P5279Pericardial inflammation basced on cardiac magnetic resonance imaging in patients with tuberculous pericarditis

Background While constrictive pericarditis has been traditionally considered a disabling disease, reversible constrictive pericarditis has been described in previous studies. But there are limited studies on cardiac imaging of tuberculous pericarditis. In particular, no studies on cardiac magnetic resonance imaging (CMR) have been reported. We aimed to investigate CMR findings including pericardial late gadolinium enhancement (LGE) and T2 fat suppression and black blood sequences in patients with tuberculous pericarditis. Methods We retrospectively analyzed medical records of patients with tuberculous pericarditis between January 2010 and January 2017 in Samsung Medical Center. Definite diagnosis of tuberculous pericarditis is based on the identification of Mycobacterium tuberculosis in pericardial fluid or tissue; probable diagnosis was made when there was other evidence of tuberculosis elsewhere in patients with unexplained pericarditis. We performed CMR at initial diagnosis. Treatment consists of the standard 4-drug antituberculosis regimen for 6 months with or without steroids. Echocardiography was also conducted at initial diagnosis and 6 months later. Results Total 39 cases with tuberculous pericarditis in immunocompetent patients were enrolled. Ten patients were diagnosed as definite tuberculous pericarditis. CMR finding at initial diagnosis divided into five groups: 1) pericardial effusion only (n=20, 51.3%), 2) effusive constrictive pericarditis (n=5, 12.8%), 3) constrictive pericarditis (n=11, 28.2%), 4) pericardial abscess formation (n=4, 10.3%) and 5) absence of pericardial effusion and constrictive physiology (n=1, 2.6%). One of the 4 patients with pericardial abscess formation was together with pericardial effusion and the other was accompanied by effusive constrictive pericarditis. Pericardial thickness increased to more than 4mm in 25 patients (64.1%) and the mean pericardial thickness was 10.0±6.9mm. Delayed enhancement of pericardium was noticed in 29 patients (74.4%). In T2 fat suppression and black blood sequences, 30 patients showed increased T2 signal intensity indicating inflammation with extensive edema. Pericardial thickening (>4mm) with constriction (n=15) was not statistically significant in the delayed enhancement and increased T2 signal intensity compared with pericardial thickening without constrictive pericarditis (n=10) (delayed enhancement 93.8% vs. 77.8% p=0.287; increased T2 signal intensity 88.9% vs. 87.5%, p=0.713). After 6 months, only 3 patients still had constrictive pericarditis in echocardiography. Effusive constrictive pericarditis Conclusions Pericardial thickening is associated with delayed enhancement and increased T2 signal intensity in patients with tuberculous pericarditis regardless of constrictive pericarditis. Even though there were hemodynamic feature of constrictive pericarditis and pericardial inflammation with extensive edema in CMR at initial diagnosis, 80% of the patients were improved from constrictive pericarditis. Acknowledgement/Funding None

Capnocytophaga Induced Acute Necrotizing and Exudative Pericarditis with Abscess Formation

We present the case of a 55-year-old gentleman, with bilateral pulmonary embolism and a large pericardial effusion that lead to a pericardial window with evacuation of creamy pus. Gram stains were negative, with culture growing Capnocytophaga. Pathology revealed acute necrotizing and exudative changes, including frank abscess formation. In developed countries, pericardial abscess and acute pericarditis are uncommon due to availability of broad-spectrum antibiotics. Pericardial abscess due to Capnocytophaga is even more uncommon.