Global longitudinal strain

GLS (2D speckle tracking) · Three apical views (4-, 2- and 3-chamber), frame rate 50–80 fps, one vendor, stable ECG

Normal range & thresholds

Pathophysiology

Raised by

• (Magnitude increases, i.e. more negative) Athletic training; hyperdynamic states; after successful revascularisation, GDMT or valve intervention
• Note the sign convention: GLS is negative, so ‘increased GLS’ is ambiguous. Report magnitude, and say ‘less negative’ or ‘more negative’

Lowered by

• (Magnitude falls, i.e. less negative) Subclinical cardiotoxicity from anthracyclines, trastuzumab, checkpoint inhibitors — the earliest detectable abnormality^[15,29,74]
• Ischaemia, prior infarction (regional bull’s-eye deficit in a coronary territory), hibernation
• Infiltrative and storage disease — amyloid (apical sparing), Fabry (basal inferolateral deficit), sarcoid (patchy, basal septal)
• HCM (reduced despite hyperdynamic LVEF), hypertensive heart disease, diabetes, obesity, CKD
• Aortic stenosis and chronic aortic/mitral regurgitation — falls before LVEF and before the dimensional thresholds are reached
• Myocarditis, chemotherapy-naive cancer cachexia, sepsis, HFpEF (GLS is abnormal in ≈half of HFpEF)
• Right-sided disease with septal involvement; LBBB and RV pacing (dyssynchrony, not necessarily disease)

Technique & pitfalls

• Non-foreshortened apical views, all three, with a clear ECG and a stable rhythm; the software must track the full myocardial thickness, not just the endocardial line.
• Frame rate 50–80 fps — too low and speckles decorrelate, too high and the signal degrades.
• Reject and re-trace any segment the software tracks badly; do not accept an automatic value with two or more excluded segments.
• Define aortic valve closure timing correctly — peak systolic strain versus end-systolic strain differ when there is post-systolic shortening.
• Read the bull’s-eye pattern, not only the single number: the pattern is what distinguishes amyloid, Fabry, sarcoid and coronary territories from each other.
• Same vendor, same version, ideally same operator for serial studies.^[16,90]

Pseudo-change & artefact

• Vendor and software version change — the commonest artefactual ‘deterioration’.^[90]
• Foreshortening, poor endocardial definition, and reverberation artefact in the lateral wall.
• Load: GLS falls with hypertension, rises after afterload reduction; it is not load-independent.
• Heart rate, arrhythmia, ectopy, atrial fibrillation (average multiple beats).
• Region-of-interest width set too wide, including pericardium, or too narrow, missing the epicardium.
• Sign confusion between reports (−18% vs 18%) — a persistent source of clinical error.

Treatment thresholds

• Cardio-oncology (the one strong, guideline-endorsed threshold): a relative reduction >15% from the patient’s own baseline defines mild asymptomatic cancer-therapy-related cardiac dysfunction and triggers cardioprotection (ACEi/ARB ± beta-blocker) and closer surveillance, without necessarily interrupting oncological treatment.^[15,29] SUCCOUR showed strain-guided management produced a smaller LVEF fall than EF-guided management.^[74]
• Amyloidosis: relative apical sparing >1.0 is one of the imaging red flags that mandates free light chains and bone scintigraphy.^[30]
• Asymptomatic valve disease: impaired GLS (commonly cited as worse than −18% in AR/MR, −15% in AS) is used by Heart Teams to bring forward intervention. It is a supportive, not a class I, criterion in the 2025 ESC/EACTS and 2020 ACC/AHA documents — say so when you report it.^[6,7]
• Heart failure with preserved EF: reduced GLS supports the diagnosis within the HFA-PEFF framework.^[100,101]

Next step

• Next: read the bull’s-eye for pattern, then correlate with wall thickness, ECG voltage and the clinical context.
• Then: CMR — LGE, T1 and ECV convert a strain pattern into a tissue diagnosis.
• Then: disease-specific confirmation — light chains and bone scintigraphy (amyloid), α-galactosidase A (Fabry), ischaemia testing or angiography (coronary territory deficit), genetic testing (cardiomyopathy).
• In cardio-oncology: repeat with the same vendor before acting on a fall — and always compare to the patient’s own baseline, never to the population range.

Drugs

• Improve GLS: ACE inhibitors/ARBs and ARNI, beta-blockers, MRAs, SGLT2 inhibitors, statins (modest); revascularisation; CRT; valve intervention; mavacamten in obstructive HCM.^[68,69,72]
• Worsen GLS: anthracyclines (dose-dependent, partly irreversible), trastuzumab (largely reversible), VEGF inhibitors and checkpoint inhibitors, radiotherapy.^[15]
• Tafamidis slows deterioration in ATTR; enzyme replacement improves strain in early Fabry.^[75]
• Acute afterload reduction improves GLS without any change in contractility — interpret peri-treatment improvement cautiously.

Reversibility