Acute pulmonary embolism multimodality imaging prior to endovascular therapy
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REVIEW PAPER
Acute pulmonary embolism multimodality imaging prior to endovascular therapy David Sin1 · Gordon McLennan1 · Fabian Rengier2 · Ihab Haddadin1 · Gustavo A. Heresi3 · John R. Bartholomew4 · Matthias A. Fink2 · Dustin Thompson1 · Sasan Partovi1 Received: 28 July 2020 / Accepted: 19 August 2020 © Springer Nature B.V. 2020
Abstract The manuscript discusses the application of CT pulmonary angiography, ventilation–perfusion scan, and magnetic resonance angiography to detect acute pulmonary embolism and to plan endovascular therapy. CT pulmonary angiography offers high accuracy, speed of acquisition, and widespread availability when applied to acute pulmonary embolism detection. This imaging modality also aids the planning of endovascular therapy by visualizing the number and distribution of emboli, determining ideal intra-procedural catheter position for treatment, and signs of right heart strain. Ventilation–perfusion scan and magnetic resonance angiography with and without contrast enhancement can also aid in the detection and pre-procedural planning of endovascular therapy in patients who are not candidates for CT pulmonary angiography. Keywords Acute pulmonary embolism · Computed tomography pulmonary angiography · Ventilation–perfusion scan · Magnetic resonance angiography
Introduction
Clinical evaluation of suspected acute PE
Acute pulmonary embolism (PE) is a frequently encountered disease associated with high morbidity and mortality [1]. Most cases of acute PE originate from lower extremity deep vein thrombosis [2]. The thirty-day mortality rate is estimated to be 4%, and the one-year mortality rate is estimated to be 13% [3]. The incidence of acute PE is higher in males (56 per 100,000 people) compared to females (48 per 100,000 people) [4–6]. Advanced age is correlated with increased incidence of acute PE [5, 7].
Acute PE presents with variable severity [8–11]. This can be explained by the varying degrees of pulmonary vasculature obstruction secondary to venous thromboembolism. Gradual increases in pulmonary artery pressure can be seen when greater than 30–50% of an arterial bed’s cross-sectional area is occluded as a result of stressed endothelial cells releasing thromboxane and other vasoactive mediators [12]. Increased pulmonary artery pressure resulting from acute PE obstruction increases right heart strain secondary to elevated right ventricular afterload [13]. Right ventricular dysfunction can be observed acutely as a result of the increased afterload as well as myocardial ischemia [2]. Continued stress on the ventricles can cause protracted contractions, ischemia, and desynchronization of the left and right ventricles [14]. Prolonged elevation of pulmonary vascular pressures can also cause pulmonary hypertension that lasts beyond the original event [15]. Dyspnea, pleuritic chest pain, and cough are the most common presenting symptoms of acute PE, while other signs of acute PE include unilateral leg edema, sinus tachycardia, and tachypnea [16, 17]. Initial testing for patients with susp
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