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 Table of Contents  
REVIEW ARTICLE
Year : 2021  |  Volume : 5  |  Issue : 1  |  Page : 16-23

The Role of Echocardiography in Heart Failure Today


1 Department of Cardiology, Father Muller Medical College, Mangalore, Karnataka, India
2 Department of Cardiology, Government Medical College, Trivandrum, Kerala, India

Date of Submission05-May-2020
Date of Decision13-Aug-2020
Date of Acceptance23-Oct-2020
Date of Web Publication27-Feb-2021

Correspondence Address:
Prof. A George Koshy
Department of Cardiology, Government Medical College, Trivandrum, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiae.jiae_20_20

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  Abstract 

Although heart failure (HF) is often defined clinically, it has a large pre-clinical spectrum and its diagnosis, staging, response to therapy, and etiology are often determined by echocardiography. Understanding of pathophysiologic nuances in HF is significantly aided by the novel parameters that modern echocardiography can assess today, especially in the field of diastolic function and imaging of strain. This article attempts to link the understanding of the progression of HF with an applicable echocardiographic approach to patients at any point in this progression, sometimes in special clinical scenarios. It also conveys that how systolic and diastolic dysfunction is not mutually exclusive but can be assessed separately or simultaneously. Early HF can be subclassified based on myocardial deformation being dysfunctional either longitudinally or circumferentially. An insight into right ventricular evaluation is also included here.

Keywords: Echocardiography, heart failure, systolic and diastolic dysfunction, strain imaging


How to cite this article:
Pinto J, Koshy A G. The Role of Echocardiography in Heart Failure Today. J Indian Acad Echocardiogr Cardiovasc Imaging 2021;5:16-23

How to cite this URL:
Pinto J, Koshy A G. The Role of Echocardiography in Heart Failure Today. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2021 [cited 2021 Jul 23];5:16-23. Available from: https://www.jiaecho.org/text.asp?2021/5/1/16/310493


  Understanding Definitions Top


The American College of Cardiology/American Heart Association (ACC/AHA) guideline defines heart failure (HF) as “a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood.”[1] The HF Association of the European Society of Cardiology (ESC) more elaborately defines HF as “a clinical syndrome characterized by typical symptoms (breathlessness, ankle swelling, and fatigue) that may be accompanied by the signs (elevated jugular venous pressure, pulmonary crackles, and peripheral edema) caused by a structural and/or functional cardiac abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or during stress.”[2] Although this definition omits patients in ACC/AHA stages A and B (described later), the ESC itself recommends that starting treatment at the precursor stages A and B may reduce mortality.[2],[3] Irrespective of the stage or symptom status, objective demonstration of a cardiac cause is central to the diagnosis of HF.[2]

In simpler terms, HF is the inability of the heart to deliver a satisfactory output at normal filling pressures.[4]


  Impact of Heart Failure Top


Globally, HF affects over 40 million people, 2% of all adults and over 10% of those above 70 years of age.[5],[6],[7] A conservatively estimated prevalence of HF in India about 10 years ago was around 1.3-4.6 million with an annual rise of 0.4-1.8 million.[8] A more recent community-based survey of 10,163 adults in rural India in 2016 showed a prevalence of 1.2 per 1000 with a mean age of 58.3 ± 10.4 years.[9]

Compared to the Western population, Indians with HF have a higher rate of hospital mortality, 1-year mortality, and younger age of onset with a greater male preponderance of 70:30.[10]


  The Spectrum of Heart Failure and the Role of Echocardiography Top


HF involves the loss of functioning myocytes after an abrupt or insidious inciting event resulting in progressive dilation or hypertrophy of the left ventricle (LV), followed by spherical remodeling.[11]

According to the 2013 ACC/AHA guideline for the management of HF, it may be classified into four stages:[1],[12]

  • Stage A: At high risk for developing HF, but no functional or structural disorder. These include patients with hypertension, coronary artery disease (CAD), diabetes mellitus, or with family history of cardiomyopathy
  • Stage B: With a structural heart disorder but without signs or symptoms. This comprises people who have suffered an acute coronary syndrome in the past, who have asymptomatic LV systolic dysfunction or who have asymptomatic valvular heart disease
  • Stage C: Previous or current symptoms of HF (shortness of breath, fatigue, and reduced exercise tolerance) with structural heart disease
  • Stage D: Advanced disease requiring hospital-based support, heart transplant, or hospice.


The number of patients with LV systolic dysfunction in stage B is four times that of stages C and D put together.[13] A population-based study of a random sample of 2029 residents aged over 45 years revealed that while only 32% of people had “no HF,” 22% were in stage A (at risk), 34% were in stage B (asymptomatic), 12% were in stage C (symptomatic), and 0.2% in stage D (refractory).[14] Survival at 5 years was 99%, 97%, and 96% for those who had no HF, those in stage A and those in stage B, respectively. Those in stage C and D, however, had a 5-year survival of only 75% and 20%, respectively.

This classification of HF by the ACCF/AHA when applied on the Olmsted County resident cohort showed that 56% of adults had asymptomatic stage A or B HF (a large subclinical spectrum) while 12% had symptomatic HF.[1],[12],[14]

Only echocardiography can truly categorize individuals into “no HF,” preclinical stage A or stage B. Stage B HF may be an incidental finding on echocardiography in the absence of not only history, symptoms and clinical signs, but also without any risk factors for HF (no prior stage A). In stages C and D, echocardiography serves as a prognostic tool to stage the severity and progression of HF.

Today, echocardiography has unmatched utility and safety in diagnosing and prognosticating systolic and/or diastolic dysfunction and suggesting an etiology. It is also essential to objectively explain a patient's symptoms as over 30% of patients with a clinical suspicion of HF may not actually have HF.[15]

Echocardiographically, HF is often classified based on LV ejection fraction (LVEF) as that with reduced (HFrEF, LVEF ≤40%), mid-range (HFmrEF, LVEF 41%–49%) or preserved (HFpEF, LVEF ≥50%) ejection fraction (EF). This classification has replaced the earlier one dividing HF into systolic and diastolic HF. The predicted survival for HFpEF after hospitalization for HF is 35%–40% at 5 years.[16] However, HFpEF seems to be more sinister as it shows a greater prevalence of hypertension and atrial fibrillation,[17],[18] noncardiac deaths,[19] and refractoriness to therapy[1] when compared to HFrEF.


  Echocardiographic Approach in Heart Failure Top


A basic echocardiographic evaluation of a patient with known or suspected HF should include M-mode, two-dimensional (2D) echocardiography, color Doppler, pulse-wave Doppler, and continuous-wave Doppler; evaluation of strain provides better insights.[20] Assessing LV diastolic function, right ventricular (RV) function and estimating right atrial (RA) pressures are as important as assessment of systolic function while evaluating for HF. Detection of co-existent valvular disease, possible intracardiac thrombi, or dilated cardiac chambers guide the need for valve interventions, anticoagulation, or treatment of arrhythmias.[4]

Tissue doppler imaging (TDI) and speckle-tracking echocardiography (STE) have increased our understanding of LV myocardial mechanics. While TDI helps us better evaluate diastolic function and myocardial performance index (MPI), STE-based strain helps us detect subclinical LV or RV systolic dysfunction. Real-time three-dimensional (3D) echo is superior to 2D echo as it minimizes the errors of formulae and fore-shortening. Contrast echocardiography helps delineate endocardial borders better, and although less frequently employed, it does help in better visualization of thrombus, aneurysm, noncompaction, and apical hypertrophic cardiomyopathy. Stress echocardiography is used predominantly in the evaluation of CAD but also has a role in HF to look for systolic reserve and early diastolic dysfunction.

Transthoracic echocardiography is recommended in HF in only select clinical scenarios:[21]

  • Initial evaluation of suspected systolic or diastolic dysfunction
  • Re-evaluation in case of change in clinical status without change in medication or diet
  • Cardiac resynchronization therapy (CRT) device optimization
  • HF suspected due to suboptimal pacing device settings
  • Potentially cardiotoxic chemotherapy.


Routine surveillance of HF without change in clinical status is not recommended.[21]

Transesophageal echocardiography is not routinely done in HF unless the patient has a co-existent cardiac condition such as valvular heart disease, prosthetic valve, or congenital heart disease.[21]

The utility of stress echocardiography has been extended into the domains of systolic and diastolic HF, nonischemic cardiomyopathy, and athlete's hearts.[22] Normally, global contractile reserve is said to be adequate if there is an increase in LVEF by >5% and flow reserve is adequate when there is an increase in forward stroke volume by >20%.[23]

As a general rule, linear internal measurements should be obtained from 2D images to avoid oblique sections. The Teichholz and Quinones methods are no longer recommended.[24] LV volumes and EF should be measured using 3D imaging or modified Simpson's biplane method. The end-diastole is measured at the first frame after mitral valve closure and end-systole is measured at the first frame after aortic valve closure.[24] Left atrial (LA) volume should be preferably measured by the biplane-area-length method.

The evaluation of the LV function and geometry in patients with HF uses various echocardiographic parameters which may be outlined, as shown in [Table 1]:[25]
Table 1: Parameters to evaluate left ventricular function and geometry

Click here to view


While assessing LV systolic function, normal LVEF by biplane method ranges between 53% and 73% for the Indian adult.[26],[27] Further LV sphericity index (LV length/diameter in apical four-chamber view) of < 1.5 is abnormal.[25] HFrEF involves the slippage of cardiomyocytes, eccentric LV remodelling (increased LV cavity size without increase in LV mass or wall thickness) or LV wall thinning and increased sphericity.[25]

In contrast, HFpEF is associated with these morphologic adaptations of the left ventricle:[25]

  • Normal LV geometry (seen in 30% of patients with HFpEF)
  • Concentric left ventricular hypertrophy (LVH) (35%): Increased LV mass with proportionally increased LV wall thickness
  • Concentric remodeling (30%): Increased wall thickness but no significant increase in LV mass
  • Eccentric LVH (8%): Increased LV mass without proportionately increased wall thickness.


Focused approach to left ventricular systolic dysfunction and heart failure with reduced ejection fraction

Systolic dysfunction may be estimated directly or indirectly based on linear measurements, 2D measurements, spectral Doppler, and 3D evaluation.

Methods of the past which are not recommended today include mitral annular plane systolic excursion, fractional area change and Teichholz method, although the latter is still employed at various centers. The magnitude of mitral valve opening called E-point septal separation (EPSS) is an indirect M-mode marker of LV systolic function. It is actually the minimum distance between the tip of the anterior mitral leaflet and the interventricular septum measured during diastole in the parasternal long-axis view. Normally, EPSS should be <6 mm; this value increases as EF falls. Similarly, aortic valve opening in M-mode is more “rounded” as it closes when forward flow reduces.

A more reliable 2D method to calculate EF is the Simpson biplane method or the rule of disks. Here, the endocardial border of the LV is traced (excluding papillary muscles and trabeculae from the cavity) in the four-chamber and two-chamber views in the systole and diastole, and the volume of the ventricle is calculated. A proper apical view requires the transducer to be at the true apex, the beam passing through the center of the LV and obtaining the greatest apex-to-base dimension. Accurate endocardial border definition may sometimes necessitate the usage of intravenous contrast. Other indirect evidences of systolic dysfunction may be observed as LV dilation, regional wall motion abnormality or absence of systolic wall thickening; however, they do not necessarily reflect the magnitude of global systolic function.

In the presence of mitral regurgitation, using spectral Doppler at a high sweep speed of 100 mm/s, LV dP/dt may be calculated from the points in time (in ms) where mitral regurgitation jet velocity changes from 1 m/s to 3 m/s (corresponding to a pressure change of 36 − 4 = 32 mmHg) and a dP/dt of <1200 mmHg/s suggests LV systolic dysfunction. As this gradient is from the LV to LA, it is a relatively load-independent measure of LV contractility.

A more accurate assessment of LV volume is obtained by advanced 3D echocardiography which is independent of the imaging plane and free from LV cavity geometric assumptions. This thus has high inter- and intra-observer reproducibility. Additional algorithms or software modules need to be in place to assess the same for the RV.

The role of deformation, strain, and torsional evaluation in the evaluation of systolic dysfunction has been discussed in a later section.

Focused approach to left ventricular diastolic dysfunction and heart failure with preserved ejection fraction

LV diastolic filling pressures may refer to any of the following:

  • Pulmonary capillary wedge pressure (PCWP)
  • Mean left atrial pressure (mLAP)
  • LV pre-A pressure
  • Mean LV diastolic pressure
  • LV end-diastolic pressure (LVEDP)


In early stages of LV diastolic dysfunction, LVEDP alone rises (mitral A velocity, deceleration time (DT) of mitral A, Ar-A >30 ms, mitral a') due to a large atrial pressure wave, while PCWP and mLAP remain normal. With tachycardia or increased LV afterload, we observe rise in PCWP and mLAP (mitral E/A, E-velocity, DT of mitral E, E/e', tricuspid regurgitation (TR) velocity, and pulmonary S/D), which support the rationale of diastolic stress echocardiography.[27]

The four recommended variables that suggest LV diastolic dysfunction are as follows:[27]

  • Average E/e' ratio >14 (most accurate)
  • Annular e' velocity (septal e' <7 cm/s, lateral e' <10 cm/s)
  • LA volume index >34 mL/m2
  • Peak TR velocity >2.8 m/s.


Using cutoffs as septal E/e' >15 or lateral E/e' >13 are also acceptable parameters, but the average E/e' is preferred. The recommended approach by the American Society of Echocardiography and the European Association of Cardiovascular Imaging is outlined in [Figure 1].[25]
Figure 1: Algorithm to grade left ventricle diastolic dysfunction.[25] CAD = Coronary artery disease, LAP = Left atrial pressure, S/D = systolic/diastolic, TR = Tricuspid regurgitation. (From: Nagueh SF, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography: An update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr 2016;29:277-314)

Click here to view


E/A >2 may also be seen in athletes and individuals under 40 years of age (due to supranormal suction force generated during early diastole), and immediately after direct current cardioversion (diminutive A wave due to atrial stunning).

Grade III LV diastolic dysfunction is often also reflected in mitral E DT <160 ms, isovolumic relaxation time (IVRT) <50 ms, and septal and lateral e' velocities <4 cm/s, but these do not form the part of routine assessment.

For an overall assessment of diastolic dysfunction, the following cutoffs may be kept in mind [Table 2], although no single parameter should be considered in isolation:[28],[29]
Table 2: Parameters to stage left ventricular diastolic dysfunction

Click here to view


Occasionally, a mitral “L wave” may be seen in LV diastolic dysfunction but may also be seen rarely in normal individuals with bradycardia. It represents ongoing LV filling in mid diastole.

Septal E/e' >15 generally reflects PCWP >20 mmHg, and if the ratio is <8, it usually means that the PCWP is normal. For intermediate values, other parameters may be evaluated.[29] Similarly, Ar-A >30 ms also suggests an elevated LVEDP of >18 mmHg.[30]

Aging can confound with the evaluation of diastolic dysfunction causing reduced mitral E/A, mitral E DT, and annular e' velocity. However, there are indices which more definitively indicate diastolic dysfunction in the elderly: E/e' >14, mitral inflow changes with Valsalva maneuver, Ar-A >30 ms, elevated resting pulmonary artery systolic pressure (PASP), LA dilation, or LV hypertrophy.[27]

Focused approach to heart failure in special scenarios

In special clinical scenarios, assessment of elevated LV filling pressures (LV diastolic dysfunction) needs additional focus on certain echocardiographic pointers, as listed in [Table 3]:[27]
Table 3: Assessing left ventricular diastolic function in special clinical scenarios - specific echocardiographic parameters

Click here to view


Novel parameters being studied include LV untwisting rate, arterial tree pathologic wave reflection, and late systolic wall stress.

LA structure and function are meaningful markers of LV filling pressure (in the absence of mitral valve abnormalities). HFpEF makes the less compliant LV overtly dependent on the atrial pump function. LA dilation is found in about half of all patients with HFpEF,[31] while atrial fibrillation is seen in nearly 40% of HFpEF.[32] Of late, “LA peak reservoir strain” has emerged as a newer parameter showing promise in recognizing earlier stages of HFpEF.[33]

Subclinical diastolic dysfunction or unexplained dyspnea is often encountered in our clinical practice and patients may have intermediate E/e' values between 8 and 15. This subset may benefit from diastolic stress echocardiography.[34],[35] Parameters are recorded at baseline, at low-level exercise, and during recovery: Mitral E, Mitral A, annular e', and PASP. Absence of new regional wall motion abmormality, LV outflow tract obstruction, dynamic mitral regurgitation, and chronotropic incompetence favors a diagnosis of HFpEF, so does an increase in the PASP to >43 mmHg or E/e' >14, peak TR velocity >2.8 m/s. Trained athletes can generate peak TR velocity >3.1 m/s after exercise. Patients with E/e' <15 at rest but >15 with leg raise are said to have unstable relaxation abnormality.

Cohesive evaluation of systolic and diastolic dysfunction

The global assessment of both systolic and diastolic function may be assessed by the Tei index or myocardial performance index (MPI)[28] which is calculated as the ratio between the durations of (isovolumic relaxation + isovolumic contraction)/(ejection time). In short, MPI = (IVRT + IVCT)/ET. The Tei index is independent of heart rate and blood pressure and is easily reproducible even in patients with poor echo windows. Further, it may be applied to the LV and the RV. Normal values of Tei index are <0.4 for LV and <0.3 for the RV.

Rationale of myocardial deformation imaging in heart failure

While the RV generates most of its ejection by longitudinal deformation, the LV is characterized by longitudinal and circumferential shortening and radial thickening, as well as shearing in the circumferential-radial, longitudinal-radial, and circumferential-longitudinal planes. The circumferential-longitudinal shear deformation is called LV twist, which becomes possible due to the double-helical orientation of LV myocardial architecture, where endocardial fibers predominantly align alone the long axis of the LV and epicardial fibers are predominantly circumferentially aligned, subtending an angle of about 60° between each other.[36] The earlier subendocardial and later subepicardial activation during systole results in rotation of the LV base (clockwise) and apex (counter-clockwise) in opposite directions, a mere 20% shortening of myocytes translates into >55% reduction in LV cavity volume.[25] This is the basis of assessing myocardial deformation to detect milder and even subclinical forms of systolic HF.

Healthy adults are expected to have a peak LV global longitudinal strain (GLS) of around -20%, which normally decreases (numerically) with age.[24]

Impaired contraction of one layer (say, subendocardial) may be compensated by another layer thereby maintaining an apparent “normal LVEF” during early stages of HF. Subendocardial fibers are more susceptible to injury/ischemia, and hence, their impairment leads to reduced longitudinal function and right-handed helix shortening with unbalanced subepicardial left-handed helix shortening and increased circumferential shortening. Reduced longitudinal strain (with exaggerated or normal circumferential function) with preserved LVEF is often seen in patients with increasing age, hypertension, diabetes mellitus, and obesity who have HFpEF.[36]

Hence, HFpEF is not necessarily caused by diastolic dysfunction alone; systolic function can still be abnormal albeit with normal LVEF. GLS quantifies the longitudinal shortening during systole and this has been shown to be impaired in HFpEF.[36],[37],[38],[39] In later stages, once the circumferential shortening also gets impaired, measured as reduced global circumferential strain (GCS), it finally leads to HFrEF.

Probably, the earliest echocardiographic indices to detect HFpEF would be impaired longitudinal strain, LV twist and untwist unmasked by exercise.[25]

The LV twist also links systole with diastole. Systolic deformation stores the mechanical energy which facilitates rapid untwisting, recoil, and thus suction during diastole.[36] Parameters to be assessed include: displacement, velocity, strain, strain rate, LV torsion, torsional rate, early diastolic untwist, and percentage of untwist.

Based on the myocardial deformation abnormalities, early HF can be subclassified into three categories as follows:[25]

  • HF with predominant longitudinal dysfunction: (seen in severe aortic stenosis) Subendocardial impairment with compensatory hypertrophy and unopposed contractility of subepicardial layers maintains a normally preserved EF. LV circumferential strain and twist may be increased. As early relaxation is the most energy-demanding phase of the cardiac cycle, this subendocardial dysfunction leads to progressive diastolic dysfunction which is worsened with the onset of myocardial fibrosis leading to HFpEF
  • HF with predominant circumferential dysfunction: (seen in myopericardial diseases) the subendocardial layer may compensate for the reduced subepicardial contraction, thus maintaining normal LVEF. The loss of LV twist, however, results in reduced LV suction and thus LV diastolic dysfunction sets in
  • HF with transmural (longitudinal, radial, and circumferential) dysfunction: (seen in acute myocardial infarction and myocarditis) characterized by reduced LVEF and progressive LV dilation, often presenting as HFrEF.


In the Treatment of Preserved Cardiac Function Heart Failure With an Aldosterone Antagonist (TOPCAT) trial, among HFpEF patients, reduced GLS was the most important echocardiographic predictor of cardiovascular death or worsening HF.[40] In the Valsartan in Acute Myocardial Infarction (VALIANT) trial, both GLS and GCS were independently associated with all-cause mortality and combined HF death or hospitalization.[41] Increased LV segmental time-to-peak velocity and strain rate also had increased risk of all-cause mortality and HF hospitalization.[42] Apart from this, strain imaging has many other applications in HF. STE-based radial strain can guide the identification of the optimal site for LV lead placement during CRT. Improved GLS after CRT has shown to predict responders and lesser all-cause mortality at 1-year follow-up.[43]


  Right Heart Evaluation in Heart Failure Top


Pulmonary hypertension and RV dysfunction are highly prevalent in HFpEF.[44] RV assessment includes measuring RA volume, RV size, systolic function, and RV systolic pressure[24] and involves parameters, as listed in [Table 4].[24],[45]
Table 4: Echocardiographic parameters of right ventricular dysfunction’

Click here to view


While assessing RA pressure using the inferior vena cava (IVC), it should be remembered that the IVC is often dilated in young athletes and in patients on positive-pressure ventilation.

Echocardiography may be used to estimate RA pressure using the IVC, RV systolic pressure using the TR jet (thus pulmonary arterial systolic pressure), pulmonary arterial diastolic pressure (equivalent to PCWP estimated by LV E/e'), and mean pulmonary pressure using the pulmonary regurgitation jet. Hence, the group of echo parameters comprised by assessment of IVC, TR jet, pulmonary regurgitation jet, and E/e' is sometimes called “Echo Right Heart Catheterization.”[11]


  Conclusion Top


Echocardiography is indeed the single most useful tool to diagnose and evaluate HF in all its forms and stages. It stages and sub-types HF, reveals its etiology and complications, and guides medical and device-based therapy. The role of echocardiography has commendable potential to delve even further into the depths of our understanding of HF and clarifying nuances in this field.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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