|Number 10-25: Constrictive Pericarditis Post Cardiac Transplant: Diagnostic Role of Cardiovascular M|
Number 10-25: Constrictive Pericarditis Post Cardiac Transplant: Diagnostic Role of Cardiovascular MRI
Case from: Patrizia Pedrotti1, Claudia Vittori2, Maria Frigerio2, and Alberto Roghi1
Cardiovascular Magnetic Resonance Unit1 and Heart Transplant Unit2, De Gasperis Department of Cardiology, Ospedale Niguarda Ca'Granda Milano, Italy
Case 1. A 56 years old male underwent heart transplantation (HTX) 8 years ago. Clinical history was unremarkable until two years ago, when he presented with acute pericarditis and development of rapid heart failure.
Echocardiography revealed thickened pericardium and abundant pericardial effusion, with signs of pericardial tamponade (restrictive filling pattern with marked respiratory variations) and the suspicion of underlying pericardial constriction (Figure 1). A pericardial window was surgically created and pericardial fluid analysis showed small and medium size lymphatic cells and Epstein-Barr virus (EBV) genoma. The pericardium was negative for lymphoproliferative disorder. Coronary angiogram and myocardial biopsy were negative.
After resolution of the pericardial temponade the patient was discharged home on NSAIDS. After 3 months he was readmitted to the hospital with heart failure. There was no significant effusion noted on echocardiography. No active inflammatory signs were present on blood work. CMR was performed to further evaluate the pericardium and rule out constrictive pericarditis.
Cardiac magnetic resonance (CMR) showed normal biventricular function with impaired right ventricular diastolic filling (movie 1, SSFP cine images), mid-apical hypertrophy (already described in previous echocardiographic evaluations) and visceral congestion (pleural effusion and ascites).
Dark-blood T1-weighted images showed diffuse pericardial thickening (Figure 2) and cine real-time images revealed pathologic ventricular interdependence with inspiratory septal flattening, characteristic of constrictive pericarditis (movie 2). Post gadolinium images did not reveal contrast enhancement of the pericardium (Fig 3) suggesting non-inflammatory constrictive pericarditis.
Figure 2 Movie 2
Pericardiectomy was performed, with rapid hemodynamic improvement. Three months after pericardiectomy CMR showed a significant reduction in pericardial thickness (Figure 4) and the absence of dynamic signs of constriction (movie 3).
Figure 4 Movie 3
CASE 2. A 63 years old male underwent HTX 6 years ago. Mild pericardial effusion was described early at echocardiography, and persisted at one year. During the first year after HTX, primary and relapsed cytomegalovirus (CMV) infection occurred and the patient received specific treatment. Coronary angiography was normal at one year. One year ago the patient developed heart failure. An coronary angiogram plus IVUS showed type B coronary artery disease. On echocardiography, mild hypokinesia and a thickened pericardium with respirophasic valvar flow changes were noticed.
CMR showed depressed right ventricular function (movie 4, SSFP cine images), pericardial thickening (Figure 5, dark blood T1 images) and pathologic ventricular coupling (movie 5 realtime cine imaging). There was no contrast enhancement of the pericardium on post gadolinium imaging (Figure 6).
Right heart catheterization showed typical dip and plateau pattern (Figure 7).
Pericardiectomy was performed. Three months after pericardiectomy the patient was well and had no signs of pericardial constriction on echocardiogram.
Perspective: Pericardial constriction is rare after HTX and is related to the presence of pericardial effusion, hematoma, mediastinitis1 or other intrathoracic infections occurring after transplantation2 or to inflammation caused by pericardial irrigation with povidone-iodine on injured serosa. Post-pericardiectomy syndrome may also play a role3. In a recent review of 17 cases of post-HTX pericardial constriction, all patients had pericardial effusion of non infectious etiology in the early post-transplant period and time to constriction ranged from 3 weeks to 11 years4. Our patients developed pericardial constriction late after HTX. Both had a history of viral infection (EBV and CMV) occurring after HTX. Acute pericarditis and constrictive pericarditis have been reported in patients with EBV or CMV infection, both in immunocompetent and in immunocompromised patients5,6. Viral infection might have played a role in the development of pericardial constriction in these two patients, either as causative or concurrent agents.
CMR plays an increasing role in the diagnostic work up of patients with suspected constrictive pericarditis, due to its capability to thoroughly depict both the morphologic aspects of the pericardium and the dynamic functional consequences of pericardial constriction and in differentiating this condition from restrictive cardiomyopathy.
COTW Handling Editor: Vikas K. Rathi, MD