Isovolumic relaxation time
IVRT · CW or PW Doppler in the apical 5- or 3-chamber view, beam positioned between LVOT outflow and mitral inflow
Normal range & thresholds
Normal 50–100 ms, lengthening with age (roughly 70–90 ms below 40 years, up to 100–110 ms above 60). 2025 ASE supplemental cut-points: IVRT ≤70 ms indicates elevated LA pressure; IVRT >110 ms indicates normal LA pressure with impaired relaxation.[2]
Special settings: in mitral annular calcification, when E/A is 0.8–1.8, IVRT <80 ms = elevated LAP and ≥80 ms = normal. In primary mitral regurgitation with a normal ejection fraction, IVRT <60 ms (or IVRT/TE-e′ <5.6) indicates elevated LAP, where E/e′ is unreliable.[2]
Special settings: in mitral annular calcification, when E/A is 0.8–1.8, IVRT <80 ms = elevated LAP and ≥80 ms = normal. In primary mitral regurgitation with a normal ejection fraction, IVRT <60 ms (or IVRT/TE-e′ <5.6) indicates elevated LAP, where E/e′ is unreliable.[2]
Pathophysiology
IVRT is the interval between aortic valve closure and mitral valve opening — the time the ventricle takes to fall from aortic diastolic pressure to left atrial pressure with both valves shut. It is therefore governed by two things: the rate of relaxation (slower relaxation, longer IVRT) and the height of the left atrial pressure (higher atrial pressure means the crossover happens sooner, shorter IVRT). This is its great value: it is the one interval that shortens as filling pressure rises, so it disambiguates a pattern where relaxation-based indices are compromised.[2]
Raised by
- Impaired relaxation with normal filling pressure — ageing, LVH, hypertension, HCM, early ischaemia
- Hypovolaemia, over-diuresis
- Elevated aortic diastolic pressure (the ventricle has further to fall)
- Bradycardia; beta-blockade in some patients
- Hypothyroidism
Lowered by
- Elevated left atrial pressure of any cause — the important one
- Significant aortic regurgitation (the AR jet raises LV pressure prematurely and the mitral valve opens early) — a false shortening, not raised LAP
- Constrictive pericarditis and restrictive cardiomyopathy
- Tachycardia; hyperthyroidism; high-output states
- Mitral stenosis (relative shortening; interpret with care)
Technique & pitfalls
- Position the sample volume or the CW beam so that the end of aortic ejection and the onset of mitral inflow appear on the same trace — apical 5- or 3-chamber, beam angled between the outflow and inflow.
- Measure from the aortic valve closure click to the onset of the mitral E wave.
- Sweep speed 100 mm/s; average 3–5 cycles at end-expiration.
- Where the click is indistinct, use the end of the LVOT spectral envelope.
- IVRT earns its place precisely where E/e′ fails — mitral annular calcification, mitral prosthesis or ring, primary MR with normal EF. Learn it for those situations, not as a routine number.[2]
Pseudo-change & artefact
- Aortic regurgitation falsely shortens IVRT — the classic error.
- Heart rate: tachycardia shortens, bradycardia lengthens; correct mentally before interpreting.
- Blood pressure on the day: a hypertensive patient has a longer IVRT for the same myocardium.
- Beam not capturing both events; measuring from the wrong click.
- Preload manipulation — the same patient before and after diuresis can move 25 ms.
- First-degree AV block and pacing alter the timing relationships.
Treatment thresholds
- No direct treatment threshold. IVRT is a filling-pressure discriminator, not a target.
- It is guideline-endorsed as the decisive step in two specific algorithms: mitral annular calcification (IVRT <80 ms → elevated LAP) and primary mitral regurgitation with preserved LVEF (IVRT <60 ms, or IVRT/TE-e′ <5.6, → elevated LAP).[2]
- It contributes to the myocardial performance (Tei) index, which is still used in right ventricular assessment and in some congenital settings.[3,19]
- A short IVRT plus a short deceleration time plus a high E/A is the restrictive triad, and it identifies patients requiring urgent decongestion and prognostic review.[2]
Next step
- Next: integrate with e′, E/e′, TR velocity and LA reservoir strain rather than reading it alone.
- Then: exclude aortic regurgitation as the explanation for a short IVRT before concluding that LAP is high.
- Then: in the annular-calcification or prosthetic-valve patient, use IVRT and pulmonary vein flow as the primary filling-pressure tools; consider invasive measurement when management hinges on it.
Drugs
- Lengthened by diuretics and preload reduction (falling LAP), and by beta-blockade through heart rate.
- Shortened by fluid loading, by anything that raises LA pressure, and by tachycardia.
- Antihypertensive therapy shortens IVRT acutely, because the ventricle has a lower aortic pressure to fall from. Over months the effect is two-sided: regression of LVH speeds relaxation (shorter IVRT), while falling filling pressures delay mitral opening (longer IVRT) — so read a serial IVRT only alongside the blood pressure and E/e′.
- Thyroid replacement normalises a long IVRT in hypothyroidism.
Reversibility
Load-dependent and therefore quickly reversible: IVRT changes within hours of diuresis or fluid loading. The relaxation-dependent component behaves like e′ — it improves slowly and incompletely with LVH regression, revascularisation of ischaemia, and rate control, over months rather than days.[2]