Early diastolic mitral annular velocity

e′ (E′) · Pulsed tissue Doppler, apical 4-chamber, sample volume on the septal and lateral mitral annulus; average the two

Normal range & thresholds

Pathophysiology

Raised by

• Youth and athletic conditioning (e′ >15 cm/s lateral is normal in the young)
• Constrictive pericarditis — annulus paradoxus: medial e′ is preserved or high (>7–8 cm/s) despite severe heart failure, because longitudinal motion is spared while the rigid pericardium restricts lateral expansion; and annulus reversus, septal e′ exceeding lateral e′ — both are among the most specific signs in echocardiography^[57]
• After successful decongestion and after relief of ischaemia (modest true improvement)
• Significant mitral regurgitation with a normal ventricle (falsely reassuring)

Lowered by

• Ageing — the dominant physiological determinant; interpret only against an age-matched threshold
• Left ventricular hypertrophy of any cause; hypertension
• Ischaemia and prior infarction (regional if the sampled wall is involved)
• Infiltrative and storage disease — amyloid (with s′ and a′ also <5 cm/s: the ‘5-5-5 sign’), Fabry, sarcoid, haemochromatosis^[2,30]
• HCM, restrictive cardiomyopathy, diabetes, chronic kidney disease, obesity
• Any cause of reduced systolic function (systolic and diastolic dysfunction travel together)
• Mechanical constraint: mitral annular calcification, annuloplasty ring, mitral prosthesis, prior mitral surgery — the annulus cannot move, whatever the myocardium is doing

Technique & pitfalls

• Angle of insonation <20° to longitudinal annular motion — this is a velocity, and cosine error is unforgiving.
• Sample volume 5–10 mm placed on the annulus, kept within its excursion throughout the cycle.
• Sweep speed 50–100 mm/s; low wall filter; gain low enough to see a clean spectral edge without spectral broadening.
• Measure and report both septal and lateral and their average. Where they diverge (regional infarct, LBBB, pacing, constriction) the divergence is itself diagnostic information.^[2,57]
• In left bundle branch block, RV pacing or after cardiac surgery, the septal value is unreliable — the 2025 guideline directs you to the lateral annulus.^[2]
• In pulmonary hypertension, use the lateral annulus, because septal flattening from RV pressure corrupts the septal signal.^[2]

Pseudo-change & artefact

• Mitral annular calcification and mitral prostheses tether the annulus and lower e′ without any relaxation abnormality — the largest single source of false diastolic dysfunction.
• Angle error and sample-volume drift into the cavity.
• Regional wall motion abnormality in the sampled segment makes a single-site value non-representative.
• Cardiac translation and respiratory motion.
• High wall filter truncating the low-velocity signal.
• Load: e′ is relatively but not completely preload-independent — in a normal ventricle (and only there) it does rise with preload.

Treatment thresholds

• e′ is the entry point of the 2025 ASE algorithm, not a treatment target. Its formal role: if e′ is reduced, one additional abnormal criterion establishes diastolic dysfunction; if e′ is preserved, two are required.^[2]
• Constrictive pericarditis: medial e′ >7–8 cm/s (annulus paradoxus) and septal > lateral (annulus reversus) support constriction over restriction, and that distinction is the decision to operate — pericardiectomy versus medical management of an infiltrative cardiomyopathy.^[31,57]
• Amyloidosis: the 5-5-5 pattern (s′, e′, a′ all <5 cm/s) is a red flag that triggers free light chains and bone scintigraphy — which lead to disease-modifying therapy.^[30]
• Heart transplant follow-up: a fall in e′ with a rising E/e′ supports the assessment for rejection or restrictive physiology, using the guideline’s transplant-specific algorithm.^[2]

Next step

• Next: compute E/e′ and measure peak TR velocity — the three primary variables must be assessed together (card 19).
• Then: if these are discordant or incomplete, add LA reservoir strain (≤18% abnormal), pulmonary vein S/D (≤0.67 abnormal), LAVI (>34 mL/m²) and IVRT.^[2]
• Then: when e′ is low with thick walls, take the infiltrative pathway — strain bull’s-eye, ECG voltage, CMR mapping, light chains, bone scintigraphy.^[30]
• Then: when e′ is low with a normal-looking heart and exertional dyspnoea, proceed to diastolic stress echocardiography.^[105,106]

Drugs

• No drug reliably and substantially raises e′. This is the honest answer, and it is worth saying in the report: relaxation abnormalities are structural.
• Small improvements follow LVH regression with RAAS blockade, relief of ischaemia by revascularisation, rate control that lengthens diastole, and effective long-term decongestion.^[66,67]
• SGLT2 inhibitors and ARNI improve E/e′ mostly by lowering E (filling pressure), with only marginal change in e′.^[68,69,82]
• Mavacamten improves e′ and E/e′ in obstructive HCM.^[72]
• Enzyme replacement in early Fabry improves e′; tafamidis slows deterioration in ATTR.^[75]

Reversibility