o Defined by thickening of pericardium (>4mm) impeding diastolic filling.
o Thickened pericardium may calcify (50%).
o Calcified pericardium almost always implies constriction, but not always.
o About 50% of calcified pericardiums are visible on conventional radiography.
o Calcification of the pericardium is most likely inflammatory in nature.
Can be seen with a variety of infections, trauma, and neoplasms.
Most common causes include:
Viral pericarditis (most common).
o Calcification most commonly occurs along the inferior diaphragmatic surface of the pericardium surrounding the ventricles.
Thin, egg-shell like calcification is more often associated with viral infection or uremia.
Calcification from old TB is often thick, confluent, and irregular in appearance, especially when compared with myocardial calcification.
Plain chest radiographs may show pericardial calcification in as many as 50% of CP patients.
The cardiac silhouette should be small in a patient with uncomplicated CP.
CP can also coexist with cardiomyopathy, and a large heart does not exclude the disease. Other, less reliable plain radiographic findings include an abnormal cardiac contour, such as straightening of the right atrial border and, more rarely, straightening of the right and left cardiac borders, with obliteration of the normal curves, on frontal images. On fluoroscopy, diminished cardiac pulsation may be seen.
The absence of calcification does not exclude the disease, and further testing should include an extensive workup in the echocardiography laboratory, with an assessment of the Doppler velocities across the mitral and tricuspid valves during inspiration and expiration.
The pericardium should be diffusely thicker than 3 mm; however, many patients do not present with this finding, and the diagnosis of CP should not be discarded if thickening is not present. The size of all 4 heart chambers should be within the normal range; however, CP can coexist with other diseases, and global or focal dilatation of the cardiac chambers does not exclude CP.
The inflow veins to the right atrium, including the SVC, inferior vena cava (IVC), and hepatic veins, should be dilated. This finding is necessary but not sufficient to make the diagnosis of CP because it commonly occurs in the setting of congestive heart failure brought on by a variety of causes. Most often, when the hepatic veins and IVC are dilated for reasons other than CP, dilatation of 1 or all of the cardiac chambers is present and caused by systolic dysfunction or valve disease. If significant cirrhosis has already occurred, the hepatic veins may not be dilated.
In CP, there should be poor opacification of liver parenchyma due to congestion and there should be no contrast enhancement in the portal vein.
NB: Dilated veins can be caused by right-sided heart failure. Liver cirrhosis can mimic the CT findings of CP.
Magnetic Resonance Imaging:
Diffuse thickening of the pericardium greater than 3 mm can be observed on multiplanar MRIs.
ECG-triggered MRI is sensitive to constrictive disease of the pericardium because the fibrous layers are bordered by fat, which produces a distinct MRI signal. MRI can be used to measure pericardial thickness; the ideal views for measuring pericardial thickness are oriented perpendicular to the long axis of the left ventricle. MRI can also be used to measure chamber sizes at successive 50-msec delays after the R wave and to determine whether or not a filling plateau is present.
Like echocardiography and/or Doppler imaging, velocity-encoded (VENC) MRI can be used to assess volumetric flow and regurgitant flow to the pulmonary veins and the hepatic vein. MRI can demonstrate focal abnormalities and can cover the heart to determine whether the disease encapsulates its entirety.
MRI dynamically shows a reversed curvature of the interventricular septum clearly.
Fast imaging can be performed during deep respiration to establish whether filling is concordant or discordant. CP restriction creates discordance with reduced left ventricular filling, which corresponds to increased right ventricular filling.
Liver sonograms show dilated hepatic veins and abnormal pulse Doppler waveforms in the portal and hepatic veins due to outflow obstruction.
Abdominal ultrasonographic findings are nonspecific and must be confirmed with echocardiography and cardiac catheterization results.
Cardiac echograms show normal contraction and systolic function. Special procedures, including an assessment of Doppler velocities across the mitral and tricuspid valves during inspiration and expiration, are needed to demonstrate ventricular interdependence.
Budd-Chiari syndrome, cirrhosis, and right-sided heart failure can mimic some of the findings of CP at liver ultrasonography.
Gated nuclear ventriculography may show rapid ventricular filling in CP. Reportedly, these findings can be used to differentiate CP from restrictive cardiomyopathy.