Leo P. Lawler, M.D
Frank M. Corl, MS
Elliot K. Fishman, M.D., FACR
Although often not considered the primary imaging modality for evaluation of the heart, when it comes to the pericardium computed tomography compliments and in some cases surpasses echocardiograms and magnetic resonance imaging in the evaluation of pericardial pathology. The combination of its spatial and contrast resolution, the ability to administer enchancing agents, the lack of field of view limitations as well as our ability to infer dynamic information serve to make this modality the test of choice in many cases of pericardial disease. The continued development of multidetector computed tomography, cardiac gated imaging and the increasing use of three-dimensional CT in the area of coronary artery evaluation make it imperative to have a clear understanding of the normal pericardium and the pathologies that affect it.
Normal anatomy and function
The normal pericardium is a double-layered fibroserosal sac embryologically forming a subdivision of the celomic cavity into which invaginates the developing heart (Fig. 1A). The thickness of the normal parietal pericardium has been determined to be 1-2mm by anatomic studies but it is non-uniform in thickness with most CT measurements being taken anterior to the plane of right and left atrium where it is best defined. The visceral and parietal serous pericardium are intimately attached to the epicardium and fibrous pericardium respectively creating between these layers the pericardial space that normally has 20-25 mls of lymph fluid . The potential spaces of the pericardium are defined by sinuses and recesses (Fig. 1B). The pericardium is anchored cranially to the adventitia of the great vessels and caudally to the central tendon of the diaphragm. Other points of fixation of the pericardium are the sternum and adjacent structures such as esophagus and spine.
The mechanical role of the pericardium is in holding the heart in position, preventing over-dilatation of the heart, facilitating the hemodynamic interdependance of the ventricles and providing a barrier between the heart and other thoracic structures. A role has also been demonstrated in lubricating heart surfaces, affecting blood pressure and heart rate and secreting immunologic mediators.
Computed Tomography Technique
The parietal pericardium is defined on CT by the low houndsfield unit epicardial fat internally and mediastinal fat and lung externally. What we are seeing on imaging is the apposed parietal serous and fibrous pericardium In most cases where thickening, fluid or calcification are the issue, oral or intravenous contrast are not required. When there are questions regarding tumor involvement, cardiac chamber effect and myocardial change intravenous contrast may be of value. Three-dimensional reconstructions are usually not required.
The standard CT coverage in most people is from the great vessels through the diaphragm. One should note that a high insertion on the great vessels is an anatomic variation and when there is a very large pericardial effusion it everts the central tendon and pushes the pericardium caudally, thus one may need to change coverage accordingly. With single detector imaging scan time is 25 seconds, with rotation speed 0.75 seconds, table speed 5mm per second, slice thickness 3-5mm (pitch of 1-1.6) and 3mm reconstruction.
Our experience is predominantly with the Somatom Plus 4 Volume Zoom (Siemens, Iselin, NJ). Our multidetector protocol uses 140 KVp 100mAs, 0.5-second rotation time, detector array 4 by 1mm, slice thickness 1.25mm, data reconstruction 2mm, table speed 6mm per rotation and pitch 6. As in electron beam CT, it has been suggested that multidetector CT may have a role in functional imaging both in perfusion and dynamic imaging of chamber size and motion but this has yet to be fully explored.
Gating may be performed. The rotation speeds of 500ms and advanced algorithms offer the possibility of 0.25ms temporal resolution which may obviate the need for cardiac gating in selected cases and motion artifact is seldom a problem in pericardial imaging.
Most commonly an absent pericardium is congenital or a result of cardiac surgery. Congenital types are thought to be due to a premature closure of the duct of Cuvier causing vascular compromise. Absence is classified as partial or complete with partial left sided defects being the most common. Although in many it is an incidental finding of no consequence, herniation of a portion of the chamber or coronary artery is a recognized complication. One third of cases are associated with a mediastinal, cardiac or lung anomaly with an atrial septal defect being the most common. Cardiac volvulus post -cardiac surgery acquired defect has been described.
CT features are an absent fibrous pericardium with lung on both sides of the right ventricle outflow tract and bulging of the main pulmonary artery to the left side. There is no preaortic recess and direct contact between heart and lung is observed(Fig.2).
In general the pericardium reacts to a wide variety of insults in a limited fashion that includes fluid exudation, fibrin production and cellular proliferation. Pericarditis may be primary or secondary with primary idiopathic being the most common. Of the many secondary causes infection (especially tuberculosis), renal failure, radiation, myocardial infarction and collagen vascular disorders are the most clinically prevalent. In many cases pericarditis is self limited or limited with medication alone and has little consequence. However in some the natural history results in calcification and/or constriction. Features of constriction include an elongated right ventricle, enlarged right atrium, paradoxical bowing of the inter-ventricular septum vena cava and hepatic engorgement in the later stages. Although a right heart problem constriction disrupts the Starling mechanism leading to left heart dysfunction and pleural effusions.
The CT features of pericarditis are a thickened (Fig. 3) or calcified pericardium (Fig. 4) with an effusion in the majority of patients. Calcification is often focal or patchy and a small strategically placed plaque may have disproportionate hemodynamic consequence. Calcified pericardium in an appropriate distribution may cause atrio-ventricular valve stenosis. Two patterns of calcification have been described-linear (Fig. 4A) or amorphous Fig. 4B). It involves the visceral and parietal layers and most commonly is found near the right and left atrio-ventricular grooves. Calcification may be seen independent of constriction and vice versa. A normal pericardium by CT, in a patient with the correct clinical picture excludes constriction and makes a restrictive cardiac disease more likely but for the rare entity of constrictive epicarditis. CT will reveal secondary effects of constriction including elongated right ventricle, bowed septum, enlarged right atrium, dilated vena cavae and possibly liver congestion (Fig. 5). Failure to see the posterolateral wall of the left ventricle on contrast enhanced CT may indicate myocardial fibrosis or atrophy, predicts a poor surgical outcome and high mortality and has been suggested as a finding that contraindicates surgical pericardiectomy.
CT is the gold standard imaging test for calcified pericarditis with a pathognomonic appearance and a clear definition of what is often a segmentally distributed condition. It is invaluable for surgical planning and for follow-up post surgery to evaluate the completeness of excision. It will be increasingly important to be aware of the distribution of pericardial calcification to distinguish it from coronary calcification for calcium scoring patients.
Pericardial effusions are seen in most conditions that cause pleural effusions and ascites (Fig. 6,7). Hydropericardium, hemopericardium, chylopericaridum and pyopericardium giving transudates and exudates with benign and malignant etiologies have all been described. The size of effusions has been graded based on their distribution with small effusions collecting dorsal to the left ventricle and left atrium, larger collections accumulating anteriorly, very large ones surrounding the heart and massive effusions being those that extend towards the abdomen. Should the fluid cause the pericardial pressures, which are normally negative or equal to pleura, to rise hemodynamic consequence is manifest in the form of tamponade. In the setting of an abnormal pericardium, smaller volumes of effusion may have greater effect.
The CT attenuation values of the effusion may reflect its character being low in chylopericardium and hydropericardium but higher in acute hemopericardium. The concern for tamponade should be raised when some of the signs of raised right heart pressures are seen such as those described above in the setting of constriction (Fig. 8). Positioning may help evaluate for the presence of loculation. Positional change and enhancement may distinguish effusion and pericardial thickening though they may coexist
Iatrogenic and traumatic are among the more common etiologies of pneumopericardium. Cardiac surgery, pericardiocentesis and esophageal sclerotherapy represent the majority of iatrogenic causes. Direct connections have been identified such as; alveolar-pericaridial, pleuro-pericardial, peritoneo-pericardial, as well as enteric fistulae particularly esophageal. In discriminating air collections CT surpasses echocardiography and MRI studies (Fig. 9). Pneumopericardium just like effusions can result in a tamponade effect.
The causes of pericardial masses are many and varied (Figs. 10-18). The most common primary mass is a congenital celomic cyst (Fig. 10). Benign and malignant pericardial solid masses are equally common (Fig. 11,12) Teratoma and malignant mesothelioma are the leading primary solid masses. Metastases are the most common malignancy of the pericardium are far more common than primary with seventy percent due to spread from lung, breast and lymphoproliferative disorders (Fig. 13,14,15). In those with pericardial metastases 25% have reduced cardiac function and for the majority tamponade is the commonest cause of death.10% of people dying of cancer have pericardial metastases. Direct spread of adjacent tumors is seen (Fig. 16,17). Although primary tumors more commonly affect the myocardium than the pericardium the reverse is true of secondary tumors.
CT features of masses that may help discriminate their etiology include; morphology, location, extent, cyst or solid character, their effect on cardiac chambers as well as their enhancement characteristics and the amount of extracardiac disease. It is in the setting of malignancy with its ability to evaluate the whole thorax that CT has much to offer.
Computed tomography has much to offer in the evaluation of pericardial disease. In routine practice effusions and thickening of the pericardium are the most common findings and an appreciation of the normal anatomy helps differentiate these entities from other mediastinal pathologies. For calcified pericarditis and pneumopericardium there is no better test than CT. Most masses are well characterized by computed tomography and a clear differential is usually possible. Multidetector CT with deceased motion artifact and higher resolution together with the possibilities of gating and functional imaging has great potential for the future.