Highlights the ongoing clinical challenge of risk stratifying hemodynamically stable patients with acute pulmonary embolism to identify those at high risk of adverse outcomes.
Management strategy and its influence on the outcomes for patients with acute pulmonary embolism (PE) has been an area of chronic debate and unresolved controversies. During the last decade at least 50 publications have provided important evidence on prognostic markers, with the hope of improving risk stratification and, consequently, treatment decisions for PE. Such markers ranged from simple clinical signs to variables, which require sophisticated laboratory tests and modern cardiovascular imaging. Paradoxically, messages most relevant to a practicing clinician confronting a patient with acute PE, so far, seem to emerge from clinical evaluation. Signs of shock or significant hypotension became universally accepted markers of high risk PE, justifying emergency thrombolysis [1]. More recently, several clinical scores have been reliably validated to identify patients at a very low risk of adverse outcomes, despite confirmed PE [2–4]. If adequately anticoagulated, such patients may be offered an option of early discharge and ambulatory therapy [5]. The trial by Bova et al . [6] attempts to solve a remaining important clinical problem , i.e. that of identifying patients with acute PE who are at a particularly high risk of adverse outcome, despite normal systemic arterial pressure. Previous similar attempts have not been successful, mostly because of a low positive prognostic value of individual laboratory-risk markers for early PE-related mortality, in this particular patient subgroup. Nevertheless, in initially hemodynamically stable patients, deaths do occur either because of early recurrence of PE or the decompensation of the right ventricle that has been submitted to excessive and prolonged overload. Progressive dilatation of right heart chambers, functional tricuspid regurgitation, increasing wall strain and oxygen myocardial, in a setting of diminished functional right ventricular coronary perfusion and hypoxaemia, may initiate and feed a rapid vicious circle, which leads …
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Adam Torbicki (2014) studied this question.
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