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Journal Article
Research Support, Non-U.S. Gov't
Signs of myocardial ischemia on electrocardiogram correlate with elevated plasma cardiac troponin and right ventricular systolic dysfunction in acute pulmonary embolism.
Cardiology Journal 2010
BACKGROUND: Plasma cardiac troponins (cTn) are frequently elevated in acute pulmonary embolism (APE). ST-segment abnormalities on electrocardiography are also commonly observed in APE patients. However, it has not been defined which ventricle is a potential source of cTn release. We assessed the potential relationship between electrocardiographic signs of myocardial ischemia, systolic dysfunction of both ventricles at echocardiography and cTn levels in APE.
METHODS: We evaluated 94 consecutive patients (42 male, 52 female, aged 63 +/- 19 years) with APE. On admission, blood samples were collected for cTnI or cTnT and standard 12-lead electrocardiogram was performed. The following signs of myocardial ischemia were analyzed: T-wave inversion [T (-)] and ST-depression or elevation (> or = 1 mV, at > or = 2 leads). The assessment of systolic function of both ventricles was performed by echocardiography.
RESULTS: In 33 (35%) patients, cTn exceeded the upper reference limit of our laboratory. The history of coronary artery disease (27% vs. 31%) and previous myocardial infarction (12% vs. 10%) did not differ in patients with elevated cTn [cTn (+)] and non-elevated cTn [cTn (-)]. In cTn (+) group T (-) or ST-depression were observed more frequently than in cTn (-) [32 (97%) vs. 46 (75%), p < 0.01]. However, both groups presented similar frequency of ST-elevation [7 (21%) vs. 11 (18%), p = NS). Interestingly, cTn levels correlated with the number of leads with T (-) or ST-depression (R = 0.30, p < 0.01). Moreover, in cTn (+) group right ventricular systolic dysfunction was more frequent [15 (54%) vs. 4 (7%), p = 0.0001], while left ventricle contractility abnormalities occurred similarly in both groups [3 (11%) vs. 8 (15%), p = NS].
CONCLUSIONS: Signs of myocardial ischemia (ST-segment changes) on electrocardiography in APE correlate with an elevated cTn and with the impairment of right, but not left, ventricle systolic function at echocardiography.
METHODS: We evaluated 94 consecutive patients (42 male, 52 female, aged 63 +/- 19 years) with APE. On admission, blood samples were collected for cTnI or cTnT and standard 12-lead electrocardiogram was performed. The following signs of myocardial ischemia were analyzed: T-wave inversion [T (-)] and ST-depression or elevation (> or = 1 mV, at > or = 2 leads). The assessment of systolic function of both ventricles was performed by echocardiography.
RESULTS: In 33 (35%) patients, cTn exceeded the upper reference limit of our laboratory. The history of coronary artery disease (27% vs. 31%) and previous myocardial infarction (12% vs. 10%) did not differ in patients with elevated cTn [cTn (+)] and non-elevated cTn [cTn (-)]. In cTn (+) group T (-) or ST-depression were observed more frequently than in cTn (-) [32 (97%) vs. 46 (75%), p < 0.01]. However, both groups presented similar frequency of ST-elevation [7 (21%) vs. 11 (18%), p = NS). Interestingly, cTn levels correlated with the number of leads with T (-) or ST-depression (R = 0.30, p < 0.01). Moreover, in cTn (+) group right ventricular systolic dysfunction was more frequent [15 (54%) vs. 4 (7%), p = 0.0001], while left ventricle contractility abnormalities occurred similarly in both groups [3 (11%) vs. 8 (15%), p = NS].
CONCLUSIONS: Signs of myocardial ischemia (ST-segment changes) on electrocardiography in APE correlate with an elevated cTn and with the impairment of right, but not left, ventricle systolic function at echocardiography.
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