期刊
EUROPEAN HEART JOURNAL-ACUTE CARDIOVASCULAR CARE
卷 12, 期 2, 页码 80-86出版社
OXFORD UNIV PRESS
DOI: 10.1093/ehjacc/zuac169
关键词
Pulmonary embolism; Clinical deterioration; Mean arterial pressure
This study assessed the prognostic role of mean arterial pressure (MAP) for 48-hour clinical deterioration in intermediate-high risk pulmonary embolism (PE) patients after admission. The results showed that a MAP of ≤ 81.5 mmHg at admission was the optimal cutoff value for predicting 48-hour clinical deterioration. Age, history of heart failure, simplified Pulmonary Embolism Severity Index, systemic thrombolysis, and a MAP of ≤ 81.5 mmHg at admission were identified as independent risk factors for 48-hour clinical deterioration. The deteriorating group had a significantly higher risk of 30-day mortality compared with the non-deteriorating group.
Aims We assess the prognostic role of mean arterial pressure (MAP) for 48 h clinical deterioration in intermediate-high risk pulmonary embolism (PE) patients after admission. Methods and results A post hoc analysis of intermediate-high-risk PE and intermediate-low-risk PE patients enrolled in the Italian Pulmonary Embolism Registry (IPER) (Trial registry: ClinicalTrials.gov; No.: NCT01604538) was performed. Clinical deterioration within 48 h was defined as patient worsening from a stable to an unstable haemodynamic condition, need of catecholamine infusion, endotracheal intubation, or cardiopulmonary resuscitation. Of 450 intermediate-high risk PE patients (mean age 71.4 +/- 13.8 years, 298 males), 40 (8.8%) experienced clinical deterioration within 48 h from admission. Receiver operating characteristic analysis established the optimal cut-off value for MAP, as a predictor of 48 h clinical deterioration, <= 81.5 mmHg [area under curve (AUC) of 0.77 +/- 0.3] with sensitivity, specificity, positive predictive value, and negative predictive value were 77.5, 95.0, 63.2, and 97.7%, respectively. Multivariate Cox regression analysis showed that independent risk factors for 48 h clinical deterioration were age [hazard ratio (HR): 1.26, 95% confidence interval (CI): 1.19-1.28, P < 0.0001], history of heart failure (HR: 1.76, 95% CI: 1.72-1.81, P < 0.0001), simplified Pulmonary Embolism Severity Index (HR: 1.52, 95% CI: 1.49-1.58, P = 0.001), systemic thrombolysis (HR: 0.54, 95% CI: 0.30-0.65, P < 0.0001), and a MAP of <= 81.5 mmHg at admission (HR: 3.25, 95% CI: 1.89-5.21, P < 0.0001). The deteriorating group had a significantly higher risk of 30-day mortality (HR: 2.61, 95% CI: 2.54-2.66, P < 0.0001) compared with the non-deteriorating group. Conclusion The mean arterial pressure appears to be a useful, bedside, and non-invasive prognostic tool potentially capable of promptly identifying intermediate-high risk PE patients at higher risk of 48 h clinical deterioration.
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