AIM: To determine whether an association exists between a known marker of platelet activation, mean platelet volume (MPV), and the severity of acute pulmonary embolism (APE), and to test whether it can be used as prognostic indicator in patients with high-risk pulmonary embolism (PE). MATERIALS AND METHODS: The study included 209 consecutive patients with APE (106 male, 103 female, mean age 62.4 ± 15.4 years) and 162 controls (86 male, 76 female) matched for age (60.5 ± 14.3 years) and concomitant diseases. Contrast-enhanced spiral computerized tomography or ventilation-perfusion scintigraphy, echocardiography, and lower extremity venous Doppler ultrasound were performed on the patients with APE. D-dimer level, troponin, arterial blood gases, platelet count, and MPV were measured in serum. RESULTS: The MPV did not differ between the patients with APE and the controls (8.0 ± 1.1 fL, 7.9 ± 0.59 fL, p = 0.22). There were no significant differences in the value of MPV among the groups of patients with massive, submassive, and nonmassive PE (MPV: 8.3 ± 0.9 fL, 8.1 ± 1.0 fL, 7.9 ± 1.1 fL, p = 0.08, respectively). The MPV was higher in non-survivors than survivors (8.6 ± 1.1 vs. 7.9 ± 1.1 fL, p = 0.02). There was a statistically weak correlation between MPV and mean pulmonary arterial pressure (r = 0.25, p < 0.001) and also between MPV and right ventricle diameter (r = 0.11, p = 0.045). CONCLUSIONS: Our results suggest that a simple baseline determination of MPV at a single time point is not a reliable indicator to determine the severity of PE or for the diagnosis of APE, but it is possible that the MPV increases in nonsurvivors.
AIM: To determine whether an association exists between a known marker of platelet activation, mean platelet volume (MPV), and the severity of acute pulmonary embolism (APE), and to test whether it can be used as prognostic indicator in patients with high-risk pulmonary embolism (PE). MATERIALS AND METHODS: The study included 209 consecutive patients with APE (106 male, 103 female, mean age 62.4 ± 15.4 years) and 162 controls (86 male, 76 female) matched for age (60.5 ± 14.3 years) and concomitant diseases. Contrast-enhanced spiral computerized tomography or ventilation-perfusion scintigraphy, echocardiography, and lower extremity venous Doppler ultrasound were performed on the patients with APE. D-dimer level, troponin, arterial blood gases, platelet count, and MPV were measured in serum. RESULTS: The MPV did not differ between the patients with APE and the controls (8.0 ± 1.1 fL, 7.9 ± 0.59 fL, p = 0.22). There were no significant differences in the value of MPV among the groups of patients with massive, submassive, and nonmassive PE (MPV: 8.3 ± 0.9 fL, 8.1 ± 1.0 fL, 7.9 ± 1.1 fL, p = 0.08, respectively). The MPV was higher in non-survivors than survivors (8.6 ± 1.1 vs. 7.9 ± 1.1 fL, p = 0.02). There was a statistically weak correlation between MPV and mean pulmonary arterial pressure (r = 0.25, p < 0.001) and also between MPV and right ventricle diameter (r = 0.11, p = 0.045). CONCLUSIONS: Our results suggest that a simple baseline determination of MPV at a single time point is not a reliable indicator to determine the severity of PE or for the diagnosis of APE, but it is possible that the MPV increases in nonsurvivors.
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