Mitral E-wave deceleration time

DT · Same pulsed Doppler trace as E and A; slope of the E-wave descent extrapolated to the baseline

Normal range & thresholds

Normal 160–240 ms (lengthens with age; >240 ms with a low E/A is the impaired-relaxation pattern). DT <160 ms with E/A ≥2 defines restrictive filling; DT <130 ms in dilated cardiomyopathy carries a particularly adverse prognosis.^[2]
In mitral stenosis the same slope yields the pressure half-time (PHT = 0.29 × DT) and hence valve area (MVA ≈ 759 / DT).^[43]

Pathophysiology

Deceleration time is a measure of how quickly the atrioventricular pressure gradient is abolished after mitral opening, and that speed is set by operating chamber stiffness. A stiff ventricle equilibrates with the atrium almost instantly — a short, steep E wave. A compliant ventricle absorbs the inflow with little pressure rise, so the gradient decays slowly — a long deceleration. In mitral stenosis the same logic is inverted: a narrow orifice sustains the gradient, so deceleration is prolonged in proportion to the obstruction.^[2,43]

Raised by

Impaired relaxation — ageing, LVH, hypertension, ischaemia (grade 1 pattern: low E/A, long DT)
Mitral stenosis — the prolongation is the basis of the pressure half-time method
Hypovolaemia; bradycardia
Constrictive pericarditis paradoxically shows a short DT, not a long one — see below

Lowered by

Restrictive filling — advanced HFrEF, restrictive and infiltrative cardiomyopathy (amyloid), acute severe mitral or aortic regurgitation
Constrictive pericarditis — abrupt cessation of filling by the rigid pericardium
Markedly elevated LA pressure of any cause; tachycardia
Significant aortic regurgitation with premature mitral closure
After acute volume loading

Technique & pitfalls

Draw the tangent along the steepest part of the E-wave downslope and extrapolate it to the zero baseline — do not measure to the point where the tracing meets the baseline, which is systematically longer.
Sweep speed 100 mm/s; sample volume at the leaflet tips.
Average 3 beats; in AF choose cycles with similar preceding RR intervals and average 5–10.
If a mid-diastolic L wave is present (marked impairment of relaxation with high filling pressures), define the E downslope before the L wave — and report the L wave, which is itself a marker of elevated LAP.
In mitral stenosis, measure the mid-diastolic slope, not the initial steep segment, and never after a long post-extrasystolic pause.

Pseudo-change & artefact

Extrapolation error — different observers routinely differ by 20–30 ms, which is enough to cross a grading boundary.
E–A fusion at high heart rates truncates the downslope and shortens DT artefactually.
Diuresis lengthens DT; fluid loading shortens it — without any change in the myocardium.
In mitral stenosis, the pressure half-time is invalidated by significant aortic regurgitation, by an atrial septal defect, by tachycardia, and immediately after balloon valvuloplasty (see card 37).^[5]
Post-extrasystolic beats and irregular rhythm.

Treatment thresholds

Mitral stenosis: DT is the source of the pressure half-time, and PHT ≥150 ms (MVA ≤1.5 cm²) defines severe mitral stenosis — the anatomical criterion for intervention (cards 34 and 37).^[5,6,7]
Restrictive filling (DT <160 ms) is a class of prognostic marker rather than a treatment threshold: it triggers intensification of decongestion, mandates a search for amyloid and constriction, and supports earlier referral for advanced heart failure therapies.^[2,30]
Atrial fibrillation algorithm: DT ≤160 ms is one of the four primary markers of elevated left atrial pressure.^[2]
Constriction versus restriction: a short DT is common to both — the discriminators are respiratory variation, septal bounce and the annular velocities, not the DT itself.^[57]

Next step

Next: place the DT in the algorithm alongside E/A, e′, E/e′ and TR velocity — never grade on it alone.
Then: if restrictive, assess for amyloid (wall thickness, ECG voltage, apical sparing) and for constriction (respirophasic septal shift, annulus reversus, hepatic vein expiratory reversal).^[30,57]
Then: CMR with T1/ECV mapping, bone scintigraphy and free light chains, or invasive simultaneous left- and right-sided pressures if constriction versus restriction is still unresolved.
If mitral stenosis: planimetry of the valve area and a Wilkins score before deciding between balloon valvuloplasty and surgery.^[45]

Drugs

Diuretics lengthen DT (restrictive → pseudonormal) — the fastest and largest effect of any intervention.
Beta-blockers and rate-limiting calcium blockers lengthen diastole and improve the trace, particularly in mitral stenosis and HCM.
GDMT lengthens DT over months as filling pressures fall.
Vasodilators and nitrates shorten E and lengthen DT acutely by reducing preload.
No drug alters DT in mitral stenosis except through heart rate; the obstruction is mechanical.

Reversibility

Follows the load with the same speed as the E wave: days for the decongestion-dependent component, months for the structural component, and not at all for mechanical mitral obstruction. Persistence of a short DT after full decongestion in a dilated ventricle is one of the more reliable echocardiographic markers of irreversible disease.^[2]