Tricuspid annular plane systolic excursion
TAPSE · RV-focused apical 4-chamber, M-mode cursor along the lateral tricuspid annulus, aligned with annular motion
Normal range & thresholds
2025 ASE graded severity:
The previous single cut-point (<1.7 cm abnormal) has been replaced by this graded scheme.[3,19]
TAPSE/PASP ratio (RV–pulmonary arterial coupling): <0.55 mm/mmHg abnormal, <0.31 mm/mmHg indicates severely uncoupled, high-risk physiology.[52,77]
| TAPSE | RV longitudinal function |
|---|---|
| ≥2.0 cm | Normal |
| 1.7–1.9 cm | Mildly reduced |
| 1.3–1.6 cm | Moderately reduced |
| <1.3 cm | Severely reduced |
TAPSE/PASP ratio (RV–pulmonary arterial coupling): <0.55 mm/mmHg abnormal, <0.31 mm/mmHg indicates severely uncoupled, high-risk physiology.[52,77]
Pathophysiology
RV shortening is predominantly longitudinal — roughly 80% of RV stroke volume comes from base-to-apex shortening of the free wall, not from radial thickening. TAPSE samples that motion at a single point. It is load-dependent in both directions: afterload (pulmonary pressure) reduces it, and preload (severe tricuspid regurgitation) increases annular excursion without any improvement in contractility. Coupling it to pulmonary pressure as TAPSE/PASP converts a load-dependent displacement into a crude but powerfully prognostic index of contractility relative to load.[3,52]
Raised by
- Volume overload with severe tricuspid regurgitation — a falsely reassuring high TAPSE in a failing ventricle
- Hyperdynamic states, exercise, inotropes
- Athletes and young subjects
- Note: an isolated high TAPSE has no independent pathological meaning; the important reading is a falsely normal TAPSE
Lowered by
- Pulmonary hypertension of any group — the commonest cause
- RV infarction (inferior MI with RV extension), ARVC, myocarditis, sarcoid, amyloid
- Acute pulmonary embolism; chronic lung disease
- After any cardiac surgery — TAPSE drops by 30–50% after pericardiotomy and stays low permanently, while RV ejection fraction by CMR is unchanged. This is the single most important pitfall with this parameter and it should be stated in every post-operative report.[3]
- Constrictive pericarditis; severe tricuspid stenosis
- Advanced left heart failure with biventricular involvement
- Poor M-mode alignment, pacemaker or defibrillator leads across the annulus
Technique & pitfalls
- Use the RV-focused apical 4-chamber view; place the M-mode cursor through the lateral tricuspid annulus and aligned with the direction of annular motion, not merely through the annulus.[3]
- Medium-to-fast sweep speed; measure leading edge to leading edge between the most basal (end-diastolic) and most apical (end-systolic) annular position.
- Anatomical M-mode helps when the annulus cannot be aligned with a straight cursor, but is not interchangeable with conventional M-mode.
- Never report TAPSE alone. The 2025 guideline is explicit: integrate TAPSE with S′, FAC, RV free-wall strain, 3D RVEF and TAPSE/PASP.[3]
- Report TAPSE/PASP whenever a TR jet is measurable — it costs nothing and adds more prognostic information than TAPSE itself.
Pseudo-change & artefact
- Cursor misalignment — always underestimates.
- Post-cardiac surgery — a real fall in longitudinal motion with preserved global RV function; misreading it as new RV failure is a common error.
- Severe tricuspid regurgitation falsely raises TAPSE.
- Whole-heart translation and respiratory motion falsely raise it.
- Constrictive pericarditis, pacing leads, catheters and poor image quality falsely lower it.
- TAPSE measures motion at one point of a crescentic chamber — regional RV disease (ARVC, RV infarct) can leave it normal.
- Loading conditions on the day: TAPSE falls with hypovolaemia and rises with volume loading.
Treatment thresholds
- Pulmonary hypertension risk stratification: TAPSE/PASP is embedded in contemporary risk assessment; low values identify high-risk patients who need upfront combination therapy, parenteral prostacyclin and early transplant referral.[8,77]
- Tricuspid intervention: the 2025 ESC/EACTS guidelines exclude patients with severe RV dysfunction from transcatheter tricuspid intervention — TAPSE, alongside FAC and strain, defines that exclusion, and this is the clearest place where the number changes the treatment offered.[6,65]
- Acute pulmonary embolism: RV dysfunction (including reduced TAPSE) with a normal blood pressure defines intermediate risk and mandates monitored admission rather than discharge.[8]
- Left ventricular assist device and transplant assessment: RV dysfunction predicts post-implant RV failure and is a central part of candidacy assessment.[11]
- Cardiac surgery: a low pre-operative TAPSE predicts prolonged inotropic support — prognostic rather than prohibitive.
Next step
- Next: add RV S′, FAC and free-wall strain in the same study, and compute TAPSE/PASP. Discordance between them is common and must be resolved before reporting ‘RV dysfunction’.
- Then: establish the mechanism — pressure load (septal flattening in systole, short PAAT, notched RVOT envelope), volume load (diastolic flattening, severe TR/PR), or primary myocardial disease.
- Then: CMR for RV ejection fraction, volumes and tissue characterisation (ARVC, sarcoid, infiltration), and CT/V-Q for thromboembolic disease.
- Then: right heart catheterisation to establish the haemodynamic diagnosis and to guide pulmonary-vasodilator therapy.[8]
Drugs
- Improved by treating the cause: pulmonary vasodilators in group 1 pulmonary hypertension, pulmonary endarterectomy or riociguat/balloon pulmonary angioplasty in CTEPH, decongestion in volume overload, revascularisation in RV infarction.[8]
- Diuretics improve RV geometry and coupling by reducing volume overload; excessive diuresis lowers TAPSE through preload.
- Inotropes and pulmonary vasodilators raise it acutely in the acute setting.
- No drug is directed at TAPSE itself.
- Beta-blockers are not RV therapy in pulmonary arterial hypertension and may be poorly tolerated.
Reversibility
Depends entirely on the cause. Acute pulmonary embolism: TAPSE recovers substantially within days to weeks of reperfusion or anticoagulation. RV infarction: substantial recovery over weeks — the RV recovers better than the LV after infarction, because of its lower oxygen demand and collateral supply. CTEPH after pulmonary endarterectomy and group 1 disease in treatment responders: large improvement over 3 to 12 months. Post-cardiac-surgery reduction: essentially permanent and benign. ARVC and established RV fibrosis: not reversible.[3,8]