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.................................................................................. Echocardiographic examination is not mandatory as part of the routine diagnostic workup in haemodynamically stable patients with suspected PE,124 although it may be useful in the differential diagnosis of acute dyspnoea. This is in contrast to suspected high-risk PE, in which the absence of echocardiographic signs of RV overload or dysfunction practically excludes PE as the cause of haemodynamic instability. In the latter case, echocardiography may be of further help in the differential diagnosis of the cause of shock, by detecting pericardial tamponade, acute valvular dysfunction, severe global or regional LV dysfunction, aortic dissection, or hypovolaemia.152 Conversely, in a haemodynamically compromised patient with suspected PE, unequivocal signs of RV pressure overload, especially with more specific echocardiographic findings (60/60 sign, McConnell sign, or rightheart thrombi), justify emergency reperfusion treatment for PE if immediate CT angiography is not feasible in a patient with high clinical probability and no other obvious causes for RV pressure overload.152

Mobile right-heart thrombi are detected by TTE or transoesophageal echocardiography (TOE), or by CT angiography, in <4% of unselected patients with PE.153155 Their prevalence may reach 18% among PE patients in the intensive care setting.156 Mobile right-heart thrombi essentially confirm the diagnosis of PE and are associated with high early mortality, especially in patients with RV dysfunction.155,157159 In some patients with suspected acute PE, echocardiography may detect increased RV wall thickness or tricuspid insufficiency jet velocity beyond values compatible with acute RV pressure overload (>3.8 m/s or a tricuspid valve peak systolic gradient >60 mmHg).160 In these cases, chronic thromboembolic (or other) pulmonary hypertension (PH) should be included in the differential diagnosis.

4.10 Compression ultrasonography

In the majority of cases, PE originates from DVT in a lower limb, and only rarely from upper-limb DVT (mostly following venous catheterization). In a study using venography, DVT was found in 70% of patients with proven PE.161 Nowadays, lower-limb CUS has largely replaced venography for diagnosing DVT. CUS has a sensitivity >90% and a specificity of 95% for proximal symptomatic DVT.162,163 CUS shows a DVT in 3050% of patients with PE,162164 and finding a proximal DVT in patients suspected of having PE is considered sufficient to warrant anticoagulant treatment without further testing.165 However, patients in whom PE is indirectly confirmed by the presence of a proximal DVT should undergo risk assessment for PE severity and the risk of early death. In the setting of suspected PE, CUS can be limited to a simple fourpoint examination (bilateral groin and popliteal fossa). The only validated diagnostic criterion for DVT is incomplete compressibility of the vein, which indicates the presence of a clot, whereas flow measurements are unreliable. A positive proximal CUS result has a high positive predictive value for PE. The high diagnostic specificity (96%) along with a low sensitivity (41%) of CUS in this setting was shown by a recent meta-analysis.165,166 CUS is a useful procedure in the diagnostic strategy of patients with CT contraindications. The probability of a positive proximal CUS in suspected PE is higher in patients with signs and symptoms related to the leg veins than in asymptomatic patients.162,163

©ESC 2019

A. Enlarged right ventricle, parasternal long axis view C. Flattened intraventricle septum (arrows) parasternal short axis view

B. Dilated RV with basal RV/LV ratio >1.0, and McConnell sign (arrow), four chamber view D. Distended inferior vena cava with diminished inspiratory collapsibility, subcostal view

E. 60/60 sign: coexistence of acceleration time of pulmonary ejection <60 ms and midsystolic “notch” with mildy elevated (<60 mmHg) peak systolic gradient at the tricuspic valve F. Right heart mobile thrombus detected in right heart cavities (arrow) G. Decreased tricuspid annular plane systolic excursion (TAPSE) measured with M-Mode (<16 mm) H. Decreased peak systolic (S’) velocity of tricuspid annulus (<9.5 cm/s)

S’

E’ A’

RV RV LV

RA RV LV RA

IVC

RV

RA RV RiHTh M-Mode TAPSE <16 mm

LV Ao

LA

AcT <60 ms TRPG <60 mmHg Tissue Doppler Imaging

S’ <9.5/s ”notch”

Figure 3 Graphic representation of transthoracic echocardiographic parameters in the assessment of right ventricular pressure overload. A0 = peak late diastolic (during atrial contraction) velocity of tricuspid annulus by tissue Doppler imaging; AcT = right ventricular outflow Doppler acceleration time; Ao= aorta; E0 = peak early diastolic velocity of tricuspid annulus by tissue Doppler imaging; IVC= inferior vena cava; LA= left atrium; LV = left ventricle; RA = right atrium; RiHTh= right heart thrombus (or thrombi); RV = right ventricle/ventricular; S0 = peak systolic velocity of tricuspid annulus by tissue Doppler imaging; TAPSE= tricuspid annular plane systolic excursion; TRPG= tricuspid valve peak systolic gradient. Downloaded from academic.oup.com/eurheartj/article/41/4/543/5556136 by guest on 07 October 2026