Cor Vasa 2016, 58(4):e403-e410 | DOI: 10.1016/j.crvasa.2015.12.001

Elevated systolic pulmonary artery pressure for prediction of myocardial necrosis and right ventricular dysfunction in acute pulmonary embolism

Karsten Keller^a,b,*, Martin Geyer^a, Meike Coldewey^a,b, Johannes Beule^c, Jörn Oliver Balzer^d,e, Wolfgang Dippold^c

^a Department of Medicine II, University Medical Center Mainz, Johannes Gutenberg-University Mainz, Mainz, Germany

^b Center for Thrombosis and Hemostasis, University Medical Center Mainz, Johannes Gutenberg-University Mainz, Mainz, Germany

^c Department of Internal Medicine, St. Vincenz and Elisabeth Hospital Mainz (KKM), Mainz, Germany

^d Department of Radiology and Nuclear Medicine, Catholic Clinic Mainz (KKM), Mainz, Germany

^e Department of Diagnostic and Interventional Radiology, University Clinic, Johann Wolfgang Goethe-University Frankfurt/Main, Frankfurt, Germany

Background: Echocardiography is currently the mainstay examination for assessment of right ventricular dysfunction (RVD) in acute pulmonary embolism (PE). RVD is associated with poorer prognosis, but there is still no generally accepted definition. Systolic pulmonary artery pressure (sPAP) is mostly not included in these RVD-criteria. We aimed to investigate sPAP for prediction of myocardial necrosis and RVD in acute PE.

Methods: Data of 182 patients with acute PE were analysed retrospectively. PE patients with sPAP ≤ 30 mmHg were compared to those with sPAP > 30 mmHg. Logistic regression models were calculated to investigate associations between sPAP and myocardial necrosis as well as RVD. Moreover ROC curves and cut-off values for sPAP predicting myocardial necrosis and RVD were computed.

Results: 134 patients (mean age 67.8 ± 15.2 years, 59.7% female) with acute PE event were included in the study. Mean sPAP value was 33.96 ± 18.14 mmHg. PE patients with sPAP > 30 mmHg (59.7%) were significantly older (71.2 ± 13.8 vs. 62.7 ± 15.7 years, p = 0.000489), more frequently female (66.3% vs. 50.0%, p = 0.0609), showed higher heart rate (98.8 ± 25.5 vs. 87.7 ± 22.1 beats/min, p = 0.00266), shock-index (0.76 ± 0.42 vs. 0.63 ± 0.26, p = 0.00892), cardiac Troponin I (0.15 ± 0.30 vs. 0.14 ± 0.32 ng/ml, p = 0.00670) and higher percentage of RVD (80.0% vs. 29.6%, p < 0.000001).
In multivariant regression model, sPAP was associated with respectively myocardial necrosis (OR 1.021, 95% CI 0.998-1.045, p = 0.0736) and RVD (OR 1.100, 95% CI 1.064-1.136, p < 0.000001).
ROC analysis for sPAP predicting myocardial necrosis revealed an AUC of 0.628 with sPAP cut-off value of 41.00 mmHg. ROC analysis for sPAP predicting RVD showed an AUC of 0.829 with sPAP cut-off value of 31.00 mmHg.

Conclusions: sPAP and respectively RVD and myocardial necrosis are both associated. sPAP is highly effective to predict RVD. sPAP values >31 mmHg indicate for RVD.

Keywords: Myocardial necrosis; Pulmonary embolism; Right ventricular dysfunction; Risk stratification; Systolic pulmonary artery pressure

Received: August 18, 2015; Revised: December 3, 2015; Accepted: December 7, 2015; Published: August 1, 2016  Show citation