Interpret an echocardiogram that shows normal left ventricular ejection fraction (71%), mild left ventricular wall thickening, normal global longitudinal strain, normal right ventricular systolic function (S′ 14.4 cm/s, TAPSE 2.9 cm), septal flattening in diastole indicating right‑ventricular volume overload, mildly enlarged right atrium, moderate tricuspid regurgitation, severe pulmonary hypertension (estimated pulmonary artery systolic pressure 62 mmHg), moderate pulmonic regurgitation, enlarged right‑ventricular outflow tract, dilated inferior vena cava with elevated right‑atrial pressure (~8 mmHg), and mild aortic regurgitation?

Echocardiographic Interpretation: Right Heart Pathology with Severe Pulmonary Hypertension

This echocardiogram demonstrates severe pulmonary hypertension (PASP 62 mmHg) with right ventricular volume overload, moderate tricuspid regurgitation, and secondary right heart remodeling—findings that mandate urgent right heart catheterization to differentiate pre-capillary from post-capillary pulmonary hypertension and guide targeted therapy. 1

Primary Pathology: Severe Pulmonary Hypertension

• Estimated pulmonary artery systolic pressure of 62 mmHg defines severe pulmonary hypertension (normal <35 mmHg; mild 36–45 mmHg; moderate 46–60 mmHg; severe >60 mmHg). 1
• The combination of moderate tricuspid regurgitation (TR), moderate pulmonic regurgitation, and elevated right atrial pressure (8 mmHg based on dilated IVC with >50% collapse) confirms hemodynamically significant pulmonary hypertension. 1
• Right heart catheterization is mandatory to measure mean pulmonary artery pressure and pulmonary capillary wedge pressure, distinguishing Group 1 (pulmonary arterial hypertension) from Group 2 (left heart disease) or other etiologies. 1

Right Ventricular Consequences

Volume Overload Pattern

• Septal flattening in mid-to-late diastole is pathognomonic for right ventricular volume overload, distinguishing this from pressure overload (which causes end-systolic flattening). 2
• This diastolic septal shift indicates that RV diastolic pressure exceeds LV diastolic pressure during mid-to-late filling, consistent with severe TR and pulmonic regurgitation creating volume overload. 2
• The enlarged right ventricular outflow tract (RVOT) and mildly enlarged right atrium (RA) further confirm chronic RV volume loading. 1

Preserved RV Systolic Function (Currently)

• TAPSE of 2.9 cm (29 mm) and S′ of 14.4 cm/s both indicate normal RV systolic function (TAPSE normal ≥1.7 cm; S′ normal ≥9.5 cm/s). 1
• However, normal TAPSE and S′ may underestimate true RV myocardial dysfunction in the setting of severe TR because these parameters are load-dependent and can be falsely elevated by the large regurgitant volume. 1
• RV longitudinal strain by speckle tracking would provide a more accurate, load-independent assessment of RV function and should be obtained if available. 1

Left Ventricular Findings: Hyperdynamic with Mild Hypertrophy

Supranormal Ejection Fraction

• An ejection fraction of 71% is hyperdynamic (normal 53–73%), which in the context of mild LV wall thickening suggests either chronic hypertension, volume depletion, or compensatory response to reduced preload from RV dysfunction. 1, 3
• Normal global longitudinal strain of -25.7% confirms preserved intrinsic LV myocardial function (normal >-18% to -20%). 1, 4
• The combination of hyperdynamic EF with normal GLS excludes primary LV systolic dysfunction or infiltrative cardiomyopathy. 4, 5

Mild LV Wall Thickening

• Mild increased LV wall thickness without chamber dilation defines concentric remodeling, most commonly due to chronic hypertension. 3
• Measure maximal LV wall thickness in all segments; if ≥15 mm, hypertrophic cardiomyopathy must be excluded. 3
• Check blood pressure urgently; if ≥130/80 mmHg, initiate aggressive antihypertensive therapy to prevent progression to heart failure with preserved ejection fraction. 3

Valvular Assessment

Tricuspid Regurgitation (Moderate)

• Moderate TR in the setting of severe pulmonary hypertension is functional (secondary), caused by annular dilation and leaflet tethering from RV enlargement. 1
• The TR jet velocity provides the basis for estimating PASP but does not quantify TR severity; semi-quantitative grading requires vena contracta width and PISA radius. 1
• Vena contracta ≥7 mm or PISA radius ≥9 mm at Nyquist 28 cm/s defines severe TR; values should be documented to track progression. 1

Pulmonic Regurgitation (Moderate)

• Moderate pulmonic regurgitation contributes to RV volume overload and explains the diastolic septal flattening pattern. 2
• The pressure half-time of pulmonic regurgitation (not reported) would help estimate pulmonary artery diastolic pressure and assess severity. 1

Aortic Regurgitation (Mild)

• Mild aortic regurgitation with a pressure half-time of 736 ms is hemodynamically insignificant (severe AR has PHT <200 ms). 1
• This finding does not contribute to the patient's symptoms or hemodynamic abnormalities. 1

Diagnostic Algorithm

Immediate Steps

1. Perform right heart catheterization to measure mean PAP, pulmonary capillary wedge pressure (Ppcw), and calculate pulmonary vascular resistance. 1

   • If Ppcw ≤15 mmHg → pre-capillary PH (Groups 1,3,4,5)
   • If Ppcw >15 mmHg → post-capillary PH (Group 2, left heart disease)
   • Consider fluid challenge (500 mL saline over 10 min) during catheterization if Ppcw is borderline (12–15 mmHg) to unmask occult diastolic dysfunction. 1

2. Complete diastolic function assessment with E/A ratio, septal and lateral E/e′, deceleration time, and pulmonary vein flow patterns. 1, 3

   • E/e′ ≥14 indicates elevated LV filling pressures and suggests Group 2 PH (left heart disease). 1, 3
   • The presence of mild LV hypertrophy and hyperdynamic EF raises suspicion for diastolic dysfunction despite normal systolic function. 1, 3

3. Quantify TR severity with vena contracta width and PISA radius to establish baseline for serial monitoring. 1

4. Measure RV longitudinal strain if available, as TAPSE and S′ may overestimate function in severe TR. 1

Etiologic Work-Up

• Screen for Group 1 PAH: connective tissue disease serology (ANA, anti-Scl-70, anti-centromere), HIV, liver function tests, ventilation-perfusion scan (to exclude chronic thromboembolic PH). 1
• Assess for Group 2 (left heart disease): blood pressure measurement, complete diastolic assessment, consider cardiac MRI if infiltrative disease suspected. 1, 3
• Evaluate for Group 3 (lung disease): pulmonary function tests, high-resolution chest CT, arterial blood gas. 1

Management Priorities

Pulmonary Hypertension-Specific Therapy

• Do NOT initiate PAH-specific drugs (endothelin receptor antagonists, phosphodiesterase-5 inhibitors, prostacyclins) until right heart catheterization confirms pre-capillary PH (Group 1). 1
• PAH-specific therapy is contraindicated (Class III) in Group 2 PH (left heart disease) and may worsen pulmonary edema. 1
• If post-capillary PH is confirmed, optimize treatment of the underlying left heart disease (blood pressure control, diuretics if volume overloaded). 1

Right Ventricular Support

• Avoid excessive diuresis, which can reduce RV preload and precipitate hemodynamic collapse in RV-dependent circulation. 1
• Maintain adequate systemic blood pressure to preserve RV coronary perfusion; avoid systemic vasodilators. 1
• Monitor for atrial arrhythmias with serial ECGs or ambulatory monitoring, as RV dilation and elevated RA pressure predispose to atrial fibrillation. 3, 6

Tricuspid Regurgitation

• Surgical or transcatheter tricuspid valve intervention is NOT indicated for functional TR unless severe (vena contracta ≥7 mm, EROA ≥40 mm²) with symptoms despite medical therapy. 1
• Serial echocardiography every 6 months to monitor TR severity, RV size and function, and PASP. 1, 3

Critical Pitfalls to Avoid

• Do not assume normal RV function based solely on TAPSE 2.9 cm and S′ 14.4 cm/s in the setting of severe TR; these load-dependent parameters may be falsely reassuring. 1
• Do not initiate pulmonary vasodilator therapy without right heart catheterization; treating Group 2 PH with PAH drugs is harmful. 1
• Do not overlook the discordance between severe pulmonary hypertension (PASP 62 mmHg) and "normal" RV systolic function; this suggests early disease with compensated RV function that will deteriorate without treatment. 1
• Do not dismiss mild LV wall thickening and hyperdynamic EF as benign; this pattern may reflect uncontrolled hypertension driving diastolic dysfunction and post-capillary PH. 1, 3
• Do not delay right heart catheterization; non-invasive parameters alone cannot distinguish pre-capillary from post-capillary PH, and this distinction is essential for appropriate therapy. 1