The Role of Echocardiography in Heart Failure
ABSTRACT: Heart failure (HF) is a fast growing worldwide clinical problem and one of the most common causes of death in developed countries. It is a complex clinical syndrome that results from any structural or functional cardiac disorder that impairs the ability of the ventricles to fill correctly or eject blood completely, leading to congestion and reduced systemic perfusion. Echocardiography is the most comprehensive imaging test in the diagnosis of HF. The test provides structural, functional, and hemodynamic information noninvasively. This first part of a 2-part series will describe the findings of echocardiography in patients with systolic and diastolic HF.
Echocardiography plays an important role in the diagnosis and management of patients with heart failure (HF). It is widely used to assess cardiac anatomy and physiology.1,2 All stages of left ventricular (LV) remodeling and failure have been characterized by two-dimensional echocardiography (2DE). Two-dimensional echocardiography has also been the single most useful diagnostic tool that can guide the management of patients with HF.
The prevalence of HF is increasing worldwide, especially in the United States, as longevity increases with an estimate of 5.7 million subjects with HF.3 In 2008, heart failure was the primary cause of death in 55,000 patients4 and contributed to the death of 280,000 patients in the United States.3 More internists and general cardiologists are involved in the care of patients with HF.
Therefore, understanding 2DE is very important to treat these patients appropriately.
Systolic Heart Failure
The degree of ventricular systolic dysfunction is a potent predictor of clinical outcome for a wide range of cardiovascular diseases. The main causes of systolic heart failure (SHF) are coronary artery disease, hypertension, cardiomyopathy, valvulopathies, and myocarditis. SHF is relatively predictable by 2DE seen by a reduction of the left ventricular ejection fraction (LVEF).1,2 This decrease in the LVEF is associated with alteration of the intracardiac geometry and hemodynamics.
The following parameters are used to characterize SHF:
• Index of sphericity. Bullet-shaped or ellipsoid shape of the normal LV is conserved lifelong. However, with SHF, this shape is distorted by the disproportionate greater increase in the short axis than the long axis of the LV. The resulting increase of the index of sphericity is defined as the ratio of the LV short axis diameter to the LV long axis length.2
• Left ventricular volumes. The American Society of Echocardiography recommends the Simpson’s method of discs to quantify the LV chamber volumes with a manual digitalization of the endocardial boundaries, ideally from the apical 4-chamber and the apical 2-chamber views.5,6
• Left ventricular ejection fraction is the most frequently used parameter to quantify systolic dysfunction and can be derived from the following formula using the LV volumes obtained through the Simpson’s method: LVEF = [End diastolic volume - End systolic volume]/End diastolic volume×100%.5-7 Most echocardiographers use visual estimation of the LVEF in clinical practice. It has been shown that experienced readers’ estimation has a very good correlation with the biplane quantifying method.8
LVEF represents the global function of the LV with the normal value greater than 55%. When managing HF, LVEF is an important parameter to consider in decision-making—such as in cases of biventricular pacing, implantable cardioverter defibrillators, valve replacement, left ventricular assist device placement, and cardiac transplantation. Contrast enhances endocardial visualization and thus improves accuracy and reproducibility of the measurement in patients where the endocardium is not well visualized.10
Cardiac output can be calculated by multiplying stroke volume (LV outflow tract area × LV outflow tract velocity time integral) x the heart rate.8,9
•Stress echocardiography is useful to differentiate between ischemic and nonischemic cardiomyopathy in patients with LV systolic dysfunction; patients with nonischemic dilated cardiomyopathy have more spherical and homogeneously hypokinetic left ventricles, whereas heterogeneous akinetic or dyskinetic areas would suggest ischemic dilated cardiomyopathy.11
Although the contractile response to β-adrenergic stimulation is generally reduced in patients with dilated cardiomyopathy and HF,11 dobutamine infusion produces an improvement of global LV wall motion in patients with normal coronary arteries. In ischemic dilated cardiomyopathy, wall motion either deteriorates or does not change from low to peak dose of dobutamine infusion.12,13
The myocardium can be divided into 17 segments and each segment is analyzed by systolic thickening and endocardial motion. Normal regional wall thickening is graded as 1, hypokinesis as 2, akinesis as 3, and dyskinesis as 4. A wall motion score index is determined as the sum of all scores divided by the number of analyzed segments. This score index provides information about the location, size, and transmurality of the infarction and how extensive the region of border zone myocardium at risk is.
•Relative wall thickness is a simple measure of ventricular geometry that can help differentiate the cause of SHF. Relative wall thickness = 2 × posterior wall thickness in diastole/LV diastolic diameter. This index is virtually unchanged through life in structurally normal hearts exposed to normal systolic blood pressure. If SHF is secondary to hypertension, relative wall thickness is increased due to concentric remodeling with increased wall thickness and decreased LV chamber capacity. However, if SHF is secondary to left-sided valvulopathy, an eccentric hypertrophy may develop with no change in the relative wall thickness due to the proportional change in wall thickness and the cavity dimensions.14
•Left ventricular mass. This parameter has received less attention in clinical cardiology than LVEF. LV mass can be calculated with M-mode by subtracting the end diastolic cavity volume from the total volume (cm3) multiplied by the density of the muscle (1.04 gm/cm3), it has a prognosis value in patients with HF without coronary disease, and higher LV mass was associated with higher rates of morbidity and mortality independently from the EF.15
•Mitral regurgitation (MR) can be due to congenital or acquired abnormalities of the valve leaflets or the associated supporting structures. For example, increasing calcification of the mitral annulus impairs the systolic contraction of the annulus leading to regurgitation; degenerative diseases of the valve leaflets or the subvalvular apparatus, such as myxomatous disease, rheumatic disease, infection, and infiltrative and inflammatory disorders can impair the mitral valve with a variable result ranging from a minimal prolapse of the leaflets into the left atrium in systole to a frank prolapse or flail of leaflet segments; and shortening of the chordae and leaflets destruction MR can also be functional, such as in the case of dilation of either the left atrium or the LV, which can improve with correction of the causative mechanism. Development of MR in nonischemic etiology is related to dilation of the mitral annulus, apical displacement of the mitral leaflets with noncoaptation of the leaflets, and distortion of papillary muscle function due to LV cavity dilation.
Ischemic MR is a different entity, usually due to significant left circumflex or right coronary artery disease, which can be corrected by revascularization. Stress echocardiography can unveil functional or ischemic mitral regurgitation not detected during resting 2DE. If MR is left untreated, it may lead to progressive LV dilation from volume overload, increased wall stress, and reduced ejection fraction, causing a vicious cycle.2 Color Doppler is usually used to visually estimate MR; proximal isovelocity surface area, effective mitral regurgitant orifice area, regurgitant volume, regurgitant fraction, and vena contracta are used to quantitatively estimate the severity and degree of the MR (Table 1).
Diastolic Heart Failure
About 35% to 50% of patients with new onset HF have preserved LV systolic function,1,5 also called HF with preserved EF (HFpEF).
This function is defined by 3 criteria:16
•LVEF >45%
•LV end systolic volume <97 ml/m2
•E/é ratio >15
It is the result of impaired diastolic relaxation and/or increased myocardial chamber stiffness.17,18 The main causes of active and passive diastolic relaxation abnormalities of the heart are myocardial hypertrophy and progressive myocardial fibrosis.
Aging is the most common cause of intrinsic isolated impaired diastolic filling, followed by hypertension.7,19 Many other conditions can also cause HFpEF, such as infiltrative diseases, constrictive pericarditis, valvular disease, congenital heart disease, and intracardiac tumors. However, most patients with DHF do not have other visible structural abnormalities.
Clinically, it is difficult to make the distinction between systolic and diastolic HF. Several 2DE clues suggest the presence of DHF. These include diminished mitral annulus motion during systole and early diastole corresponding to active mitral relaxation, increased LV wall thickening, and left atrial enlargement.
Doppler is more specific instrument in the diagnosis of DHF by evaluating the following parameters:
•Early E and late A diastolic velocities of the mitral inflow
•Deceleration time of mitral E velocity
•Early diastolic mitral annular velocity é, which is preferably calculated using averaged velocities from the septal and lateral aspects of the mitral annulus. Measurements from the lateral annulus are more reproducible than septal measurements, especially in patients with normal LVEF
•Pulmonary vein and hepatic vein velocities
•Mitral inflow propagation velocity obtained by M-mode
•Isovolumic relaxation time, which provides insight into the rate of early diastolic LV relaxation, and is measured as the time from the middle of the aortic closure click to the onset of mitral flow. Impaired relaxation is associated with prolonged isovolumic relaxation time, while increase in left atrial pressure is associated with a shorter isovolumic relaxation time.
DHF is divided classically into stages summarized in Table 2.1,9,19-22
Diastolic wall strain is usually low in patients with HFpEF, suggesting higher stiffness when compared to control despite normal EF. Among patients with HFpEF, patients with lower diastolic wall strain have more abnormal geometry, impaired relaxation, higher filling pressures, and worse prognosis, when assessed by Doppler. Increased brain natriuretic peptide, left atrial volume index, and E/é ratio are load-dependent and do not directly reflect the intrinsic passive myocardial stiffness.Diastolic wall strain correlates with the diastolic stiffness even with changes in the volume load18;global LV longitudinal strain was also low in patients with HFpEF. When compared to normal control despite having normal EF, strain rate analysis is likely to provide more reliable information than tissue Doppler integral velocities which is influenced by extra-cardiac motion due to breathing, translational motion, septum displacement, and tethering by adjacent myocardium.23
LV torsion or twist is a mechanism that generates energy during systole, which is released during early diastole to produce ventricular recoil, upward annular motion, and suction, confirming the close relation of systolic function to early diastole.24 In the normal heart, all of these aspects of ventricular function increase on exercise to aid fast ejection and, more importantly, enable rapid filling of the ventricle during a shortened diastole period while maintaining a low filling pressure. Speckle tracking echocardiography, has demonstrated a combination of systolic and diastolic abnormalities of ventricular function in HFpEF patients that is more obvious on exercise than at rest and that includes reduced myocardial systolic strain, rotation, LV suction, longitudinal (annular) function, and delayed untwisting.25-27 Morris et al28 found that patients with HFpEF have a systolic and diastolic myocardial impairment, largely as a result of the alteration of the longitudinal, circumferential, and radial function of the LV and that these patients have increased LV filling pressures, decreased cardiac output, and worse clinical presentation.
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 in SHF and DHF patients. The second part will discuss the value of echocardiography in right HF, pulmonary vascular diseases, cardiac resynchronization therapy, ventricular assist device, and heart transplantation.
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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.
