An Illustrative Case of Constrictive Pericarditis

A 72-year-old man, treated for hypertension and type II diabetes, presented with a few months history of inferior limbs oedema, legs ulcerations, weight gain (4–5 kg in the last 2 months), nycturia, abdominal tension, and gradually increasing dyspnea.

Clinical examination demonstrates prominent jugular veins, hepato-jugular reflux, oedema and ulcerations of inferior limbs and signs of bilateral pleural effusions. The cardiac auscultation was normal.

Chest X-ray (Figure 1A,B) shows diffuse pericardial calcifications and right pleural effusion. Thoracic CT scan confirms pleural effusion and circumferential pericardial thick-ening (6 mm) with calcifications (fig. 2A) together with dilatation of the inferior vena cava, hepatomegaly and ascites. 3-dimensional reconstruction (Figure 2B) nicely delineates the spatial extension of pericardial calcifications.

Due to poor echogenecity of the patient, cardiac MRI is performed and demonstrates: important pericardial thickening (6–7 mm) (Figure 3A), normal left ventricular function, interventricular interference during inspirium and a protodiastolic “septal bounce” (cine-MRI images). No late pericardium or myocardium enhancement is observed after Gadolinium injection (Figure 3B).

Simultaneous right- and left-heart catheterisation demonstrates rapid filling (“dip and plateau” pattern) and elevation and equalisation of LV and RV end-diastolic pressures at a value of 20 mm Hg. During inspirium, a discordant pattern of RV and LV systolic pressure changes diagnostic of pericardial constriction (Figure 4) is observed.

In summary, careful examination of chest X-ray raised the suspicion of calcific constrictive pericarditis in this patient with overt right heart failure. Standard chest CT-scan allows a nice anatomic delineation of the pericardium and its calcifications. Cardiac MRI provides systolic function of both ventricles as well as signs of diastolic interaction like “septal bounce”. Respiratory variations in chambers filling can be observed using “real-time” cine sequences [1]. The definitive diagnosis relies on a careful haemodynamic evaluation by right and left heart catheterisation including respiratory recordings of RV and LV pressure changes [2].