Aortic valve velocity–time integral

AV VTI (transvalvular) · Continuous-wave Doppler across the aortic valve from apical 5-/3-chamber plus right parasternal and suprasternal windows

Normal range & thresholds

Normal transaortic peak velocity <1.7–2.0 m/s. The VTI itself is used as a ratio, not as an absolute number.
Aortic stenosis severity^[5]:

	Mild	Moderate	Severe
V_max	2.6–2.9 m/s	3.0–3.9 m/s	≥4.0 m/s
Mean gradient	<20 mmHg	20–39 mmHg	≥40 mmHg
DVI (LVOT VTI / AV VTI)	>0.25		<0.25

‘Very severe’: V_max ≥5.0 m/s or mean gradient ≥60 mmHg.^[5,7]

Pathophysiology

Velocity across a fixed orifice is set by the pressure drop across it (the simplified Bernoulli relation, ΔP = 4V²) and by the flow crossing it. That second dependence is the entire difficulty of aortic stenosis assessment: a severely stenotic valve with a poorly contracting or small, underfilled ventricle generates a low velocity and a low gradient, and looks moderate. Conversely a high-flow state — anaemia, fever, arteriovenous fistula, or significant aortic regurgitation — can push a moderate valve into the severe velocity range.^[5]

Raised by

Aortic stenosis — valvular, and (with a different envelope shape) subvalvular or supravalvular
High flow: significant aortic regurgitation, anaemia, thyrotoxicosis, fever, pregnancy, arteriovenous fistula, sepsis, dialysis fistula
Bicuspid valve with an eccentric jet
Prosthetic valve obstruction, thrombosis, pannus, or patient–prosthesis mismatch
Falsely: contamination by a mitral regurgitation jet on the CW trace (see below)

Lowered by

Low-flow states — LV systolic dysfunction, small hypertrophied ventricle with a low stroke volume, mitral stenosis or severe MR reducing forward flow, tachyarrhythmia, hypovolaemia
Failure to interrogate from enough windows — the commonest reason for underestimating aortic stenosis, and it is entirely operator-dependent
After relief of obstruction

Technique & pitfalls

Interrogate from multiple windows — always. Apical 5-chamber, apical 3-chamber, right parasternal (patient in the right lateral decubitus, with a dedicated non-imaging Pedof probe if available) and suprasternal. The right parasternal window gives the highest velocity in roughly a quarter of patients, and skipping it systematically under-grades aortic stenosis.^[5,17]
Trace the outer edge of the dense CW envelope (the opposite convention from the pulsed LVOT trace).
Report V_max, mean gradient, VTI, the window used, the heart rate and the blood pressure.
In atrial fibrillation, average 5–10 beats and avoid post-extrasystolic beats, which exaggerate the gradient.
Distinguish the aortic envelope from a mitral regurgitation jet: MR starts earlier (during isovolumic contraction), lasts longer, is usually higher velocity, and has no clear opening/closing clicks aligned to ejection.

Pseudo-change & artefact

Mitral regurgitation contamination of the CW beam — the classic false ‘severe aortic stenosis’; check timing and duration against the ECG.
Pressure recovery in a small aorta (ascending aorta <3.0 cm): Doppler overestimates the net gradient; energy loss index corrects for it.^[5]
High-flow states overestimate severity; low-flow states underestimate it.
Non-parallel alignment — underestimates.
Gain set too high, so spectral noise is traced — overestimates.
Systemic hypertension at the time of study lowers the transvalvular gradient; a study performed while the patient is markedly hypertensive under-grades the valve.^[5]

Treatment thresholds

Severe aortic stenosis (V_max ≥4 m/s or mean gradient ≥40 mmHg) plus symptoms → aortic valve replacement, class I.^[6,7]
Asymptomatic severe AS with LVEF <50% → AVR, class I.^[6,7]
Asymptomatic very severe AS (V_max ≥5.0 m/s), or rapid progression (≥0.3 m/s per year), or a markedly raised natriuretic peptide, or an abnormal exercise test → AVR, class IIa. The RECOVERY and AVATAR trials, and more recently EARLY TAVR, support earlier intervention in asymptomatic severe disease.^{[6,7,61,62,63]}
2025 ESC/EACTS: the age threshold favouring TAVI over surgery in tricuspid-valve aortic stenosis has moved from 75 to 70 years.^[6]
Prosthetic valves: a rising mean gradient with a falling DVI defines prosthetic obstruction and triggers TOE, CT and consideration of reintervention or thrombolysis.^[20,21]

Next step

Next: reconcile velocity, gradient, valve area, dimensionless index and stroke volume index. If they disagree, the study is not finished.
Then: if low-gradient with low flow and reduced LVEF → low-dose dobutamine stress echocardiography to separate true-severe from pseudo-severe stenosis and to test contractile reserve.^[5,28]
Then: if low-gradient with preserved LVEF (paradoxical low-flow) → aortic valve calcium score by non-contrast CT (≥3000 AU men, ≥1600 AU women highly likely severe).^[5,80]
Then: exercise testing in the truly asymptomatic patient — symptoms, a fall in blood pressure or arrhythmia convert a IIa into a I.^[6,7]
Then: Heart Team, coronary assessment, and gated CTA for access and annular sizing.

Drugs

No medical therapy modifies aortic stenosis. Statins do not slow it; RAAS blockade does not reverse it. Say this plainly to patients who expect otherwise.^[7]
Treat hypertension — but measure the gradient at a controlled blood pressure, because afterload alters the number.
Vasodilators need care in severe stenosis with a fixed output.
Beta-blockade lowers the gradient by lowering flow, not by improving the valve.
Correct anaemia and thyrotoxicosis before finalising severity in a high-flow patient.

Reversibility

0% for the native valve. Aortic stenosis is progressive: the untreated gradient rises by roughly 7 mmHg and V_max by about 0.3 m/s per year on average, faster with heavier calcification and renal disease. The velocity falls only when the obstruction is relieved — immediately and permanently after surgical or transcatheter replacement, subject to prosthesis–patient mismatch. In pseudo-severe, low-flow stenosis, restoring flow with dobutamine raises the gradient without the valve having changed — the diagnostic use of that reversibility.^[5,60]