Heart failure

The Role of Echocardiography in Heart Failure, Part 2

Kamel Sadat, MD, Masood Ahmad, MD, Qiangjun Cai, MD, Mohamed Morsy, MD, Navin Nanda, MD, Alejandro Barbagelata, MD, Wissam Khalife, MD

ABSTRACT: Echocardiography is the most comprehensive imaging test in the diagnosis of heart failure (HF). The test provides structural, functional, and hemodynamic information noninvasively. The first part described the findings of echocardiography in patients with systolic HF and diastolic HF. In the second part of the series, we will discuss the value of echocardiography in right HF, pulmonary vascular diseases, cardiac resynchronization therapy, ventricular assist device, and heart transplantation.


Right ventricle (RV) dysfunction predicts mortality in heart failure (HF) patients independent of left ventricle (LV) function.1 It is often difficult to image the RV in 1 plane because of its complex spacial geometry.2 

Tricuspid annular planar systolic excursion is one of the best methods to estimate RV systolic function and is measured as the extent of movement of the tricuspid lateral annulus from M-mode through the annulus in the apical 4-chamber view. A value greater than 14 mm to 16 mm and a doubling of the tricuspid annular planar systolic excursion measurement predicts improved mortality independent of left ventricular ejection fraction (LVEF).3,4 

Right ventricular myocardial performance index provides an index of global RV function, which is calculated as myocardial performance index = isovolumic relaxation time + isovolumic contraction time/systolic ejection period.5,6 If the value is >0.4 by pulsed Doppler or >0.55 by tissue Doppler, RV dysfunction is indicated. 

Right ventricular stroke index is also a good marker of the RV function and can be calculated by the following formula: (mean pulmonary artery pressure - mean right atrial [RA] pressure) x stroke volume index.7

Three and 4-dimensional echocardiography may have a potential advantage in determining RV volumes and image reconstruction.2 The RV diastolic function is analogous to the LV with a tricuspid early mitral flow diastolic velocity (E)/A ratio <0.8, suggesting impaired relaxation (stage 1 diastolic HF [DHF]). A tricuspid E/A ratio of 0.8 to 2.1 with an E/ mitral annular early diastolic velocity (é) >6 or diastolic flow predominance in the hepatic veins suggests pseudonormal filling (stage 2 DHF). A tricuspid E/A ratio >2.1 with deceleration time <120 ms, suggests restrictive filling (stage 3 DHF).5

Right atrial pressure reflects the amount of blood returning to the heart and is often used as a surrogate  for the preload, it can be estimated by 4 methods:

o Inferior vena cava (IVC) maximal diameter 1 cm to 2 cm from RA-IVC junction and the IVC collapsibility index can be used to estimate the right atrial pressure (RAP)(Table 1).5 

o Tissue Doppler measures RAP through RV regional isovolumic relaxation time—the time between the end systolic annular motion and the onset of the é wave—when <59 ms correlates with a mean RAP greater than 8 mm Hg.1

o The maximum velocity across the tricuspid valve (TV) during early diastolic filling of the RV increases with high RAP but also with active relaxing RV sucking the blood across the TV. To differentiate between these 2 entities, tissue Doppler placed laterally to the TV annulus measures the maximum relaxation velocity of the RV myocardium é wave. A fast signal signifies a rapid relaxation while a slow signal implicates impaired relaxation. Therefore, a high E wave velocity with a slow é wave indicate a high RAP with a correlation of E/é >4 for a RAP >10 mm Hg8 on the other hand, high E wave velocity with a fast é wave indicate a normal relaxing RV.

o Hepatic vein flow can also be used for RAP assessment, with normal flow directed toward the RA in most of systole and early diastole followed by a reversal flow with atrial contraction. Higher RAP reduces the systolic forward flow and augments the atrial reversal. The hepatic vein systolic fraction = velocity time integral (VTI) of systole forward flow/VTI (systole+ diastole) forward flow. A value of <55% predicts RAP >8 mm Hg.9

atrial pressure

Pulmonary Vasculature and Echocardiography

Estimation of pulmonary vascular hemodynamic variables is an essential component for HF evaluation. The estimation of pulmonary arterial systolic pressure is crucial among patients with suspected pulmonary hypertension. It is estimated by continuous wave Doppler measurement of the tricuspid regurgitation jet with the modified Bernoulli equation in the absence of pulmonary valvular stenosis, pulmonary artery stenosis, or RV outflow tract obstruction: pulmonary arterial systolic pressure = tricuspid regurgitation gradient + RAP.10 Pulmonary arterial systolic pressure = 4 (max velocity of tricuspid regurgitation jet2) + RAP. Normal values are up to 30 mm Hg at rest and up to 40 mm Hg during exercise. 

Pulmonary artery diastolic pressure can also be derived from the velocity of the end diastolic pulmonary regurgitation by using the modified Bernoulli equation: pulmonary artery diastolic pressure = 4 x (velocity of the end-diastolic pulmonary regurgitation2) + RAP.1,5 Once systolic and diastolic pressures are known, mean pressure may be estimated by the standard formula: mean pulmonary artery pressure = 1/3 pulmonary arterial systolic pressure + 2/3 pulmonary artery diastolic pressure (mm Hg).

Pulmonary capillary wedge pressure (PCWP) can be invasively measured by wedging a pulmonary catheter with an inflated balloon into a small pulmonary arterial branch. It is used as surrogate for left atrial pressure when there is no significant transpulmonary gradient. Noninvasively, by transthoracic echocardiogram (TEE), it can be estimated by the ratio of E by continuous wave Doppler to é by tissue Doppler—either the medial, lateral or average of the medial and lateral. It is a simple measurement and well-accepted method to estimate left ventricular filling pressure in patients with sinus rhythm. 

In patients with atrial fibrillation, we can average the ratio of E/é over 10 cardiac cycles and use it as surrogate for the PCWP. E/é ratio has been compared with LV end diastolic pressure; ratio <8 did accurately predict normal LV end diastolic pressure and higher than 15 did predict a high LV end diastolic pressure.6 

The American Society of Echocardiography/European Association of Echocardiography guidelines for the estimation of LV filling pressures in patients with depressed ejection fraction (EF) came with an algorithm that is when the E/A ratio is <1 and with an E velocity ≤50 cm/s, a normal left atrial pressure is likely. When the E/A ratio is ≥2, or with deceleration time <150 ms, an increased left atrial pressure is assumed. When the E/A ratio is ≥1 but <2, or when it is <1 but with an E velocity >50 cm/s, the presence of abnormally elevated values in 2 of the following Doppler measurements was needed to support the conclusion that LV filling pressures are elevated: average E/é ratio >15, flow propagation velocity (E/Vp) ratio ≥2.5, pulmonary venous systolic to diastolic ratio <1, or a pulmonary atrial reversal duration - transmitral atrial flow duration ≥30 ms, and pulmonary artery systolic pressure (PASP) >35 mm Hg.11 Table 2 summarizes the hemodynamic formulas calculated by 2-dimensional gel electrophoresis (2DE).


Resynchronization Therapy

Biventricular pacing has been shown to improve functional status and survival of patients with reduced LVEF and ventricular conduction delay. The standard indications for cardiac resynchronization therapy (CRT) are patients with LVEF ≤35%, left bundle branch block, New York Heart Association class III or IV, and wide QRS complex ≥120 ms.12,13 2DE has been used to assess the outcome of the device therapy by demonstrating decreased LV volume, increased LVEF, increased rate of ventricular pressure rise, and decreased mitral regurgitation, all of which are signs of reverse remodeling. 

Another role of 2DE is to identify nonresponder to CRT as 30% to 50% of patients may not respond to therapy,4,12 which usually predicts a poor prognosis. Mechanical dyssynchrony measured by tissue Doppler is better than only assessing LVEF to identify responders to resynchronization therapy. Time interval from onset of QRS to the peak systolic velocity of 2 to 12 segments of the LV are used to determine the maximum of standard deviation interval. 

An interval of 100 ms has the highest predictive value for positive responders.1 Three-dimensional echocardiography proved its superiority compared to 2DE and tissue Doppler in evaluating LV dyssynchrony. An accurate analysis of the LV volumes serves as a strong marker for LV reverse remodeling after CRT.13

Echocardiography and Ventricular Assisted Device

The left ventricular assist device (LVAD) is designed for mechanical support of patients with severe systolic HF (Figure 1). This device provides effective long-term circulatory support as a bridge to recovery, transplantation, or as a destination therapy.14 Echocardiography plays an important role in selecting patients for LVAD placement and identifying other structural abnormalities that can affect patients’ selection or the need for concomitant surgical intervention, such as atrial septal defect/patent foramen ovale, significant valvular disease ascending aorta disease, LV apical thrombus, and severe RV failure.1,14 The detection of significant aortic insufficiency is crucial. If present, it reduces the forward flow produced by the LVAD; 2DTEE has very good sensitivity to assess aortic insufficiency (AI) and guide the surgeon to correct it before LVAD placement.15 


Figure 1. Echocardiographic assessment of left ventricular assist device (LVAD) A. Normal color flow Doppler recorded from the inflow cannula (arrow) in apical 4-chamber position. B. Pulsed wave Doppler signal from the LVAD inflow cannula with a peak velocity of 1.1 m/s. C. Color flow Doppler from the outflow cannula (arrow).D. Pulsed wave Doppler signal from outflow cannula with a peak velocity of 1.5 m/s

One of the important intraoperative roles of 2DTEE is to provide guidance to surgeons in the deairing of the heart prior to unclamping the aorta after LVAD placement. Large air bubbles present in the LVAD can embolize the coronary or cerebral circulation with devastating consequences. Left-sided output increase leads to increased venous return to RV. In some cases, a failing RV cannot handle the increased preload in proportion to the increased pump speed, real-time echocardiography can be used to adjust the pump speed setting and decrease the severity of the tricuspid regurgitation. If unsuccessful, this real-time modality can predict the need for right ventricular assist device (RVAD).14,16,17 

The use of 2DE can visualize VAD malfunction through regurgitation of the forward flow propulsed by the LVAD, either to the atrium in the case of mitral regurgitation or to the LV in case of aortic regurgitation. It can also detect cannula kinking by absence of flow, cannula obstruction by thrombus, or cardiac structure if malpositioned with velocity >2.5 m/s for pulsatile pumps with intermittent interruptions of the usual laminar cannula flow14-17 versus high turbulent peak inflow velocity >2 m/s with the continuous-flow pumps.17 

Infection is the major cause of morbidity and mortality. TEE has a good sensitivity in detecting vegetation on VAD or native cardiac structures. Finally, ventricular recovery and VAD’s weaning can be decided when LVEF >40% to 45% and LV end diastolic dimension ≤5.5 cm in off-pump studies with RV fractional area change greater than 40%.14-18 

Ramp test is performed to monitor the appropriateness of the LVAD programmed setting and aid in changing the device speed. Additionally, this test also allows detection of device malfunction. Baseline images of the ventricular diameters, frequency of aortic valve opening, degree of AI, mitral regurgitation, and RV pressures are obtained with a speed set at 8000 revolutions per minute (rpm). After a few minutes, the speed is increased subsequently by 400 rpm at few minute intervals with repeat acquisition of the echo images. The increment continues to 1200 rpm or until any suction event occurs. Suction events occur when the pump is set high enough to cause partial collapse of the LV, resulting in obstruction of the inflow cannula by adjacent myocardium; the speed of the pump is lowered typically by 400 to 800 rpm below the fixed speed setting. If the patient has a device thrombosis, an uncoupling of the relationship between the device speed and the LV end diastolic volume occurs.19

Impella is a left intraventricular assist device for short term (5 to 7 days) mechanical circulatory assistance as a bridge to recovery, LVAD placement, or transplantation.20,21 Esophageal echocardiography was initially used to look for contraindications for VAD placement as detailed above. Before placement of the Impella, 2DE is crucial in detecting any possible contraindication for placement, such as LV thrombus, significant AI, significant ascending aortic disease, 2DTEE can be used to guide appropriate placement and 2DE (Figure 2), it can also ensure proper position as spontaneous displacement is not uncommon, reposition can be done at bed site with 2DE guidance.22

2d thoracic


Figure 2. Echocardiographic assessment of Impella placement. A. 2D transthoracic parasternal long axis view showing a malpositioned device with the catheter tip abutting against the posterior wall of the left ventricle (arrow). B. 2D transthoracic parasternal long axis view shows a correctly repositioned Impella catheter (arrow). 

Cardiac Transplantation 

Echocardiography is important in posttransplant patients by providing accurate assessment of the graft function (Figure 3). Left ventricular systolic dysfunction might signify either ischemic injury or rejection. Acute or chronic allograph rejection can be expressed through an increased wall thickness and left ventricular mass, or decreased systolic function.23,24 Left ventricular diastolic dysfunction can be secondary to ventricular hypertrophy, acute rejection, myocardial edema, and fibrosis.25,26 It usually correlates well with the shortening of the isovolumic relaxation time and early mitral inflow deceleration time. Changes in the E and A wave velocities and the E/A ratio have been less consistent.23 A better approach to detect acute allograph rejection is the use of allograph myocardial performance index which measures both systolic and diastolic performance.19,25 2DE can also detect iatrogenic damage to the tricuspid valve secondary to endomyocardial biopsy with flail tricuspid leaflets and eccentric regurgitant jets.24-26

Two-dimensional echocardiography is ideally suited to identify mechanical complications, such as constriction of the anastomosis that can be recognized with Doppler flow. Sometimes the atrial anastomosis can protrude into the atria and be mistaken for a mass. Thrombus formation on a prominent suture line may be best detected by 2DTEE.25 


Figure 3. Echocardiographic assessment of acute heart transplant rejection:A,B. 2D transthoracic apical 4-chamber view in end diastole and end-systole respectively after acute heart transplant rejection. Arrow points to an apical thrombus. C,D. Same views are shown after recovery from rejection and after resolution of the apical thrombus. AO: aorta; LA: left atrium; LV: left ventricle; m: meter; RA: left atrium; RV: right ventricle; s: second

Right ventricular failure is important to recognize early in the transplantation course. Right ventricular failure can be secondary to the exposure of donor RV to the elevated pulmonary vascular resistance encountered in some recipients which is often transient.24,26 Right ventricular failure could also be secondary to acquired cor triatriatum, which necessitates surgical excision of the atrial tissue. It also identifies patent foramen ovale, which requires surgical repair to avoid embolization. Early regional wall motion abnormality of the LV immediately after transplantation can be a sign of acute rejection or acute coronary syndrome that is often silent. A size mismatch between the donor heart and the recipient pericardial cavity can be corrected by pericardial reduction plasty. Aortic dissection and fistula can occur following transplant; 2DTEE is the main tool to make this diagnosis.27

The blunted heart rate response to exercise due to cardiac denervation limits the sensitivity of exercise testing to detect allograph vasculopathy. Pharmacological stress testing is more sensitive in this population.22,23 Dobutamine stress echocardiography can detect transplant-related coronary artery disease through the evaluation of inducible ischemia. This is especially important since transplant vasculopathy is usually a diffuse disease that can be underestimated and not well visualized by invasive angiography.22, 24,26

Echocardiography is the imaging modality of choice in patients with HF for multiple reasons including cost compared to other imaging modalities, reproducibility, availability, noninvasiveness, as well as diagnostic and prognostic values. It is the most useful tool in guiding HF management, especially advanced HF therapy including pre- and post-LVAD and heart transplant. Diagnosing and managing patients with HF will not be possible without echocardiography.


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Kamel Sadat, MD, is a fellow in advanced heart failure and transplant cardiology at the University of Texas Medical Branch
at Galveston.

Masood Ahmad, MD, is a professor in medicine and director of the echocardiography laboratory at the University of Texas Medical Branch in Galveston.

Qiangjun Cai, MD, is on faculty in the department of cardiology at McFarland Clinic in Ames, IA.

Mohamed Morsy, MD,is an assistant professor at the University of Texas Medical Branch in Galveston.

Navin Nanda, MD, is a professor of medicine and director of the echocardiography laboratory at the University of Birmingham, AL.

Alejandro Barbagelata, MD, is an associate professor of medicine at University of Texas Medical Branch in Galveston.

Wissam Khalife, MD, is an associate professor and director of heart failure, assist devices, and transplant at the University of Texas Medical Branch in Galveston.