E/A ratio

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The E/A ratio is a marker of the function of the left ventricle of the heart; it is determined on echocardiography, an ultrasound-based cardiac imaging modality. Abnormalities in the E/A ratio on Doppler echocardiography suggest that the left ventricle, which pumps blood into the circulation, cannot fill with blood properly in the period between contractions. This phenomenon is referred to as diastolic dysfunction and can eventually lead to the symptoms of heart failure.[1]

The heart is a biological pump designed to move blood through the brain and body. It has four collecting chambers: two upper chambers, the atria (single:atrium), stacked on top of two lower chambers (the ventricles). The atria are separated from the ventricles beneath by valves that act like trap doors. They transfer blood to the ventricles in 2 steps: in the first step, the weight of the collected blood in each atrium causes it to fall into the ventricles below when the "trap door" valves open; focusing on the left side, the speed at which the blood moves during this initial action is called the "E" ( for early) filling velocity. But some blood always remains, so toward the end of the atrial emptying cycle (diastole), the second step occurs in which the atria contract to squeeze out that last bit ("atrial kick"). The speed of the blood filling the ventricle in this step is the "A" (for atrial) filling velocity.

The E/A ratio is the ratio of the early (E) to late (A) ventricular filling velocities. In a healthy heart, the E velocity is greater than the A velocity. In certain pathologies and with aging, the left ventricular wall can become stiff, increasing the back pressure as it fills, which slows the early (E) filling velocity, thus lowering the E/A ratio.

The reversal of the E/A ratio ('A' velocity becomes greater than 'E' velocity) is often accepted as a clinical marker of diastolic dysfunction, in which the left ventricular wall becomes so stiff as to impair proper filling, which can lead to diastolic heart failure. This can occur, for instance, with longstanding untreated hypertension.

The late phase is dependent upon atrial contraction and is therefore absent in patients with atrial fibrillation, making the E/A ratio very large.[citation needed]

The E:A ratio is a first generation test for diastolic performance of the heart.

Diastolic relaxation is divided into four distinct phases during the cardiac cycle:[1]

  1. isovolumetric relaxation (abbreviated as IVRT)
  2. early filling
  3. diastasis
  4. atrial contraction.

In short, there are a number of factors that influence ventricular filling during each of these phases, but remember that the main factor is the driving gradient between the atrial and ventricular pressure.

The E/A ratio is measured by placing a pulse wave doppler across the mitral valve, and measuring the velocities across the valve. Hence the other names for the test - transmitral velocity profile or transmitral doppler waveforms.

Pulse wave doppler allows measurement of velocities at a specific point, but has the disadvantage of aliasing, so often has to be adjusted (baseline shifted etc.) to best fit the individual point of measurement.

IVRT is measured as the time between the closure of the aortic valve and the opening of the mitral valve.

The normal transmitral flow profile has two peaks - an E and an A wave.

The E peak arises due to early diastolic filling. Most filling (70-75%) of the ventricle occurs during this phase.

The A peak arises due to atrial contraction, forcing approximately 20-25% of stroke volume into the ventricle.

The deceleration time (DT) is the time taken from the maximum E point to baseline. Normally in adults it is less than 220 milliseconds.

Below is a transthoracic image - for those with TEE/TOE experience, simply invert the image mentally, but the concept is the same.

On the left is a heart with normal diastolic function, and on the right is a heart of impaired relaxation (note the different height of the E and A waves). Note the DT is prolonged - another hallmark of impaired relaxation.

Note too the timing according to the ECG - the waves are being measured prior to the commencement of the QRS complex (the start of systole). The A wave corresponds to the mechanical action of the electrical P wave on the ECG.

Grading of ventricular diastolic dysfunction[edit]

From this, a number of grades of diastolic function can be determined:

  1. Normal diastolic function (E > A)
  2. Impaired relaxation (E:A reversal i.e. E is < A)
  3. Pseudonormal (E:A ratio appears normal)
  4. Restrictive filling (E:A ratio often > 2)

Pseudonormalisation shows a transmitral profile that appears normal, however with the use of pulmonary vein pulse wave doppler, it can be shown that the relaxation pattern is abnormal (systolic blunting, a decrease in the height of the S wave). In addition, performance of a valsalva manoeuvre will result in unmasking of the pseudonormal state.


  • Cursor position is important - if the PW sample window is incorrect, it will produce artifact. The cursor should be placed at the level of the open leaflets in diastole.
  • Presence of mitral valve abormalities e.g. mitral stenosis will alter the pressure gradients and change loading conditions of the LV.
  • Presence of AI - aortic incompetence will result in a rapid rise in LV diastolic pressure, limiting the gradient across the mitral valve during diastole.
  • Heart rate & rhythm - loss of a normal atrial rhythm e.g. atrial fibrillation will cause loss of the A wave. The height of the E wave now becomes dependent on the length of the cardiac cycle (variable) rather than a true measure of diastolic function. Similarly, pacing and tachycardia can result in alterations, whereas bradycardia actually increases the E/A ratio.

These are some of the disadvantages of first generation testing methods.

Diastolic function should be assessed normally in addition to the twenty views. It is important in establishing a number of cardiac conditions - e.g. pericardial tamponade (where E/A ratios across the tricuspid valve are often more important), restrictive pericarditis vs constrictive cardiomyopathy etc.