Interpret the complete transthoracic echocardiogram (two‑dimensional, motion mode, Doppler) for a 188 cm, 110 kg (BMI 31 kg/m²) adult with blood pressure 117/67 mm Hg, evaluating aortic valve anatomy and gradients, left ventricular dimensions, concentric hypertrophy, ejection fraction, global longitudinal strain, diastolic function, and any other significant cardiac findings.

Echocardiogram Interpretation: Structurally Normal Heart with Subclinical Myocardial Dysfunction

This echocardiogram reveals a structurally normal heart with preserved ejection fraction (61%) but demonstrates subclinical left ventricular systolic dysfunction evidenced by borderline-reduced global longitudinal strain (-15.8%) in the setting of mild concentric left ventricular hypertrophy, likely related to the patient's obesity (BMI 31.3 kg/m²) and requiring aggressive cardiovascular risk factor modification to prevent progression to overt heart failure. 1, 2

Aortic Valve Assessment

• The aortic valve is trileaflet with normal structure and function, showing no evidence of stenosis or regurgitation 1
• Peak aortic velocity is 1.37 m/s with mean gradient of 4.2 mmHg, well below thresholds for any degree of stenosis (severe AS requires mean gradient ≥40 mmHg or peak velocity ≥4 m/s) 1
• Calculated aortic valve area by continuity equation is 3.0-3.1 cm² (indexed 1.3 cm²/m²), confirming no stenosis (severe AS defined as <1.0 cm² or <0.6 cm²/m²) 1
• The aortic root diameter is 3.1 cm, which is normal for body size 1

Left Ventricular Structure and Systolic Function

Concerning Finding: Discordance Between Ejection Fraction and Strain

• The ejection fraction of 61% appears reassuring but masks early myocardial dysfunction revealed by the global longitudinal strain of -15.8%, which falls below the normal threshold of -20% 1, 2
• This discordance between preserved LVEF and reduced GLS is characteristic of patients with concentric left ventricular hypertrophy, where circumferential shortening compensates for impaired longitudinal function to maintain pump function 2, 3

Left Ventricular Hypertrophy Analysis

• Mild concentric LVH is present with interventricular septum 1.0 cm and posterior wall 1.2 cm in diastole 1
• LV mass calculated at 207-222 grams (indexed 87.7 g/m²) confirms mild hypertrophy 1
• The IVS/LVPW ratio of 0.85 indicates symmetric (concentric) hypertrophy pattern 1
• Concentric hypertrophy geometry is a significant independent predictor of impaired GLS (odds ratio 22.4) even when LVEF appears normal 2

Clinical Significance of Reduced GLS

• GLS of -15.8% indicates subclinical myocardial dysfunction that precedes decline in ejection fraction and predicts progression to overt heart failure 1, 4, 5
• In hypertensive patients with concentric LVH and preserved LVEF, approximately 13% progress to systolic dysfunction over 3 years of follow-up 6
• The reduced GLS reflects early myocardial fibrosis and impaired longitudinal fiber function despite preserved circumferential shortening 1, 3

Diastolic Function Assessment

• Left ventricular filling pattern is reported as normal 1
• Mitral E velocity 82.8 cm/s, A velocity 60.8 cm/s, yielding E/A ratio of 1.4 1
• Lateral e' velocity 13.8 cm/s and medial e' velocity 12.8 cm/s are preserved 1
• Average E/e' ratio would be approximately 6.2, indicating normal left ventricular filling pressures 1
• However, the presence of concentric LVH with reduced GLS suggests early diastolic dysfunction may develop despite currently normal parameters 5, 3

Right Heart and Pulmonary Pressures

• Right ventricular size and function are normal with TAPSE 3.0 cm (normal ≥1.7 cm) 1
• Estimated right ventricular systolic pressure is 33.2 mmHg (derived from TR velocity 2.74 m/s plus estimated RA pressure 3 mmHg), which is normal 1
• Right atrial area 20.9 cm² is within normal limits 1

Valvular Function Summary

• Mitral valve: Trace mitral regurgitation, which is physiologic and requires no intervention 1
• Tricuspid valve: Trace tricuspid regurgitation, which is physiologic 1
• Pulmonic valve: Normal structure and function without stenosis or regurgitation 1

Critical Management Implications

Immediate Priorities

• Aggressive blood pressure control is mandatory with target <130/80 mmHg to prevent progression of LVH and further GLS deterioration 5
• Uncontrolled hypertension increases risk of GLS decline by 3.55-fold in patients with LVH 5
• Weight reduction is essential given BMI 31.3 kg/m²; obesity is independently associated with reduced GLS (odds ratio 2.01) and progression to systolic dysfunction 5

Cardiovascular Risk Factor Optimization

• Screen for and aggressively treat diabetes mellitus, as diabetes increases risk of GLS decline by 2.21-fold in hypertensive patients with LVH 5
• Evaluate and treat dyslipidemia, which increases risk of reduced GLS by 2.16-fold 5
• Assess renal function, as renal impairment increases risk of GLS decline by 4.27-fold 5

Surveillance Strategy

• Repeat echocardiography in 6-12 months to monitor for progression of LVH or further GLS deterioration 1
• Serial GLS measurements are more reproducible than LVEF for detecting early changes in myocardial function 1
• Monitor for development of symptoms (dyspnea, reduced exercise tolerance, chest pain) that would indicate progression to symptomatic heart failure 1

Risk Factors for Progression to Systolic Dysfunction

• QRS duration >120 ms on ECG increases risk of progression to systolic dysfunction by 2-fold 6
• Elevated arterial impedance >4.0 mmHg/ml/m² increases risk by 2-fold 6
• Presence of both factors increases risk by >4-fold 6
• Interval myocardial infarction is the strongest predictor (present in 43% of patients who develop systolic dysfunction) 6

Pitfalls to Avoid

• Do not be falsely reassured by the normal ejection fraction of 61%; the reduced GLS of -15.8% indicates early myocardial dysfunction requiring intervention 1, 2
• Do not attribute the concentric LVH solely to "normal aging"; this represents pathologic remodeling requiring aggressive risk factor modification 5, 6
• Do not delay intervention until symptoms develop or LVEF declines, as myocardial fibrosis may become irreversible 1, 6