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Clinical Echocardiography

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  1. Introduction to echocardiography and ultrasound imaging
    12 Chapters
  2. Principles of hemodynamics
    5 Chapters
  3. The echocardiographic examination
    3 Chapters
  4. Left ventricular systolic function and contractility
    11 Chapters
  5. Left ventricular diastolic function
    3 Chapters
  6. Cardiomyopathies
    6 Chapters
  7. Valvular heart disease
    8 Chapters
  8. Miscellaneous conditions
    5 Chapters
  9. Pericardial disease
    2 Chapters
Section 7, Chapter 7
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Aortic regurgitation

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Aortic regurgitation

Aortic regurgitation implies that the aortic valve leaks during diastole, such that blood regurgitates back from the aorta into the left ventricle. This results in volume overload in the left ventricle during diastole. The hemodynamic consequences of aortic regurgitation depend on whether the condition develops acutely or gradually.

Acute aortic regurgitation

Acute aortic regurgitation results in rapid volume overload on the left ventricle. The rapid onset results in a sudden increase in LVEDP (left ventricular end-diastolic pressure) and LAP (left atrial pressure). The left ventricle compensates by increasing cardiac output (CO); this is achieved by increasing heart rate and producing larger stroke volumes. Failure to increase cardiac output sufficiently will result in the following compilations:

  • Pulmonary edema develops due to rising LAP and LVEDP.
  • Cardiogenic shock develops if the cardiac output is insufficient.

Aortic regurgitation may cause myocardial ischemia because cardiac output diminishes in parallel with increasing myocardial load (and hence oxygen demand).

The most common causes of acute aortic regurgitation are aortic dissection, endocarditis and trauma.

Chronic aortic regurgitation

If aortic regurgitation develops gradually, then the ventricle will adapt to the volume overload. Unfortunately, adaptation implies that the left ventricle dilates, which induces irreversible cellular and extracellular processes that ultimately lead to heart failure. This initially results in greater diastolic volume and increased compliance. Increasing diastolic volumes requires that the myocardium becomes hypertrophic. Dilation and hypertrophy allow the ventricle to maintain cardiac output and prevent, or alleviate, the pressure increase in the left ventricle and left atrium.

Chronic aortic regurgitation leads to dilatation and hypertrophy of the left ventricle.

Cardiac remodeling

Ventricular dilatation and hypertrophy lead to myocardial remodeling and neurohormonal changes that further worsen the hemodynamic situation. Thus, chronic aortic regurgitation gradually leads to impaired contractile function and the development of myocardial fibrosis. Contractile dysfunction further aggravates the regurgitation (the regurgitation volume increases). Mechanically, wall stress (the load on individual muscle fibers) increases while the contractile function worsens.

Chronic aortic regurgitation also leads to increasing LVEDP and LAP, which in turn results in pulmonary hypertension and pulmonary edema.

Table 1. Causes of aortic regurgitation
Bicuspid aortic valve
Rheumatic heart disease
Calcified aortic valves
Idiopathic aortic dilatation (aneurysm)
Aortic dissection, proximal
Marfan syndrome (may also cause aortic dissection)
Vasculitis, rheumatic diseases
Ehlers-Danlos syndrome (may also cause aortic dissection)
Subaortic membrane

Echocardiography in aortic regurgitation

2D Echocardiography

The images are acquired in PLAX (parasternal long-axis view) and PSAX (parasternal short-axis view), with the valve zoomed. The following parameters are evaluated:

  • Can all three cusps be visualized, or is the valve bicuspid?
  • Is there cusp prolapse?
  • Are there vegetations on the valve?
  • Is the valve calcified?
  • Is the aortic root dilated?
  • Is the left ventricle dilated?
  • Is the left ventricle hypertrophic?
  • Is left ventricular ejection fraction (LVEF) normal?

A normal-sized ventricle with hyperdynamic contractility suggests acute aortic regurgitation.

The severity of aortic regurgitation can be evaluated using the following parameters.

Diameter of the regurgitant jet

The diameter of the regurgitant jet is measured in PLAX, and then compared with the diameter of the LVOT. A jet diameter smaller than 25% of the LVOT diameter suggests moderate aortic regurgitation. A jet diameter >65% of the LVOT diameter suggests severe aortic regurgitation (Figure 1).

Figure 1. Diameter of the regurgitant jet (aortic regurgitation).
 Table 1. Severity of aortic regurgitationJet size ratio
Severe> 65

Vena contracta

Vena contracta is also measured in PLAX with the aortic valve zoomed (Figure 2). Vena contracta is the narrowest diameter of the jet and reflects the regurgitant orifice area. A vena contracta <0.3 cm wide suggests mild aortic regurgitation, whereas vena contracta >0.6 cm indicates severe aortic regurgitation.

Figure 2. Measurement of the width of vena contracta in aortic regurgitation.

PHT (Pressure Half Time)

Pressure half time (PHT) is defined as the time it takes for the initial maximal pressure gradient across the aortic valve to fall by 50% during diastole. The drop in the pressure gradient is gradual in patients with mild aortic regurgitation. The drop is rapid in patients with severe aortic regurgitation (Figure 3, Table 2). Pressure half time is measured with continuous Doppler in apical views (3C or 5C).

Figure 3. Assessing severity of aortic regurgitation using pressure half time (PHT).
  Table 2. Severity of aortic regurgitationPressure Half Time (ms)
Mild>500 ms
Moderate500-349 ms
Moderate-severe349-200 ms
Severe< 200 ms

It is important to note that the estimated severity of aortic regurgitation depends on the hemodynamic circumstances; severity is overestimated in patients with a significantly increased LVEDP.

Diastolic flow reversal

Diastolic flow reversal can be detected with Doppler recordings in the suprasternal window. Pulsed wave Doppler is placed along the ascending or descending aorta (Figure 4). The Doppler signal reveals whether there is flow reversal in the aorta during diastole; this backflow is referred to as diastolic flow reversal.

Note that the elasticity of the aorta depends on age; young patients have high compliance in the aorta, which during diastole produces a recoil that forces blood in the retrograde and antegrade direction. Hence, mild (physiological) flow reversal is normal in young individuals.

Normal and pathological flow reversal can be distinguished by means of the spectral curve. Pathological diastolic flow reversal exists throughout diastole and, generally, has velocity >20 cm/s at the end of diastole. The term holodiastolic flow reversal is used to denote flow reversal proceeding throughout diastole.

Figure 4. Diastolic flow reversal in aortic regurgitation.

Estimation of regurgitation volume and effective regurgitant orifice area (EROA)

Regurgitation volume (Vregurg) can be calculated using the following three methods.

Method 1: Stroke volume

According to the continuity equation, flow across the mitral valve is equal to flow across the aortic valve. Using pulsed wave Doppler, the volume flowing across the aortic valve (i.e stroke volume) and the mitral valve can be calculated. The difference between these two volumes is equivalent to the regurgitation volume (Vregurg). The stroke volume across the aortic valve (SVaorta) is equivalent to the volume of blood flowing through the aortic valve in anterograde direction minus the volume leaking back during diastole. This volume can be calculated by the following formula:

SVaorta = areaLVOT × VTILVOT

The volume of blood flowing across the mitral valve is equivalent to the anterograde stroke volume across the valve (SVmitral):

SVmitral = Areamitral × VTImitral

Thus, the regurgitation volume (Vregurg) can be calculated as follows:

Vregurg = SVaorta – SVmitral

This formula must not be used in the setting of mitral regurgitation.

It is also possible to calculate SVaorta using the following formula:

(Simpson’s method)
LVEDV = Left ventricular end-diastolic volume; LVESV = left ventricular end-systolic volume

Method 2: PISA (Proximal Isovelocity Surface Area)

The regurgitation volume is the product of the effective regurgitation orifice area (EROA) and the regurgitant jet VTI:

Vregurg = EROA × VTIAR jet

EROA is the effective regurgitant orifice area and is calculated using PISA (Proximal Isovelocity Surface Area). PISA is the semicircle visualized with color Doppler. PISA should be measured carefully, which requires zooming the area and minimizing the color sector in order to increase the resolution (higher frame rate). If the regurgitation is obliquely directed, a parasternal view should be used for the measurement. If the regurgitation is centrally directed, an apical view should be used. The Doppler baseline (Nyquist limit) should be adjusted to optimize the image. The following measurements are made:

  1. rPISA (PISA radius)
  2. vmax AR (maximum velocity of the regurgitation, measured using CW doppler)
  3. VTIAR jet

Calculation of EROA:

PISA = 2𝛑 × rPISA2

EROA = PISA × valiasing / vmax AR

If the regurgitation volume (Vregurg) has already been calculated, EROA can be obtained using the following formula:

EROA = Vregurg / VTIAR jet

Grading the regurgitation using EROA

EROA <0.1 cm2 suggests mild aortic regurgitation. If EROA is >0.3 cm2, then the regurgitation is severe.

Grading the regurgitation using Vregurg

Regurgitation volume <30 ml/stroke implies that aortic regurgitation is moderate. Regurgitation volume >60 ml/stroke is classified as severe aortic regurgitation.

Method 3: Regurgitation fraction (Fregurg)

Regurgitation fraction (Fregurg) is the proportion of blood that regurgitates back into the ventricle. The fraction is calculated by the following formula:

Fregurg = Vregurg / SVaorta

SVaorta = areaLVOT x VTILVOT

  • Regurgitation fraction < 30% indicates moderate aortic regurgitation.
  • Regurgitation fraction > 50% indicates severe aortic regurgitation.


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