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Cardiac troponin I in acute pericarditis.
Massimo Imazio, Brunella Demichelis, Enrico Cecchi, Riccardo Belli, Aldo Ghisio, Marco Bobbio, Rita TrincheroJournal of the American College of Cardiology 2003 December 17
OBJECTIVES: This study was designed to investigate the prognostic value of cardiac troponin I (cTnI) in viral or idiopathic pericarditis.
BACKGROUND: Idiopathic acute pericarditis has been recently reported as a possible cause of nonischemic release of cTnI. The prognostic value of this observation remains unknown.
METHODS: We enrolled 118 consecutive cases (age 49.2 +/- 18.4 years; 61 men) within 24 h of symptoms onset. A highly sensitive enzymoimmunofluorometric method was used to measure cTnI (acute myocardial infarction [AMI] threshold was 1.5 ng/ml).
RESULTS: A cTnI rise was detectable in 38 patients (32.2%). The following characteristics were more frequently associated with a positive cTnI test: younger age (p < 0.001), male gender (p = 0.007), ST-segment elevation (p < 0.001), and pericardial effusion (p = 0.007) at presentation. An increase beyond AMI threshold was present in nine cases (7.6%), with an associated creatine kinase-MB elevation, a release pattern similar to AMI, and echocardiographic diffuse or localized abnormal left ventricular wall motion without detectable coronary artery disease. After a mean follow-up of 24 months a similar rate of complications was found in patients with a positive or a negative cTnI test (recurrent pericarditis: 18.4 vs. 18.8%; constrictive pericarditis: 0 vs. 1.3%, for all p = NS; no cases of cardiac tamponade or residual left ventricular dysfunction were detected).
CONCLUSIONS: In viral or idiopathic acute pericarditis cTnI elevation is frequently observed and commonly associated with young age, male gender, ST-segment elevation, and pericardial effusion at presentation. cTnI increase is roughly related to the extent of myocardial inflammatory involvement and, unlike acute coronary syndromes, is not a negative prognostic marker.
BACKGROUND: Idiopathic acute pericarditis has been recently reported as a possible cause of nonischemic release of cTnI. The prognostic value of this observation remains unknown.
METHODS: We enrolled 118 consecutive cases (age 49.2 +/- 18.4 years; 61 men) within 24 h of symptoms onset. A highly sensitive enzymoimmunofluorometric method was used to measure cTnI (acute myocardial infarction [AMI] threshold was 1.5 ng/ml).
RESULTS: A cTnI rise was detectable in 38 patients (32.2%). The following characteristics were more frequently associated with a positive cTnI test: younger age (p < 0.001), male gender (p = 0.007), ST-segment elevation (p < 0.001), and pericardial effusion (p = 0.007) at presentation. An increase beyond AMI threshold was present in nine cases (7.6%), with an associated creatine kinase-MB elevation, a release pattern similar to AMI, and echocardiographic diffuse or localized abnormal left ventricular wall motion without detectable coronary artery disease. After a mean follow-up of 24 months a similar rate of complications was found in patients with a positive or a negative cTnI test (recurrent pericarditis: 18.4 vs. 18.8%; constrictive pericarditis: 0 vs. 1.3%, for all p = NS; no cases of cardiac tamponade or residual left ventricular dysfunction were detected).
CONCLUSIONS: In viral or idiopathic acute pericarditis cTnI elevation is frequently observed and commonly associated with young age, male gender, ST-segment elevation, and pericardial effusion at presentation. cTnI increase is roughly related to the extent of myocardial inflammatory involvement and, unlike acute coronary syndromes, is not a negative prognostic marker.
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