Mitral inflow E and A velocities, E/A ratio

E, A, E/A · Pulsed Doppler, apical 4-chamber, 1–3 mm sample volume at the mitral leaflet tips, sweep 100 mm/s

Normal range & thresholds

Age matters more than any single cut-point. 2025 ASE age-stratified normal ranges:

Age (y)	E (m/s)	A (m/s)	E/A
20–39	0.54–1.11	0.24–0.68	0.88–2.73
40–60	0.47–1.02	0.33–0.82	0.69–2.07
60–80	0.39–0.92	0.43–0.97	0.50–1.40

Decision cut-points: E/A ≤0.8 (impaired relaxation pattern) · E/A 0.8–2 (grading depends on the other markers) · E/A ≥2 with a short deceleration time (restrictive filling, markedly elevated LAP).^[2]

Pathophysiology

E is generated by the left atrium-to-left ventricle pressure gradient in early diastole, which is the product of two opposing forces: how high the atrial pressure is (pushing) and how fast the ventricle relaxes and recoils (sucking). A reduces to how hard the atrium can contract into a ventricle whose stiffness it must overcome. The clinical trap follows directly: as disease progresses, impaired relaxation first lowers E (E/A ≤0.8), then rising atrial pressure pushes E back up through the normal range (pseudonormalisation, E/A 0.8–2), and finally dominates completely (E/A ≥2). The E/A ratio traverses the normal range twice, which is why it can never be interpreted alone.^[2]

Raised by

E raised: elevated LA pressure of any cause; significant mitral regurgitation (transmitral volume); mitral stenosis; high-output states, anaemia, pregnancy, thyrotoxicosis; left-to-right shunt; youth
A raised: impaired relaxation with a preserved, hypertrophied atrium — the compensatory phase; first-degree AV block with a well-timed atrial kick; bradycardia
E/A ≥2: restrictive filling — advanced HFrEF, restrictive and infiltrative cardiomyopathy, constrictive pericarditis, acute severe MR or AR

Lowered by

E reduced: impaired relaxation (ageing, LVH, ischaemia, hypertension); hypovolaemia; tachycardia; significant mitral stenosis reduces the gradient decay rather than E itself
A reduced or absent: atrial fibrillation (absent by definition), atrial standstill, LA mechanical failure after cardioversion or ablation (‘atrial stunning’), amyloid atrial infiltration, markedly elevated LV end-diastolic pressure that opposes atrial emptying
E/A ≤0.8: grade 1 diastolic dysfunction — normal above the age of 60–65, abnormal below it

Technique & pitfalls

Sample volume at the leaflet tips, where velocities are maximal — at the annulus, E is lower and the ratio changes.
Sweep speed 100 mm/s; measure at end-expiration; average 3 cycles in sinus rhythm, 5–10 in AF.
Do the Valsalva manoeuvre when the pattern looks normal but the clinical picture does not: a fall in E/A of ≥50% unmasks pseudonormal filling; in grade 3, reversal to E/A <2 defines ‘reversible restrictive’ physiology and carries a better prognosis.^[2]
Report the deceleration time from the same trace (card 15).
Record with the patient in a steady state — not immediately after exertion, coughing, or a fluid bolus.

Pseudo-change & artefact

E–A fusion at heart rates >100/min or with PR >200 ms merges the waves and invalidates the ratio (2025 guideline: PR >280 ms with impaired relaxation almost guarantees fusion).^[2]
Sample volume placed at the annulus, or angled >20° to inflow — both underestimate.
Respiration: velocities vary by 10–15% normally, and >25% variation is itself a sign of constriction or tamponade — always measure at end-expiration.
Preload: acute diuresis converts grade 3 to grade 2 or even 1 within hours — the ventricle has not improved, only the load.
Significant mitral regurgitation, mitral stenosis, prosthesis or annular calcification: E is no longer a filling-pressure signal.
Ectopy and post-extrasystolic beats.

Treatment thresholds

No intervention threshold is defined by E, A or E/A in isolation — they are inputs to the grading algorithm and to the filling-pressure estimate.
E/A ≥2 with deceleration time <160 ms (restrictive filling) identifies a high-risk phenotype in HFrEF, amyloid and restrictive cardiomyopathy, and is used to intensify decongestion and accelerate advanced-therapy referral.^[2,30]
Mitral stenosis: the same trace gives the mean gradient and the pressure half-time that define severity and the intervention threshold (cards 34 and 37).^[5,6]
Valsalva-reversible restrictive filling (grade 3a) has substantially better outcomes than fixed restrictive filling (grade 3b) — a prognostic, not a therapeutic, threshold.^[2]
In the 2025 atrial fibrillation algorithm, mitral E ≥100 cm/s and deceleration time ≤160 ms are two of the four primary criteria for elevated LAP.^[2]

Next step

Next: complete the three primary variables — e′, E/e′ and peak TR velocity — then apply the 2025 algorithm (card 19).
Then: where the primaries are discordant, add LA reservoir strain, pulmonary vein S/D, LAVI and IVRT.
Then: if resting filling pressures are normal but the patient is breathless, perform a diastolic stress echocardiogram.^[105,106]
Then: natriuretic peptides, and right heart catheterisation with exercise if the diagnosis still matters and remains unresolved.

Drugs

Diuretics move this pattern faster and further than anything else — E falls, E/A falls, deceleration time lengthens, within hours. Always note the diuretic status on the report.
Beta-blockers and non-dihydropyridine calcium blockers lengthen diastole, separate E and A, and improve filling in tachycardia and HCM.
RAAS blockade, ARNI and SGLT2 inhibitors improve the pattern over months by lowering filling pressures and promoting reverse remodelling.^[68,69]
Nitrates and other preload reducers lower E acutely; fluid loading and transfusion raise it.
Restoration of sinus rhythm restores the A wave — though atrial stunning delays it by days to weeks.

Reversibility

Highly and rapidly reversible in its load-dependent component, slowly reversible in its structural component. Decongestion alone converts a restrictive pattern to a pseudonormal or impaired-relaxation pattern within days in most patients — documented in essentially every heart failure admission. The underlying relaxation abnormality (e′) barely moves over the same period. Persistent restrictive filling despite adequate decongestion identifies fixed disease and predicts poor outcome.^[2]