Septal & posterior wall thickness
IVSd, PWd (+ LV mass, RWT) · PLAX end-diastole, 2D-guided, just below the mitral leaflet tips, perpendicular to the long axis
Normal range & thresholds
IVSd and PWd: men 0.6–1.0 cm · women 0.6–0.9 cm.[1]
LV mass index (Devereux linear formula[41]): men ≤115 g/m², women ≤95 g/m². Relative wall thickness RWT = (2 × PWd) / LVIDd; normal ≤0.42.
LV mass index (Devereux linear formula[41]): men ≤115 g/m², women ≤95 g/m². Relative wall thickness RWT = (2 × PWd) / LVIDd; normal ≤0.42.
| Geometry | LV mass index | RWT |
|---|---|---|
| Normal | Normal | ≤0.42 |
| Concentric remodelling | Normal | >0.42 |
| Concentric hypertrophy | Increased | >0.42 |
| Eccentric hypertrophy | Increased | ≤0.42 |
Pathophysiology
Wall thickness is the myocyte’s answer to systolic wall stress (Laplace: σ ∝ P × r / 2h). Pressure overload raises P, so sarcomeres are added in parallel — thicker wall, smaller cavity, normalised stress: concentric hypertrophy. Volume overload raises r, so sarcomeres are added in series — a longer, dilated ventricle with only proportionate thickening: eccentric hypertrophy. A third group is not hypertrophy at all: infiltration (amyloid), storage (Fabry, Danon, PRKAG2) and myocyte disarray (HCM) thicken the wall without a pressure stimulus, which is why the ECG voltage and the strain pattern separate them from hypertensive LVH.[23,30]
Raised by
- Hypertension — commonest by an order of magnitude; concentric, symmetric
- Aortic stenosis and other fixed outflow obstruction (subaortic membrane, coarctation)
- HCM — asymmetric, ≥15 mm (or ≥13 mm with family history/positive genotype)[13,14]
- Infiltration — AL and ATTR amyloidosis: thick walls, low ECG voltage, granular texture, biatrial dilatation, apical sparing on strain[30]
- Storage/metabolic — Fabry (males, concentric, low native T1), Danon, PRKAG2, mitochondrial disease; Friedreich ataxia
- Athlete’s heart — usually ≤13 mm (rarely to 15 mm in black male endurance athletes), with a dilated cavity and normal diastolic function
- Obesity, chronic kidney disease and dialysis, acromegaly, phaeochromocytoma
- Endomyocardial fibrosis, radiation, chronic anaemia (eccentric pattern)
Lowered by
- Prior transmural myocardial infarction — regional thinning <6 mm with akinesia is scar, not viable myocardium
- Dilated cardiomyopathy (walls thin relative to a very large cavity; total mass may still be high)
- Burnt-out or end-stage HCM
- Myocarditis in the healed phase; muscular dystrophies (Duchenne/Becker — inferolateral thinning)
- Arrhythmogenic cardiomyopathy with LV involvement; severe cachexia; anorexia nervosa
- Constitutionally thin walls in small women — index to BSA before calling it abnormal
Technique & pitfalls
- End-diastole = the frame at the onset of the QRS, or the frame with the largest cavity.
- 2D-guided, perpendicular to the long axis, at or immediately below the mitral leaflet tips; blood–tissue interface to blood–tissue interface.
- Do not include RV trabeculations, the moderator band, a false tendon, or the pericardium.
- Beware the sigmoid/basal septal bulge of the elderly — measure below it, or it will manufacture ‘HCM’.
- For HCM, report the maximal wall thickness anywhere in the LV, not the PLAX septum; apical and anterolateral variants are missed without contrast or off-axis sweeps.[13,87]
- Report LV mass index and RWT, not just millimetres — geometry carries the prognostic information.[23]
Pseudo-change & artefact
- Oblique M-mode is the classic error: a cursor not perpendicular to the walls overestimates both walls and the cavity, and inflates calculated mass by 10–20%.
- Including the RV moderator band or trabeculae in the septum — a frequent cause of a spurious 1.3 cm septum.
- Harmonic imaging thickens endocardial borders slightly compared with fundamental imaging.
- Near-field clutter and inadequate lateral resolution over-thicken the anteroseptum.
- Systolic frame instead of diastolic: 30–50% overestimate.
- Volume status: a dehydrated or dialysed patient has a smaller cavity and apparently thicker walls; RWT is particularly load-sensitive.
- Pericardial fat and a lipomatous septum mimic hypertrophy — check tissue texture and the interatrial septum.
Treatment thresholds
- Maximal wall thickness ≥15 mm (≥13 mm with family history or positive genotype) with a non-dilated LV = diagnosis of HCM when loading conditions do not explain it.[13,14]
- Maximal wall thickness ≥30 mm is a major sudden-death risk marker → ICD reasonable (class IIa); it is also a continuous variable in the ESC HCM Risk-SCD calculator.[13,14,38]
- Septal thickness at the point of SAM contact must be adequate (generally ≥15–16 mm) for safe alcohol septal ablation or myectomy; a thin septum is a contraindication to ablation.[13]
- Echocardiographic LVH is hypertension-mediated organ damage — it reclassifies the patient upward and mandates treatment regardless of the absolute BP.[26]
- Wall thickness ≥12 mm plus a red flag (low voltage, discordance, apical sparing, aortic stenosis in the elderly, carpal tunnel, neuropathy) → amyloidosis pathway: free light chains and bone scintigraphy.[30]
Next step
- Next: compute LV mass index and RWT; review the ECG for voltage–mass concordance; look at global longitudinal strain for apical sparing.
- Then: CMR — T1/ECV mapping and LGE distinguish hypertensive LVH, HCM, Fabry (low native T1) and amyloid (high ECV, subendocardial LGE), and refine maximal thickness.[13,30]
- Then: serum/urine free light chains + 99mTc-DPD/PYP scintigraphy if amyloid is possible; α-galactosidase A / GLA genotyping if Fabry; HCM gene panel and cascade family screening.[13,30]
- Also: ambulatory BP and exercise BP if hypertensive LVH; detraining for 3–6 months resolves the athlete’s grey zone.
Drugs
- ACE inhibitors / ARBs produce the greatest LVH regression (≈10–13% mass reduction); calcium-channel blockers similar; diuretics intermediate; beta-blockers least (≈6%).[66]
- SGLT2 inhibitors reduce LV mass independently of glycaemia (EMPA-HEART: −2.6 g/m² at 6 months).[83]
- Tirzepatide in obesity-related HFpEF reduced LV mass by ≈11 g at 52 weeks.[84]
- Mavacamten (cardiac myosin inhibitor) reduces wall thickness and LV mass in obstructive HCM.[72,73]
- Tafamidis slows — does not reverse — ATTR cardiomyopathy.[75] Enzyme replacement / chaperone therapy regresses Fabry hypertrophy if started before fibrosis.
- Beware: anabolic steroids and stimulants increase wall thickness.
Reversibility
Hypertensive LVH: 10–15% LV mass index regression at 6–12 months with an ACE inhibitor/ARB, and up to ≈25–30% with sustained tight control; regression is independently associated with fewer cardiovascular events beyond BP reduction alone (LIFE).[66,67]
Aortic stenosis: LV mass falls ≈20–30% within the first year after AVR and continues for several years, but replacement fibrosis on CMR does not regress — the argument for intervening before fibrosis is established.[86]
Athlete’s heart: essentially complete regression after 3–6 months of detraining.
HCM: partial (mavacamten, myectomy). Amyloid: effectively irreversible; treatment stabilises. Fabry: substantially reversible if treated early, minimal once LGE is present.
Aortic stenosis: LV mass falls ≈20–30% within the first year after AVR and continues for several years, but replacement fibrosis on CMR does not regress — the argument for intervening before fibrosis is established.[86]
Athlete’s heart: essentially complete regression after 3–6 months of detraining.
HCM: partial (mavacamten, myectomy). Amyloid: effectively irreversible; treatment stabilises. Fabry: substantially reversible if treated early, minimal once LGE is present.