Is a tricuspid regurgitation (TR) peak velocity of 2.4m/s in an elderly male patient with impaired renal function close enough to the 2.5m/s threshold to be a concern?

TR Velocity of 2.4 m/s Should Not Be Considered a Concern in This Context

A TR peak velocity of 2.4 m/s falls below the established 2.5 m/s threshold and, combined with a normal pulmonary artery systolic pressure of 26 mmHg and normal right atrial pressure of 3 mmHg, indicates this patient has low probability for pulmonary hypertension and does not require further cardiac workup based on these right heart findings alone. 1

Evidence-Based Thresholds for TR Velocity

The guideline literature establishes clear cutoffs that should not be arbitrarily lowered:

• The ESC/ERS guidelines classify TR velocity ≤2.8 m/s as "PH unlikely" when no additional echocardiographic variables suggestive of pulmonary hypertension are present 2
• The American Thoracic Society confirms that TR velocity ≥2.5 m/s is the specific threshold associated with increased mortality risk, and values below this threshold do not carry the same prognostic significance 1
• This patient's TR velocity of 2.4 m/s places them in the "low probability" category for pulmonary arterial hypertension, requiring no additional workup in the absence of symptoms or associated risk factors 2

Why 2.4 m/s Is Not "Close Enough"

The distinction between 2.4 and 2.5 m/s matters clinically for several reasons:

• Thresholds exist because they represent statistically validated cutpoints where outcomes diverge—they are not arbitrary suggestions 2
• The ESC/ERS guidelines specifically tested multiple TR velocity cutoffs (including 3.0 m/s and 3.2 m/s) and found that even at 3.0 m/s, 45% of diagnoses were false positives, demonstrating that higher thresholds reduce false positive rates 2
• The calculated pulmonary artery systolic pressure of 26 mmHg is definitively normal (normal is <35 mmHg, with values <30 mmHg being unequivocally normal), providing additional reassurance that this TR velocity is physiologic 1

Context: Renal Dysfunction and TR

While your concern about the proximity to threshold is understandable given the patient's renal impairment, the causality flows in the opposite direction:

• Significant TR (moderate or severe) can contribute to renal dysfunction through venous congestion and elevated renal venous pressure, but this patient does not have significant TR 3, 4, 5
• The research demonstrates that moderate/severe FTR combined with right ventricular dysfunction is independently associated with renal dysfunction, but mild or trivial TR (which this patient has based on velocity) is not 5
• The renal impairment in this elderly male should be evaluated for non-cardiac causes including intrinsic renal disease, nephrotoxic medications, volume status, and left ventricular diastolic dysfunction (age >65 years is a risk factor) 1, 2

Clinical Recommendation

Focus your evaluation on the documented renal impairment itself rather than pursuing cardiac causes based on normal right heart parameters:

• Calculate creatinine clearance using the Cockcroft-Gault formula for medication dosing decisions, as serum creatinine alone significantly underestimates renal insufficiency in elderly patients 6, 7
• Review all current medications for nephrotoxic agents (NSAIDs, ACE inhibitors, certain antibiotics) and assess for appropriate renal dose adjustments 6
• Evaluate for left ventricular diastolic dysfunction, which is common in elderly patients and can contribute to both renal dysfunction and mild TR 2
• Do not pursue right heart catheterization or additional cardiac workup based solely on these echocardiographic findings 2, 1

Common Pitfall to Avoid

The most important pitfall here is over-interpreting borderline normal values and initiating unnecessary cardiac workups when clear guideline thresholds have not been met. The 2.5 m/s threshold exists precisely to prevent this scenario—it balances sensitivity for detecting true pulmonary hypertension against specificity to avoid false positives 2. Lowering thresholds arbitrarily based on clinical anxiety rather than evidence leads to diagnostic cascades that expose patients to unnecessary testing, cost, and potential harm without improving outcomes.