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Echocardiography, troponins and lower extremity ultrasound: the ‘Three Musketeers’ lead the prognosis of acute pulmonary embolism
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  1. Antonio Vitarelli
  1. Sapienza University, Cardio-Respiratory Department, Rome, Italy
  1. Correspondence to Professor Antonio Vitarelli, Via Lima 35, 00198 Rome, Italy; vitar{at}tiscali.it

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The European guidelines1 and American guidelines2 highlight that, in the diagnosis and management of acute pulmonary embolism (PE), the functional consequences determined by right ventricular (RV) dysfunction and elevation of cardiac biomarkers are more relevant for risk stratification than assessment of the anatomical burden and distribution of the pulmonary artery thrombus. The mortality rate associated with massive PE may reach 30%, while that associated with so-called submassive PE (defined as the presence of RV dysfunction without systemic hypotension) is between 5% and 10% and that associated with non-massive PE is <5%.1 While there is consensus that thrombolytic therapy, catheter embolectomy or surgery are indicated in patients with right heart failure and haemodynamic instability, the appropriate treatment of patients with submassive PE remains controversial. In this subset of patients, the ‘tricks of the trade’3 should be identified and clinical-laboratory aspects evaluated to judge the level of severity. RV echocardiographic parameters, cardiac troponins and peripheral ultrasound data are described as poor prognostic factors in the currently available literature.

Each of these tests has its own advantages and limitations. A number of studies have shown that RV dysfunction and dilation is a robust prognostic factor in acute PE. Still, some questions arise. First, the different pathophysiology of acute versus chronic pulmonary hypertension has recently been outlined.4 Similarities between PE (acute occlusive pulmonary hypertension) and chronic pulmonary hypertension include the fact that pulmonary circulatory resistance increases, RV function may decline and mortality and morbidity are correlated with the extent of RV dysfunction in both cases. Nevertheless, the mechanisms of cardiopulmonary changes are very different and result in different modes of RV injury …

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