**1. Introduction**

168 Pulmonary Embolism

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Acute pulmonary embolism (PE) is a common and potentially fatal disease (Goldhaber et al., 1999). The most frequent cause of death within 30 days is right ventricular (RV) failure (Goldhaber & Elliott, 2003). Rapid risk stratification is paramount for identifying high-risk patients and for helping to select the appropriate treatment strategy. According to European guidelines (Torbicki et al., 2008), high-risk PE (formerly 'massive' PE) implies the presence of shock or hemodynamic instability (mortality >15%) (Goldhaber et al., 1999). Non highrisk PE can be further stratified by the presence of markers of RV dysfunction and/or myocardial injury as intermediate- and low-risk PE. Intermediate-risk PE (formerly 'submassive' PE) is diagnosed by the presence of at least one marker of RV dysfunction or myocardial injury. Low-risk PE (formerly 'non-massive' PE) is diagnosed when RV dysfunction markers are negative (mortality <1%). Reperfusion therapy, including thrombolysis or surgical embolectomy, is indicated for patients with high-risk PE. However, the risks and benefits of reperfusion therapy for patients with intermediate risk PE are less clear. Based on pathophysiological knowledge of the impact of RV dysfunction on acute PE, risk stratification is based on imaging modalities for the visualization of RV dysfunction. Therefore, echocardiographic assessment of RV dysfunction in acute PE may predict early mortality, and may guide decisions regarding reperfusion therapy (Grifoni et al., 2000; Kucher et al., 2005). Echocardiography, however, is time-consuming, operator-dependent, and not always available in an emergency situation, and echocardiographic criteria for assessing RV have not yet been determined. The development of narrow collimation, multi–detector row computed tomography (CT) imaging, and modern workstations for image postprocessing and analysis have made CT pulmonary angiography the modality of choice for the assessment of patients with pulmonary emboli (Ghaye et al., 2006; Schoepf & Costello, 2004). At times, CT is more rapidly accessible in emergency settings, and is more widely available than echocardiography. CT enables the direct visualization of emboli and provides information about cardiac morphology. CT findings, including RV enlargement, the ratio of RV diameter to the diameter of the left ventricle (LV) (RV/LV ratio), interventricular septal bowing, and pulmonary vascular obstruction score, have been associated with early mortality and clinical outcomes (Araoz et al., 2003; Collomb et al., 2003; Coutance et al., 2011; Ghuysen et al., 2005;

Risk Stratification of Submassive Pulmonary Embolism:

**2.1.1 Echocardiographic RV/LV ratio** 

**2.1.2 Echocardiographic RV hypokinesis** 

0.9 (OR, 2.66; p < 0.01).

assessed.

The Role of Chest Computed Tomography as an Alternative to Echocardiography 171

view (Fig. 1); as RV systolic free wall hypokinesis (McConnell sign); or as systolic pulmonary arterial hypertension, defined as a tricuspid regurgitant velocity >2.6 m/s (Goldhaber, 2002). Indirect signs of RV pressure overload include a flattened interventricular septum, paradoxical systolic motion of the interventricular septum toward the LV, and a dilated inferior vena cava with reduced respiratory variability (Table 1). Signs of RV dysfunction have been found in 40-70% of patients with PE, and numerous studies have demonstrated that echocardiography is a useful tool for estimating the prognosis of normotensive patients with acute PE (Goldhaber et al., 1999; Ribeiro et al., 1997; Grifoni et al., 2001). A recent meta-analysis found that echocardiographic evidence of RV dysfunction was associated with a significantly elevated risk of death during the acute phase of PE (OR, 2.5; 95% CI, 1.2-5.5%) (Sanchez et al., 2008). However, since large populations of patients with signs of RV dysfunction have low mortality rates, echocardiographic detection of RV dysfunction alone does not justify more aggressive treatment strategies (Goldhaber et al., 1999; Konstantinides, 2008). More importantly, definitions of RV dysfunction differed greatly among these studies, and patients with chronic obstructive pulmonary disease were not excluded (Jimenez et al., 2007). In addition, it is difficult to differentiate chronic from acute RV overload based on standardized criteria (e.g. RV free wall thickness > 6 mm or tricuspid valve regurgitation jet velocity > 2.6 m/sec).

A retrospective study of 950 patients showed that the echocardiographic RV/LV ratio was prognostic in the evaluation of PE, with a critical cutoff for prediction of in-hospital mortality of 0.9 (Fremont et al., 2008). Echocardiograms were electrocardiogram (ECG) gated to allow end-diastolic diameter measurement on the R wave. The minor axes of the RV and LV were measured in apical 4-chamber views from the septum to the lateral wall endothelium at their widest point just above the mitral valve and tricuspid valve annulus. The prognostic value of this easily measurable echocardiographic parameter was independent of patient history and clinical data. Multivariate analysis showed that the independent predictors of in-hospital mortality included systolic BP < 90 mm Hg (odds ratio [OR], 10.73; p < 0.0001), history of left heart failure (OR, 8.99; p < 0.0001), and RV/LV ratio >

Moderate or severe RV free-wall hypokinesis may be accompanied by relatively normal contraction and "sparing" of the RV apex, a phenomenon called the McConnell sign (McConnell et al., 1996). In patients with PE, the McConnell sign had a sensitivity of 77%, a specificity of 94%, a positive predictive value of 71%, and a negative predictive value of 96%. This sign appeared useful in distinguishing between RV dysfunction due to PE and dysfunction due to other conditions, such as primary pulmonary hypertension. For patients with RV hypokinesis due to acute PE, the excursion diminished markedly when measured in the middle of the RV free wall. However, the excursion improved progressively when segments closer to the apex were measured. This pattern of regional RV dysfunction appeared highly specific for acute PE; in patients with RV dysfunction due to primary pulmonary hypertension, RV hypokinesis was not improved when apical segments were

Jimenez et al., 2010; Lu et al., 2009; Qanadli et al., 2001; Sanchez et al., 2008; Schoepf & Costello, 2004; van der Meer et al., 2005; Wu et al., 2004).

This chapter will focus on recent studies comparing CT and echocardiographic findings of RV dysfunction. The data obtained in these trials provide the background for emerging risk stratification algorithms, which we hope will lead to the use of chest CT as an alternative to echocardiography in the successful identification of RV dysfunction.
