorta and the pulmonary trunk, above the left atrium. The superior extent of the transverse sinus is the superior aortic recess; it has a crescentic posterior and lateral and anterior components around the aorta. The right and left pulmonic recesses form the lateral extent of the transverse sinus. The right pulmonic recess is inferior to the right pulmonary artery. The left pulmonic recess is bound superiorly by the left pulmonary artery, inferiorly by the left superior pulmonary vein, and medially by the ligament of Marshall. The oblique sinus is immediately superior and posterior to the left atrium and anterior to the esophagus. The right and left pulmonary vein recesses are in relationship to the pulmonary veins. It is important to be aware of normal recesses and pericardial sinuses. For instance, fluid that has accumulated in the superior aortic recess of the transverse sinus may mimic aortic dissection, a thickened aortic wall from arteritis, or enlarged lymph nodes. On rare occasions, a surgeon may opt to pull a venous bypass graft through the transverse sinus, if the graft is too short to be placed in the typical position anterior to the pulmonary artery ( Figure 6-3 ). This is also a surgically favored placement for a right internal mammary artery graft to the left-sided vessels.

Normal Appearance on Chest Imaging

The visceral and parietal pericardium and the fluid in the normal pericardial space cannot usually be differentiated on computed tomography (CT) or magnetic resonance imaging (MRI) because the thickness of the pericardial layers is below the limits of the resolution. If a thickened pericardium is described, it usually refers to the combination of visceral pericardium, pericardial fluid, and parietal pericardium. On CT, secondary signs are helpful to differentiate the cause of the thickening of the pericardial complex. Nodularity and enhancement of the thickened pericardium is suggestive of metastatic disease. Calcification indicates chronic pericarditis. A smoothly thickened pericardial contour is suggestive of, although not diagnostic of, pericardial effusion. One great aid in imaging the pericardium is the fat that covers the outside of the parietal pericardium (pericardial fat) and the fat over the surface of the heart (epicardial fat). On CT and MRI, the pericardium is easily visualized in the area of the right ventricle, because it is located between the bright mediastinal and epicardial fat. The normal thickness of the pericardium between the sternum and the right ventricular free wall is less than 3 mm. Of note, pericardial thickness depends upon the anatomical level, and increases toward the diaphragm. The measurement of pericardial thickness is, therefore, most reliable at the midventricular level.

Laterally, the pericardium is usually not visible on CT. On MRI images, chemical shift artifacts may cause the pericardium to look like a thick black line in the frequency encoding direction. Special techniques can be used to investigate the different components of the pericardial contour: Phase contrast images allow for detection of freely moving fluid within the pericardial space.

Pericardial Effusion

The normal pericardial space in the adult can be distended with 150 to 250 mL of fluid acutely before cardiac tamponade results. Cardiac tamponade is caused by excess fluid in the pericardial space, which compresses the heart and thus causes a low cardiac-output state. In tamponade, the cardiac size on the chest radiograph is slightly to markedly increased. The heart may have a water-bottle appearance in which both sides are rounded and displaced laterally ( Figure 6-4 ). The differential diagnostic considerations for a water-bottle heart are global cardiomegaly, large anterior mediastinal mass, or pericardial effusion. If you are lucky, you may see the Oreo cookie sign on the lateral chest radiograph ( Figure 6-5 ). In this sign, a radiolucent stripe behind the sternum (pericardial fat), then a more radiopaque stripe (pericardial effusion), followed by yet another radiolucent stripe (epicardial fat) will be noticed.

Appearance of Effusion on Computed Tomography and Magnetic Resonance Imaging

The appearance of a pericardial effusion on CT and MRI depends on the type of fluid. When there is blood in the pericardial cavity, CT will show dense material with Hounsfield units above 40. A simple pericardial effusion typically has CT numbers in the range of 10 to 20 Hounsfield units.

On MRI spin echo sequences, pericardial effusions are of low signal intensity, which in part is from low protein content and from the motion of the fluid, which causes phase dispersion ( Figure 6-6 ). Balanced steady-state free precession (B-SSFP) images, called FIESTA, True-FISP, or FFE sequences depending upon the vendor, demonstrate typical bright fluid signal of simple pericardial fluid. Phase contrast images allow for quantification of flow and can be helpful in the characterization of pericardial fluid. The appearance of pericardial hematomas depends heavily on the type of hemoglobin present (e.g., oxyhemoglobin, deoxyhemoglobin, and methemoglobin).

Pericardial Effusion Syndromes

Infection, Collagen Disease, Metabolic Disease, and Tumors

Many infectious and metabolic diseases, tumors, radiation, drug reactions, and collagen disorders, such as systemic lupus erythematosus and scleroderma, typically cause small pericardial effusions. Uremic pericarditis occurs in about 50% of patients with chronic renal failure and is an indication for dialysis. Most effusions do not lead to cardiac tamponade. Common diseases that form pericardial effusions are listed in Box 6-1 . Infectious agents that cause pericarditis with resultant effusions are usually coxsackievirus group B and echovirus type 8. Tuberculous pericarditis is uncommon except in patients with acquired immune deficiency syndrome (AIDS).

Box 6-1

Common Causes of Pericardial Effusions

Serous

• Congestive heart failure

• Hypoalbuminemia

• Radiation

• Collagen vascular disease (including systemic lupus erythematosus, rheumatoid arthritis, and scleroderma)

• Acute pericarditis

• Myxedema

• Drug reaction

Bloody

• Acute myocardial infarct

• Trauma, including cardiac surgery

• Chronic renal disorder

• Anticoagulants

• Neoplasm

Purulent

Bacterial

• Staphylococcus

• Streptococcus

• Pneumococcus

• Neisseria

Viral

• Coxsackievirus

• Human immunodeficiency virus (HIV)

• Echovirus

• Tuberculosis

• Fungal and parasitic

Although many bacterial, viral, or fungal agents can cause pericarditis, the most common organisms are Staphylococcus, Haemophilus influenzae, and Neisseria meningitidis ( Figure 6-7 ). In addition to a hematogenous source, pericardial infections result from extension from a myocardial abscess related to infective endocarditis, from mediastinal abscess caused by fistula, and from carcinoma of the lung and the esophagus. A loculated pericardial fluid can represent hematoma, abscess, or lymphocele or may be secondary to fibrous adhesions from previous pericarditis. Loculated pericardial effusions can appear similar to pericardial cysts. Neoplastic pericardial effusions are usually related to systemic metastatic disease. The pericardium demonstrates nodular thickening with enhancement of the nodules. Infiltration of the epicardial or pericardial fat, myocardium, or adjacent vascular structures may be seen ( Figures 6-8 and 6-9 ).

Myocardial Infarction (Dressler Syndrome)

The most common cause of pericardial effusion is myocardial infarction with left ventricular failure. An increase in either right or left heart pressure may also cause a pericardial effusion. About 5% of patients with acute myocardial infarction develop a pericardial effusion. Dressler syndrome is the development of pericardial and pleural effusions 2 to 10 weeks after a myocardial infarction ( Figure 6-10 ). An autoimmune reaction to a viral infection has been implicated as a possible etiologic factor. These effusions may be hemorrhagic and can result in cardiac tamponade, particularly if the patients have been given anticoagulant medication.