Novel use of parametric mapping in the assessment of acute pericarditis and hemopericardium in the setting of constrictive pericarditis (QF_TH_014)

A 34-year-old male with no past medical history presented with signs and symptoms of fatigue, hepatomegaly, jaundice and lower extremity edema. Initial work-up by hepatology were consistent with chronic congestive hepatopathy

Diagnostic Techniques and Their Most Important Findings:

Echocardiography features of septal bounce and tissue doppler annulus reversus, were confirmed with cardiac catheterization and suggested right heart failure with constrictive physiology.

Cardiovascular magnetic resonance (CMR) imaging performed on a 3 Tesla system revealed pericardial thickening (4 mm) with late gadolinium enhancement (LGE) around the left ventricle, indicative of pericardial inflammation. Elevated pericardial mapping values were noted, with T1 at 1447 ms and T2 at 37 ms, both higher than myocardial values. These findings, along with septal bounce and tubular left ventricular morphology, were consistent with constrictive pericarditis

Additional material was observed in the pericardial space adjacent to the lateral border of the left ventricle. This material appeared dark on TruFISP cine sequences, did not exhibit LGE, and was T2-weighted hypointense, suggestive of thrombus. Mapping values of T1 1085 ms and T2 33 ms indicated the presence of chronic thrombi..

Learning Points from this Case:

Although CMR is utilized for diagnosing pericardial inflammation, conventional imaging techniques can still pose challenges. Few studies have explored the quantitative assessment of pericardial inflammation using parametric mapping, which may serve as a novel, contrast-independent marker. Elevated mapping values correlate with pericardial inflammation, burden of pericardial LGE, and inflammatory biomarkers.
In this case, parametric values provided objective confirmation of the suspicion of acute pericarditis, supported by pericardial thickening, and enhancement. Moreover, mapping was helpful in identifying the chronicity of hemopericardium, as recent thrombi typically exhibit shorter native T1 times compared to older thrombi. Signs of septal bounce and tubular left ventricular morphology on CMR were consistent with constrictive physiology, concordant with findings on both echocardiography and cardiac catheterization. No pericardial calcification was evident on computed tomography imaging. The etiology of the constriction may be related to the inflammatory process of the pericardium, compounded by the mass effect of chronic thrombi, which may indicate an acute-on-chronic relapsing history of pericarditis.
This case highlights the utility of parametric mapping in facilitating diagnostic decision-making regarding pericardial inflammation and the etiology of constrictive pericarditis.