Echocardiographic Assessment of Patients with Systolic Heart Failure

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2 Echocardiographic Assessment of Patients with Systolic Heart Failure

Sorin Pislaru, Maurice Enriquez-Sarano

Definition, Staging, and Etiology of Systolic Heart Failure

• Heart failure (HF): abnormality of cardiac function responsible for inability of the heart to provide blood flow at rates commensurate with tissue requirement, or to do so only at increased filling pressures.
• HF stages1

Stage A: risk factors for HF, but normal ventricular function, no symptoms
Stage B: ventricular dysfunction (systolic/diastolic), but no symptoms
Stage C: ventricular dysfunction and mild symptoms
Stage D: ventricular dysfunction and severe symptoms
• Systolic heart failure

• Implies impairment of systolic ventricular function.
• It is a common end stage for a variety of cardiac diseases.
• It can be left ventricular, right ventricular, or biventricular.

• Various etiologies2

• Coronary artery disease—approximately 60% to 70% of systolic HF
• Dilated cardiomyopathy

• Idiopathic
• Infectious (viral, HIV, Chagas’ disease, Lyme disease)
• Toxic (alcohol, cocaine, anthracyclines)
• Metabolic (thiamine and selenium deficiencies, thyroid disorders, hemochromatosis)
• Genetic

• Valvular disease
• Other (peripartum, tachycardia-induced, autoimmune, familial, sarcoidosis, obstructive sleep apnea, etc.)
• The single most useful diagnostic test in the evaluation of patients with HF is the comprehensive two-dimensional (2D) echocardiogram coupled with Doppler flow studies.1 The goals of echocardiography in systolic HF are:

• Define etiology and in particular determine if systolic HF is due to a primary myocardial disease (including consequences of coronary disease) or a primary valve disease.
• Define the degree of systolic ventricular dysfunction and remodeling (Table 2-1).
• Define the degree of diastolic ventricular dysfunction (addressed in Chapter 3).
• Define the presence and severity of functional mitral regurgitation (MR) and/or tricuspid regurgitation.
• Define the hemodynamic consequences (cardiac output, pulmonary and atrial pressures).

TABLE 2-1 LEFT VENTRICULAR QUANTIFICATION METHODS: USE, ADVANTAGES, AND LIMITATIONS

Dimension/Volumes Use/Advantages Limitations
Linear
M-mode Reproducible Beam frequently off-axis
High frame rates Single dimension not representative in distorted ventricles
2D-guided Assures orientation perpendicular to LV axis Lower frame rates than in M-mode
  Single dimension only
Volumetric
Biplane Simpson’s method Corrects for shape distortions Apex frequently foreshortened
Minimizes mathematic assumptions Endocardial dropout
  Relies on only two planes
Area-length method Partial correction for shape distortion Based on mathematic assumptions
3D echocardiography Best correlation with MRI Endocardial definition
Further enhanced by contrast use  

Echocardiographic Methods for Assessment of Left Ventricular Systolic Function

Image Acquisition and Interpretation

• Various imaging modalities can be used for assessment of left ventricular systolic function (see Table 2-1).
• Classical indexes of left ventricular function are derived from linear and volumetric data.3
• Image optimization is a key step in obtaining accurate measurements. Always adjust focus depth, sector size, and lateral gains to optimize axial and temporal resolution.
• Harmonic imaging increases wall thickness and decreases internal dimensions slightly.
• Color B-mode maps and/or intravenous contrast may be needed for wall motion analysis.
• Assessment by Doppler echocardiography is always comprehensive, integrating all methods available (e.g., ejection fraction [EF] is judged visually and compounded with calculated EF from M-mode or 2D diameters or LV volumes).

Indexes of Global Left Ventricular Systolic Function

• Left ventricular size

• LV size is measured by the diameter at the mitral leaflet tips; calculation is simple but not linearly related to LV volumes.
• Left ventricular volumes can be calculated from 2D imaging (area-length or method of disks) and from three-dimensional (3D) imaging with specific software. End-systolic volume index is an important index of LV remodeling and function.

• EF by visual assessment

• This value is an estimation based on appreciation of ventricular area change in systole from multiple views.
• Calculation is simple but underestimates EF in the very low range (an area change of 10% equals an EF of 19%).
• It serves as a background check for calculation methods.

• EF by linear measurements (Figure 2-1)

• Calculation is based on the LV internal diameter at end-diastole and end-systole.
• Electrocardiography (ECG) serves only as a guidance; valve and wall motion should also be considered in selecting end-diastolic and end-systolic frames.3
• EF calculations are based on Teichholz or Quiñones methods.
• Linear measurements (M-mode, 2D) have several disadvantages (see Table 2-1).
• EF by volumetric measurements (Figure 2-2)

• Calculation does not have geometric assumptions.
• LV apical foreshortening and lateral resolution on 2D images can be significant limitations (see Table 2-1).
• 3D contrast-enhanced echocardiography has the best correlation with magnetic resonance imaging (MRI) in terms of assessment of LV and RV volumes.
• Stroke volume and cardiac output (Figure 2-3)

• These values are based on 2D (LV outflow tract [LVOT] dimension and calculated area) and Doppler (blood velocity) measurements, with calculation of stroke volume as the product of LVOT area by time-velocity integral (TVI).
• LVOT diameter measurement can be underestimated, and small errors in LVOT measurements are squared in area calculation. Careful zoomed imaging with decreased gain, and learning curve with calculation of cardiac index, are essential in accuracy.
• Other parameters used in assessment of global LV systolic function

• Mitral annular systolic velocity (tissue Doppler imaging [TDI])
• Global left ventricular peak systolic strain (Figure 2-4)
• Estimated left ventricular dP/dt (Figure 2-5)
• LV mass is measurable using wall thickness and LV size and is particularly important in hypertensive patients. LV mass is always increased with LV dilatation, but prognosis is more based on quality than on quantity of muscle.

image

Figure 2-1 Left, M-mode measurement of left ventricular end-diastolic (LVEDD) and end-systolic (LVESD) dimensions. EF can be then calculated based on Teichholz or Quiñones formulas. Right, Note that only the M-mode obtained along the center line is perpendicular to the LV long axis. M-mode images obtained on the outer lines would overestimate left ventricular size, a common problem in M-mode measurements.

image

Figure 2-2 EF measurement based on the method of disks. End-systolic and end-diastolic frames are used to trace the endocardial border on standard apical 4-chamber (top panel, left ventricle on the left side) and 2-chamber (bottom panel ) views.

image

Figure 2-3 Stroke volume (SV) calculations are based on measurement of LVOT diameter and LVOT TVI. The LVOT is assumed to be circular and the area is calculated by the formula: A = π × d2/4 = 0.785 × d2. The cardiac output is then calculated by multiplying the SV and the heart rate at the time of acquisition.

image

Figure 2-4 Measurement of left ventricular peak longitudinal systolic strain in a patient with hypertrophic cardiomyopathy. The software automatically tracks the area of interest and calculates left ventricular strain based on speckle tracking (left panel—example of tracking in 4-chamber view). The average peak negative systolic strain can be then calculated from measurements performed on each of the 17 segments, and can be displayed as a bull’s-eye diagram (right panel); this can also serve for assessment of regional left ventricular function. The peak negative longitudinal systolic strain has gained importance in assessment of early changes in systolic function in patients with infiltrative and hypertrophic cardiomyopathies.

image

Figure 2-5 Measurement of left ventricular systolic dP/dt is based on the mitral regurgitant signal. Since in the very early phase of systole the MR does not significantly increase the atrial pressure, it can be assumed that the increase in MR regurgitant velocity directly reflects changes in intraventricular pressure. By measuring the time needed for the MR velocity to increase from 1 to 3 m/s, dP/dt can be calculated according to the formula: dP/dt = (4 × 32 − 4 × 12)/time = 32/time.

Assessment of Regional Left Ventricular Function

• Assessment of regional wall motion abnormalities (RWMAs)

• The American Society of Electrocardiography (ASE) recommends a 17-segment LV model (Figure 2-6).
• Motion of each segment is evaluated on a semiquantitative scale (1 = normal or hyperkinesis; 2 = hypokinesis; 3 = akinesis or negligible thickening; 4 = dyskinesis/paradoxical systolic motion; 5 = aneurysmal).

• RWMA due to ischemia does not occur at rest until epicardial coronary artery stenosis is greater than 85%.
• Echocardiography overestimates the area of ischemic or infarcted myocardium as adjacent regions are affected by tethering, regional loading conditions, and stunning.
• The presence of regional left ventricular dysfunction not respecting coronary distribution can be seen in various diseases, such as post–coronary artery bypass grafting, infiltrative cardiomyopathies (sarcoidosis), cardiac tumors, myocarditis, etc.
• Other tools are gaining momentum in assessing regional wall motion, particularly segmental left ventricular strain or strain rate (see Figure 2-4).
image

Figure 2-6 The 17-segment model used for assessment of left ventricular regional wall motion. Top panel: Short-axis schematic with six basal and midventricular segments and four apical segments. Bottom panel: Corresponding long-axis parasternal and apical 4-chamber and 2-chamber views. The 17-segment model adds an apical cap segment.

Assessment of LV Diastolic Function

• LV relaxation is always slowed when systolic function is reduced.
• Diastolic dysfunction analysis is based on the combination of mitral and pulmonary venous flows and TDI.
• Simple relaxation abnormality (stage I) is benign, while restrictive filling (stage III/IV) indicates elevated filling pressures.

Assessment of Functional Regurgitation (Mitral, Tricuspid)

• Assess structural normalcy of valves.
• Estimate or, better, quantify regurgitation.

Assessment of Hemodynamic Consequences

• Estimate right atrial pressure using inferior vena cava size and variation, and right ventricular pressure using tricuspid regurgitation velocity.
• Calculate cardiac index.

Key Points

• Left ventricular internal diameter and EF are key parameters in the diagnosis and follow-up assessment of systolic dysfunction.
• Several guidelines include LV size and EF in decision making.
• The ASE recommends use of biplane method of disks (modified Simpson’s method) for EF calculations.
• Erroneous LVOT measurements can introduce large errors in estimation of cardiac output and severity of valvular disease.
• RWMAs at rest can occur both with ischemic and nonischemic cardiomyopathies.
• Assessment of LV strain and strain rate are increasingly used.

Echocardiographic Assessment of Specific Causes of Systolic Heart Failure

Ischemic LV Dysfunction

• Ischemic LV dysfunction is the most common cause of systolic HF.
• The presence of resting RWMAs in a coronary artery distribution pattern and/or evidence of old myocardial infarction (thinned, scarred myocardial wall; LV aneurysm) are key echocardiographic findings.
• Resting RWMAs can also be seen with stunned/hibernating myocardium and occasionally in non-ischemic disease.
• Intravenous contrast should be used whenever endocardial border definition is suboptimal in two or more contiguous segments.
• Stress echocardiography is an established method of assessment of myocardial ischemia.

• Exercise (treadmill or stationary bike) is the preferred stress method. It can be combined with oxygen consumption for better quantification of exercise ability. Dobutamine is the most commonly used pharmacologic stress agent.
• Interpretation is based on regional wall motion analysis and global response to stress (change in left ventricular dimension and EF with stress).
• With stress, RWMAs can occur with epicardial coronary stenoses as low as 50%.
• A biphasic response to dobutamine in at least two segments with resting RWMAs (improvement at low dose followed by worsening at high dose) is suggestive of viable myocardium and epicardial coronary artery disease (hibernating myocardium).

• MR can be associated with ischemic left ventricular dysfunction, and is most commonly due to tethering of the posterior mitral leaflet (Figure 2-7); an effective regurgitant orifice (ERO) greater than 0.20 cm2 and a regurgitant volume greater than 30 mL are associated with poor prognosis.
• Always assess for intraventricular thrombus in patients with low EF and aneurysmal changes (Figure 2-8). This is best done by administration of intravenous contrast.
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