Echocardiography in Chronic Thromboembolic Pulmonary Hypertension

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Chronic thromboembolic pulmonary hypertension (CTEPH) is a significant complication of venous thromboembolism and is caused by incomplete resolution of pulmonary emboli. The persistent chronic pulmonary hypertension leads to right-ventricle pressure overload. As a result, there is often significant functional and morphological alteration of both the right and the left ventricle. Transthoracic echocardiography, which allows for the estimation of pulmonary arterial pressures, not only plays an important role in the diagnosis of pulmonary hypertension but also provides insights in the pathophysiology of CTEPH. This article reviews the echocardiographic techniques and findings in CTEPH patients.

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Overview of Echocardiography in PHTN and CTEPH

PHTN results in increased right ventricular afterload and myriad of subsequent hemodynamic and structural changes, many of which can be assessed by echocardiography. These findings are not pathognomonic for CTEPH but can be seen in other causes of PHTN. The salient features of significant pulmonary hypertension include (Fig. 1) the following: right ventricle (RV) enlargement, RV hypertrophy followed by RV systolic dysfunction, tricuspid valve annular dilation and tricuspid regurgitation,

Diagnosis of PHTN

While some patients with significant chronic thromboembolic disease may have little to no PHTN, most present with significant elevations in pulmonary arterial pressures. Echocardiography provides a simple noninvasive technique to estimate pulmonary arterial pressure and therefore diagnose PHTN.

During systole, in the absence of significant pulmonary valve stenosis, the pressure in the RV and pulmonary artery are essentially identical. RV pressures can be easily estimated by echocardiography

Degree of Tricuspid Regurgitation

PHTN is associated with RV hypertrophy and ultimately RV enlargement, leading to a dilation of the tricuspid valve annulus. This along with chordal traction of the valve leaflets results in tricuspid regurgitation (Fig. 4). The tricuspid regurgitation does not correlate directly with the degree of PHTN per se but rather more directly with the degree of RV enlargement and changes in RV geometry. Here again echocardiography allows for the evaluation of the degree of tricuspid regurgitation both

RV Size and Function

As PHTN progresses, the RV enlarges and its function may become depressed. Echocardiography can provide helpful information on both RV size and function, although the assessment is often qualitative, given the complexity of RV geometry. The most helpful view to assess RV enlargement is the apical four-chamber view. In normal individuals (in the apical four-chamber view) the left ventricle (LV) is larger than the RV and fills the apex. In the presence of RV enlargement, the RV area exceeds the

Pericardium and Coronary Sinus

The marked elevations in RV and RA pressures in CTEPH may lead to impaired lympathic and venous drainage from the pericardium with resultant pericardial effusions, easily detected on echocardiography. The presence of pericardial effusion correlates with increased RA pressures.12

Similarly elevated RA pressure may impair coronary sinus drainage and lead to enlargement of the coronary sinus, again easily visualized with echocardiography.13

The LV and Septum in CTEPH

The overload on the right heart in CTEPH results in the septum being frequently distorted with flattening and even bulging into the LV cavity. This results in a characteristic D-shaped LV (Fig. 5), in contrast to a normally circular LV, in the parasternal short-axis view. By measuring the two axes of the LV in the parasternal short-axis view, an eccentricity index can be determined. Normally with a circular LV this index is 1 during both systole and diastole.14

The overload on the right heart in

Mitral Valve in CTEPH

The marked distortion of the LV caused by the pressure overload in CTEPH may lead to distortion of the mitral valve annulus and subsequent mitral valve prolapse and mitral regurgitation. Following PTE surgery this “pseudo” mitral valve prolapse often reverses.15

Diastolic Function in CTEPH

CTEPH has also been associated with abnormal LV diastolic falling. Initial studies demonstrated that abnormal LV diastolic function seen in RV pressure overload was largely mediated through the intraventricular septum. Subsequent more detailed analysis of echocardiographic diastolic filling parameters E and A revealed E/A reversal (E/A ratio <1.5) in CTEPH patients. Postsurgery and with the resolution of pulmonary hypertension there was a significant improvement in the ratio. In fact, following

Preoperative Assessment of Potential CTEPH Candidates

There have been preliminary reports that echocardiography can distinguish between CTEPH and primary pulmonary hypertension (PPH) as a cause of pulmonary hypertension.18, 19, 20 However, in a follow-up prospective study of 142 patients, echocardiography was not sufficiently accurate to differentiate between the two entities.21 At UCSD we have relied primarily on ventilation-perfusion (V/Q) scanning and pulmonary angiography/angioscopy to differentiate the two entities. However, routine

Postoperative Assessment of PTE Surgery

Following successful PTE surgery significant changes occur rapidly in cardiac morphology and function (Fig. 8). RV volumes and function improve rapidly, even before discharge, and continue to improve in the subsequent months. The eccentricity index may normalize immediately postoperatively in conjunction with the decrease in pulmonary pressures. Tricuspid regurgitation and cardiac output also improve. All of these parameters are easily evaluated by echocardiography.17 Furthermore patients who

Conclusions

Echocardiography plays an integral role in the diagnosis of CTEPH patients, and also in their preoperative as well as postoperative assessment. Further studies of newer echocardiography techniques such as tissue Doppler and 3D echo may continue to provide insight in the pathophysiology of this disease.

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