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PREDICTORS OF CONSTRICTIVE PERICARDITIS FOLLOWING PERICARDIOCENTESIS FOR SIGNIFICANT PERICARDIAL EFFUSION
A27.E254 JACC March 9, 2010 Volume 55, issue 10A
CARDIAC FUNCTION AND HEART FAILURE PREDICTORS OF CONSTRICTIVE PERICARDITIS FOLLOWING PERICARDIOCENTESIS FOR SIGNIFICANT PERICARDIAL EFFUSION ACC Poster Contributions Georgia World Congress Center, Hall B5 Monday, March 15, 2010, 9:30 a.m.-10:30 a.m.
Session Title: Comorbidities and Cardiomyopathies Abstract Category: Cardiomyopathies/Myocarditis/Pericardial Disease Presentation Number: 1121-42 Authors: Kye Hun Kim, Lawrence Sinak, Gellian Nestbitt, Raul E Espinosa, A. Jamil Tajik, Jae K Oh, Mayo Clinic, Rochester, MN, Chonnam National University Hospital, Gwangju, South Korea Background: Constrictive pericarditis (CP) may develop following pericardiocentesis, but the predictors related to the development of CP are not well known. The aim of this study was to investigate the predictors of CP after pericardiocentesis for significant pericardial effusion (PE). Methods: A total of 205 patients who underwent pericardiocentesis were divided into 2 groups according to the transthoracic echocardiographic (TTE) evidence of CP; patients with CP (group I, n=33, 53.8±17.8 years) versus patients without CP (group II, n=172, 60.1±15.6 years). Clinical, laboratory, TTE findings were compared. Results: Clinical findings including etiology, symptoms and signs of PE were not different between the groups. Laboratory findings were also not different between the groups except for the results of pericardial fluid analysis. In pericardial fluid analysis, the percentage of neutrophils was significantly higher (50.6±25.6 vs 28.2±25.4%, p=0.003), and the percentage of monocytes was significantly lower (15.5±19.1 vs 31.4±25.7%, p=0.010) in group I than in group II. The early diastolic velocity of septal mitral annulus (Em) (9.4±4.0 vs 7.0±2.3 cm/s, p=0.002) increased significantly, and the incidence of loculated (43.5 vs 21.1%, p=0.024) or fibrinous (43.5 vs 17.8%, p=0.007) PE were significantly higher in group I than in group II on pre-centesis TTE. The echo-lucent or low echo soft tissue density within pericardial space (pericardial rind) (75.0 vs 20.0%, p<0.001) and the simultaneous movement of pericardium with liver capsule to same direction on subcostal view (43.5 vs 87.5%, p<0.001) were developed frequently in group I than in group II on post-centesis TTE. Conclusion: The present study suggested that several pre- and post-centesis TTE findings, and higher proportion of acute inflammatory cells within pericardial fluid were significantly associated with the development of CP after pericardiocentesis. Careful follow up echocardiography should be considered in patients with these findings.
CARDIAC FUNCTION AND HEART FAILURE PREDICTORS OF CONSTRICTIVE PERICARDITIS FOLLOWING PERICARDIOCENTESIS FOR SIGNIFICANT PERICARDIAL EFFUSION ACC Poster Contributions Georgia World Congress Center, Hall B5 Monday, March 15, 2010, 9:30 a.m.-10:30 a.m.
Session Title: Comorbidities and Cardiomyopathies Abstract Category: Cardiomyopathies/Myocarditis/Pericardial Disease Presentation Number: 1121-42 Authors: Kye Hun Kim, Lawrence Sinak, Gellian Nestbitt, Raul E Espinosa, A. Jamil Tajik, Jae K Oh, Mayo Clinic, Rochester, MN, Chonnam National University Hospital, Gwangju, South Korea Background: Constrictive pericarditis (CP) may develop following pericardiocentesis, but the predictors related to the development of CP are not well known. The aim of this study was to investigate the predictors of CP after pericardiocentesis for significant pericardial effusion (PE). Methods: A total of 205 patients who underwent pericardiocentesis were divided into 2 groups according to the transthoracic echocardiographic (TTE) evidence of CP; patients with CP (group I, n=33, 53.8±17.8 years) versus patients without CP (group II, n=172, 60.1±15.6 years). Clinical, laboratory, TTE findings were compared. Results: Clinical findings including etiology, symptoms and signs of PE were not different between the groups. Laboratory findings were also not different between the groups except for the results of pericardial fluid analysis. In pericardial fluid analysis, the percentage of neutrophils was significantly higher (50.6±25.6 vs 28.2±25.4%, p=0.003), and the percentage of monocytes was significantly lower (15.5±19.1 vs 31.4±25.7%, p=0.010) in group I than in group II. The early diastolic velocity of septal mitral annulus (Em) (9.4±4.0 vs 7.0±2.3 cm/s, p=0.002) increased significantly, and the incidence of loculated (43.5 vs 21.1%, p=0.024) or fibrinous (43.5 vs 17.8%, p=0.007) PE were significantly higher in group I than in group II on pre-centesis TTE. The echo-lucent or low echo soft tissue density within pericardial space (pericardial rind) (75.0 vs 20.0%, p<0.001) and the simultaneous movement of pericardium with liver capsule to same direction on subcostal view (43.5 vs 87.5%, p<0.001) were developed frequently in group I than in group II on post-centesis TTE. Conclusion: The present study suggested that several pre- and post-centesis TTE findings, and higher proportion of acute inflammatory cells within pericardial fluid were significantly associated with the development of CP after pericardiocentesis. Careful follow up echocardiography should be considered in patients with these findings.