Aortic regurgitation pressure half-time
AR PHT · CW Doppler of the AR jet from the apical 5- or 3-chamber view; slope of the diastolic decay
Normal range & thresholds
| AR PHT | Severity |
|---|---|
| >500 ms | Mild |
| 200–500 ms | Moderate |
| <200 ms | Severe |
Pathophysiology
The AR jet velocity encodes the instantaneous pressure difference between the aorta and the left ventricle in diastole. A large regurgitant orifice equalises those pressures quickly — aortic pressure falls, LV diastolic pressure rises — so the velocity decays steeply and the half-time is short. In a small leak the gradient is preserved throughout diastole and the decay is flat. The same steep decay therefore has two different causes, which the number cannot distinguish: a large orifice, or a stiff, non-compliant ventricle whose pressure rises fast for any given regurgitant volume — which is exactly the situation in acute severe aortic regurgitation.[4]
Raised by
- Chronic, well-compensated aortic regurgitation with a dilated compliant ventricle — the PHT can remain >400 ms even when the regurgitation is severe: the important false negative
- Systemic hypertension at the time of the study (a higher aortic diastolic pressure sustains the gradient)
- Milder regurgitation (the intended signal)
- Bradycardia (a longer diastole to measure across)
Lowered by
- Severe aortic regurgitation (the intended signal)
- Acute severe AR — endocarditis, aortic dissection, trauma: a very short PHT (often <150 ms) with a small, non-dilated, non-compliant ventricle, premature mitral valve closure, and a patient in cardiogenic shock. A surgical emergency
- Reduced LV compliance for any reason — restrictive disease, hypertrophy, ischaemia
- Vasodilators, hypotension and a low aortic diastolic pressure
- Tachycardia
- Elevated LV end-diastolic pressure of any cause
Technique & pitfalls
- Align the CW beam with the regurgitant jet, which is frequently eccentric — use both the 5-chamber and 3-chamber views and accept only a complete, dense envelope.
- Measure the slope of the mid-diastolic decay; ignore the initial and terminal portions.
- Record the systemic blood pressure with the measurement — without it the value is not interpretable and not comparable with a previous study.
- Never grade aortic regurgitation on the pressure half-time alone: combine vena contracta width, the jet-to-LVOT width and area ratios, holodiastolic flow reversal in the proximal descending aorta (end-diastolic velocity >20 cm/s), regurgitant volume, regurgitant fraction and effective regurgitant orifice area.[4]
- In acute severe AR, look for the supporting signs — premature mitral closure, diastolic mitral regurgitation, a short mitral deceleration time, and a non-dilated LV.
Pseudo-change & artefact
- Chronic compensated severe AR with a long PHT — the clinically dangerous false negative.
- Hypertension lengthens PHT; hypotension and vasodilators shorten it. Grading changes with the blood pressure on the day.
- Eccentric jets and poor alignment — an incomplete envelope cannot be measured.
- Tachycardia truncating the diastolic envelope.
- Reduced LV compliance shortening PHT independently of the leak.
- Confusion between the AR jet and the mitral inflow or the LVOT signal on a poorly aligned CW trace.
Treatment thresholds
- AR PHT does not itself define an operative threshold. It contributes to establishing severe aortic regurgitation, and the operative triggers are then symptoms, LVEF and left ventricular dimensions or volumes.[6,7]
- Chronic severe AR → surgery for symptoms (class I); if asymptomatic, for LVEF ≤55% (2025 ESC/EACTS) or ≤50–55% (ACC/AHA), LVESDi >22 mm/m² or LVESVi >45 mL/m² (2025 ESC/EACTS), or LVESD >50 mm / >25 mm/m² (2020 ACC/AHA).[6,7]
- Acute severe AR → urgent surgery. A short PHT with premature mitral closure and a non-dilated ventricle is an emergency finding: intra-aortic balloon counterpulsation and beta-blockade are contraindicated in acute AR, and vasodilators plus inotropes are a bridge to theatre, not a treatment.[6,7]
- 2025 ESC/EACTS introduces TAVI as an option for selected high-risk patients with aortic regurgitation after Heart Team evaluation — a genuinely new pathway for the inoperable patient.[6]
Next step
- Next: complete the multiparametric grading — vena contracta (card 39), descending aortic flow reversal, regurgitant volume and fraction.
- Then: define the mechanism — cusp prolapse, perforation, retraction, or an aortic root or STJ problem (cards 02 and 03) — because it determines repairability.
- Then: measure LV dimensions and volumes indexed to BSA, LVEF and GLS; TOE and CMR (regurgitant fraction) where echo is equivocal.
- Then: if the mechanism is root dilatation with normal cusps, refer for valve-sparing root replacement assessment; otherwise Heart Team for AVR.
Drugs
- Vasodilators (dihydropyridine calcium blockers, ACE inhibitors/ARBs) are indicated for hypertension in chronic AR — but they do not delay surgery in asymptomatic severe AR with a dilated ventricle, and should not be used as a substitute for it.[7]
- Beta-blockers are used cautiously: they lengthen diastole and can increase the regurgitant volume; they remain indicated where there is aortopathy or a syndromic diagnosis.
- In acute severe AR: vasodilators and inotropes as a bridge; avoid beta-blockade and intra-aortic balloon pump.
- Antibiotics and prompt surgery in endocarditis.
- Note that all of these alter the pressure half-time without altering the valve.
Reversibility
The regurgitation itself is abolished immediately by valve replacement or repair. Ventricular recovery is the variable that matters: LV dimensions fall most in the first 6 months and normalise in the majority when pre-operative LVESD is <50 mm, but rarely when it exceeds 55 mm, and LVEF frequently fails to recover when it was already depressed pre-operatively. That gradient of reversibility is the entire rationale for the dimensional and volumetric triggers — and for the 2025 ESC/EACTS decision to lower them.[6,94,95]