RESUMEN
INTRODUCTION: Although in the non-vitamin K oral anticoagulants (NOAC) era majority of low-risk acute pulmonary embolism (APE) patients can be treated at home, identifying those at very low risk of clinical deterioration may be challenging. We aimed to propose the risk stratification algorithm in sPESI 0 point APE patients, allowing them to select candidates for safe outpatient treatment. MATERIALS AND METHODS: Post hoc analysis of a prospective study of 1151 normotensive patients with at least segmental APE. In the final analysis, we included 409 sPESI 0 point patients. Cardiac troponin assessment and echocardiographic examination were performed immediately after admission. Right ventricular dysfunction was defined as the right ventricle/left ventricle ratio (RV/LV) > 1.0. The clinical endpoint (CE) included APE-related mortality and/or rescue thrombolysis and/or immediate surgical embolectomy in patients with clinical deterioration. RESULTS: CE occurred in four patients who had higher serum troponin levels than subjects with a favorable clinical course (troponin/ULN: 7.8 (6.4-9.4) vs. 0.2 (0-1.36) p = 0.000). Receiver operating characteristic (ROC) analysis showed that the area under the curve for troponin in the prediction of CE was 0.908 (95% CI 0.831-0.984; p < 0.001). We defined the cut-off value of troponin at >1.7 ULN with 100% PPV for CE. In univariate and multivariate analysis, elevated serum troponin level was associated with an increased risk of CE, whereas RV/LV > 1.0 was not. CONCLUSIONS: Solely clinical risk assessment in APE is insufficient, and patients with sPESI 0 points require further assessment based on myocardial damage biomarkers. Patients with troponin levels not exceeding 1.7 ULN constitute the group of "very low risk" with a good prognosis.
RESUMEN
INTRODUCTION: SARS-CoV-2 infection leads to a hypercoagulable state. The prevalence of pulmonary embolism (PE) seems to be higher in this subgroup of patients. PATIENTS AND METHODS: We combined data from two tertiary referral centers specialized in the management of PE. The aims of this study were as follows: (1) to evaluate the prevalence of PE among a large population of consecutive patients admitted for COVID-19 pneumonia in two centers, (2) to identify a plasma D-dimer threshold that may be useful in PE diagnostic assessment, (3) to characterize the abnormalities associated with PE and mortality in COVID-19 patients. RESULTS: The incidence of symptomatic acute PE was 19.3%. For diagnosing PE in COVID-19 patients, based on ROC curve analysis, we identified a D-dimer concentration/patient's age ratio of 70, which improved D-dimer diagnostic capacity for PE and led to a reclassification improvement of 14% (NRI 0.14, p = 0.03) when compared to a cut-off level of 1000 ng/mL. Especially in severe COVID-19 lung involvement, D-dimer/age ratio cut-off equal to 70 was characterized by high diagnostic feasibility (sensitivity, specificity, negative predictive value, positive predictive value of 83%, 94%, 96%, and 73%, respectively). Apart from PE status, lung involvement and troponin T concentration were also independent predictors of in-hospital mortality. In the subgroup of PE patients, mortality was comparable with non-PE patients (19/88 (21.5%) vs. 101/368 (27.4%) for non-PE, p = 0.26) and was associated with older age, higher Bova scores, and higher troponin T concentrations. Age was the sole independent predictor for mortality in this subgroup. CONCLUSIONS: PE in COVID-19 patients is common, but it may not influence mortality when managed at a specialized center. In suspected PE, age-adjusted D-dimer levels (upper limit of normal obtained from the formula patient's age × 70) may still be a useful tool to start the diagnostic workup. In COVID-19 patients without PE, older age, more extensive parenchymal involvement, or higher D-dimer levels are factors predicting mortality.