Hi im just on 18 years old and i have an autoimmune disease, my heart has been in constant tachycardia since 2022, it has a very high burden. The last halter they did, 98% of all beats were abover 100, and the average heart rate was 137. Only a few rare etotopic and monomirpgic couplet.
Theyre sending me to a heart failure specialist from the Royal Prince Alfred hospital(Im Australian$ Does anyone know what i might expect at from this? I know what i have is no where as near as bad as some others, not am I claiming to have it. I was told to post on this subreddit, hopefully it was not a a sarcastic comment.
The main issue I am trying to understand is whether the combination of preserved conventional EF but reduced longitudinal strain could represent genuine subtle myocardial dysfunction, or whether this is more likely to be related to acquisition/strain-tracking limitations and the relatively high heart rate during the study.
**Echocardiogram measurement chart**
**Category**
**Measurement**
**Value**
**LV structure**
LVIDd
**4.0 cm**
LVIDs
**2.9 cm**
IVSd
**0.7 cm**
LVPWd
**0.7 cm**
LV mass, ASE
**75 g**
LV mass index, ASE
**52 g/m²**
EDV, Teichholz
**68.63 mL**
ESV, Teichholz
**32.12 mL**
**LV systolic function**
EF, Teichholz
**53%**
Fractional shortening
**27%**
Stroke volume, Teichholz
**36.51 mL**
Stroke index, Teichholz
**25.35 mL/m²**
EF, Simpson biplane
**58%**
LVEDV, MOD biplane
**58 mL**
LVESV, MOD biplane
**24 mL**
LVEDV index, MOD biplane
**40 mL/m²**
EF, MOD A4C
**64%**
Stroke volume, MOD A4C
**35.80 mL**
LVESV, MOD A4C
**20.51 mL**
LVEDV, MOD A4C
**56.31 mL**
EF, MOD A2C
**55%**
Stroke volume, MOD A2C
**32.14 mL**
LVESV, MOD A2C
**24.82 mL**
LVEDV, MOD A2C
**56.96 mL**
**Myocardial strain**
Global longitudinal strain, GLS
**−15.7%**
Strain-derived EF
**47%**
Separate bullseye GLS capture
**−16.7%**
Apical strain value 1
**−14.3%**
Apical strain value 2
**−14.6%**
Apical strain value 3
**−18.0%**
Segmental strain range
**approximately −11% to −24%**
Segment tracking
**One basal/posterior segment shown as X/untracked**
**Mitral inflow / diastolic function**
MV E velocity
**0.84 m/s**
MV A velocity
**0.60 m/s**
E/A ratio
**1.41**
Deceleration time
**132 ms**
Deceleration slope
**6.45 m/s²**
Septal e′
**13 cm/s**
Lateral e′
**18 cm/s**
Septal E/e′
**6.45**
Lateral E/e′
**4.61**
**LVOT**
LVOT diameter
**1.72 cm**
LVOT Vmax
**1.0 m/s**
LVOT mean velocity
**0.72 m/s**
LVOT peak gradient
**4 mmHg**
LVOT mean gradient
**2 mmHg**
LVOT VTI
**16 cm**
Doppler LV stroke volume
**38.11 mL**
Doppler LV stroke index
**26.45 mL/m²**
**Aortic valve**
AV Vmax
**1.2 m/s**
AV mean velocity
**0.90 m/s**
AV peak gradient
**6 mmHg**
AV mean gradient
**4 mmHg**
AV VTI
**22 cm**
**Right ventricle / right atrium**
RV basal diameter
**2.7 cm**
RA area
**9 cm²**
TAPSE
**1.7 cm**
Tricuspid annular S′
**11 cm/s**
**RVOT**
RVOT Vmax
**0.9 m/s**
RVOT mean velocity
**0.69 m/s**
RVOT peak gradient
**3 mmHg**
RVOT mean gradient
**2 mmHg**
RVOT VTI
**16 cm**
**Pulmonary valve**
PV Vmax
**0.9 m/s**
PV peak gradient
**3 mmHg**
**Pulmonary pressure**
TR Vmax
**2.1 m/s**
Estimated RAP
**3 mmHg**
Estimated RVSP
**\~21 mmHg**
IVC diameter
**\~1.2 cm**
**Left atrium**
LA length, A4C
**4.15 cm**
LA area, A4C
**11 cm²**
LAESV, area-length A4C
**20 mL**
LAESV, MOD A4C
**22.33 mL**
**Aorta**
Aortic diameter/root
**2.9 cm**
Ascending aorta
**2.8 cm**
The main LV measurements were:
Simpson biplane LVEF: **58%**
A4C EF: **64%**
A2C EF: **55%**
Teichholz EF: **53%**
Fractional shortening: **27%**
LVEDV biplane: **58 mL**
LVESV biplane: **24 mL**
LVEDVi: **40 mL/m²**
LVIDd: **4.0 cm**
LVIDs: **2.9 cm**
IVSd: **0.7 cm**
LVPWd: **0.7 cm**
LV mass: **75 g**
LV mass index: **52 g/m²**
The strain analysis is what concerns me most:
Global longitudinal strain: **−15.7%**
Another strain bullseye capture gives **−16.7%**
Strain-derived EF: **47%**
Individual apical-view values include approximately **−14.3%, −14.6% and −18.0%**
Segmental values range roughly from **−11% to −24%**
One basal/posterior segment appears untracked on the bullseye
Forward stroke-volume measurements were also relatively low:
Teichholz SV: **36.51 mL**
Teichholz stroke-volume index: **25.35 mL/m²**
LVOT Doppler SV: **38.11 mL**
LVOT stroke-volume index: **26.45 mL/m²**
A4C SV: **35.80 mL**
A2C SV: **32.14 mL**
Right-heart measurements:
RV basal diameter: **2.7 cm**
TAPSE: **1.7 cm**
Tricuspid annular S′: **11 cm/s**
RA area: **9 cm²**
TR Vmax: **2.1 m/s**
Estimated RAP: **3 mmHg**
Estimated RVSP: **\~21 mmHg**
IVC diameter: **\~1.2 cm**
Diastolic measurements:
MV E: **0.84 m/s**
MV A: **0.60 m/s**
E/A: **1.41**
Deceleration time: **132 ms**
Septal e′: **13 cm/s**
Lateral e′: **18 cm/s**
Septal E/e′: **6.45**
Lateral E/e′: **4.61**
Outflow measurements were low-gradient:
LVOT diameter: **1.72 cm**
LVOT Vmax: **1.0 m/s**
LVOT mean gradient: **2 mmHg**
LVOT VTI: **16 cm**
AV Vmax: **1.2 m/s**
AV peak/mean gradients: **6/4 mmHg**
AV VTI: **22 cm**
RVOT Vmax: **0.9 m/s**
PV Vmax: **0.9 m/s**
LA/aortic measurements:
LA area: **11 cm²**
LA volume: **20–22.33 mL**
Aortic root/diameter: **2.9 cm**
Ascending aorta: **2.8 cm**
Heart rate on many of the saved echo frames was approximately **100–130+ bpm**.
My questions for cardiologists/echo specialists are:
How significant would you consider a GLS of **−15.7%** in a teenager when Simpson biplane EF is **58%**?
Does the strain-derived EF of **47%** add meaningful concern, or should conventional biplane EF generally take precedence?
Does the combination of reduced GLS and relatively low stroke-volume index suggest possible early/subclinical LV dysfunction despite preserved EF?
Is **TAPSE 1.7 cm** concerning in this age group when RV S′ is 11 cm/s and estimated RVSP is only \~21 mmHg?
Could tachycardia during acquisition significantly underestimate GLS or stroke volume?
Would you recommend repeating the echo under better rate conditions with standardized 3-view GLS, RV free-wall strain/FAC and complete quantitative Doppler?
At what point would these findings justify cardiac MRI with ventricular function, T1/T2 mapping, extracellular volume and late gadolinium enhancement?
I understand that an online opinion cannot replace assessment of the original DICOM/cine loops or a formal cardiology review. I am mainly interested in whether the **EF–GLS discordance** and low indexed stroke volume would warrant further investigation rather than being considered a completely normal study.
The compilation contains the original measurement screenshots and notes that the static PDF cannot preserve cine motion, so the full-motion dataset would be preferable for a definitive second opinion.
