[Pulmonary CT angiography in pulmonary embolism: beyond diagnosis].

c Right ventricular dysfunction (RVD) is the most common cause of short-term mortality in patients with acute pulmonary embolism (PE).1 Shock and hemodynamic instability, defined as systolic blood pressure below 90mmHg or a fall of more than 40mmHg, is a clinical marker of high risk and identifies patients who may benefit from early thrombolysis.2 However, in PE patients without hemodynamic compromise, the cost/benefit ratio of fibrinolytic therapy is less clear. In order to determine the therapeutic strategy in such patients, a more detailed and accurate stratification is essential, based on early detection of RVD. The pathophysiology of RVD in PE is thought to be due to a sharp increase in right ventricular (RV) afterload caused by both mechanical pulmonary arterial obstruction and pulmonary vasoconstriction mediated by neurohumoral factors.3 Although compensatorymechanisms tomaintain RV systolic function come into play, including catecholamineinduced tachycardia and recruitment of preload reserve via the Frank-Starling mechanism, cardiac output from the RV decreases, resulting in reduced left ventricular (LV) filling. Increased wall stress and decreased oxygen supply can trigger ventricular ischemia, which in turn leads to systolic dysfunction and hemodynamic instability. Depending on clinical conditions, including comorbidities and clot burden, this vicious cycle may prove rapidly fatal, particularly