Grading of Pulmonary Hypertension by Tricuspid Regurgitant Velocity (TRV)
Pulmonary hypertension probability is graded using TRV combined with additional echocardiographic signs into three categories: low probability (TRV ≤2.8 m/s without signs), intermediate probability (TRV ≤2.8 m/s with ≥2 categories of signs OR TRV 2.9-3.4 m/s without signs), and high probability (TRV 2.9-3.4 m/s with ≥2 categories of signs OR TRV >3.4 m/s regardless of other signs). 1
The TRV-Based Grading System
The current approach uses peak TRV measured by continuous wave Doppler as the primary variable, not estimated pulmonary artery systolic pressure (PASP), because RAP estimation introduces significant measurement error 2. The 2015 ESC/ERS guidelines and 2022 ACR appropriateness criteria establish this framework:
Three Probability Categories:
Low Probability:
- TRV ≤2.8 m/s AND no additional echocardiographic signs of PH 1
Intermediate Probability:
- TRV ≤2.8 m/s WITH presence of ≥2 categories of echocardiographic signs, OR
- TRV 2.9-3.4 m/s WITHOUT additional signs 1
High Probability:
- TRV 2.9-3.4 m/s WITH ≥2 categories of echocardiographic signs, OR
- TRV >3.4 m/s (regardless of other signs) 1
Required Additional Echocardiographic Signs
At least two of the following three categories must be positive to count toward PH probability 1, 2:
Category A - Right Ventricular Findings:
- RV/LV basal diameter ratio >1.0
- Flattening of interventricular septum (LV eccentricity index >1.1 in systole and/or diastole)
Category B - Pulmonary Artery Findings:
- PA diameter >25 mm
- Early diastolic pulmonary regurgitation velocity >2.2 m/s
- RV outflow Doppler acceleration time <105 ms and/or mid-systolic notching
Category C - IVC/Right Atrial Findings:
- IVC diameter >21 mm with decreased inspiratory collapse (<50% with sniff or <20% with quiet inspiration)
- End-systolic RA area >18 cm²
Clinical Decision Algorithm
For symptomatic patients:
- Low probability + no risk factors → Consider alternative diagnosis
- Low probability + risk factors for PAH/CTEPH → Echo follow-up
- Intermediate probability + no risk factors → Further investigation may be considered
- Intermediate probability + risk factors → Right heart catheterization (RHC) should be considered
- High probability (with or without risk factors) → RHC is recommended before initiating PH-specific therapy 1
Important Caveats and Pitfalls
Measurement Limitations:
- TRV may be significantly underestimated in severe tricuspid regurgitation and cannot exclude PH in this setting 2
- Overestimation can also occur 2
- Echocardiography performs poorly in detecting mild PH, particularly PH secondary to lung diseases 1
- TRV is measurable in only about two-thirds of echocardiograms 3
Context-Dependent Interpretation:
- TRV varies with clinical status and may be acutely elevated during acute illness 4
- The quality of the tricuspid regurgitation spectrum matters more than the volume of regurgitation for accuracy 5
- Use agitated saline contrast if TRV is difficult to measure due to trivial/mild TR 2
Evolving Thresholds
Recent evidence suggests the traditional thresholds may need revision given the updated hemodynamic definition of PH (mean PAP >20 mmHg rather than ≥25 mmHg):
- A TRV of 2.7 m/s may provide better sensitivity (95%) for detecting PH under the new definition while maintaining acceptable specificity 6, 7
- The conventional 2.8 m/s threshold aligns more closely with the 2022 guidelines (mPAP >20 mmHg) 8
- For tertiary referral centers, a lower threshold of approximately 2.7 m/s provides high sensitivity for screening 6
However, the established guideline thresholds (≤2.8 m/s, 2.9-3.4 m/s, >3.4 m/s) remain the current standard for clinical practice 1, 2, as these are embedded in the most recent major society guidelines from ESC/ERS (2015) and ACR (2022).
Special Populations
In sickle cell disease, mortality risk stratification uses different TRV cutoffs:
- TRV <2.5 m/s: ~2% mortality
- TRV 2.5-2.9 m/s: ~10% mortality
- TRV ≥3.0 m/s: ~20% mortality 4
High-risk populations warranting screening include those with genetic mutations for PAH, first-degree relatives with PAH, scleroderma spectrum disorders, congenital heart disease, and portal hypertension before liver transplant 1.