Measure the thickest segment on short-axis cine at end-diastole, find where it is (septal, apical, mid-ventricular), look for LV outflow obstruction and an apical aneurysm, then quantify scar — and rule out the phenocopies before you call it HCM.
Orient first
- HCM is unexplained LV wall thickening: in adults a maximal end-diastolic thickness of 15 mm or more in any segment (13–14 mm with a family history or a positive gene) — verify the threshold against the current ESC/AHA guideline.
- The phenotype varies: asymmetric septal (commonest), apical (spade-shaped cavity on the vertical long axis), mid-ventricular with an apical aneurysm, and concentric.
- Phenocopies thicken the wall for other reasons — hypertension, aortic stenosis, athlete's heart, amyloidosis, Fabry disease — and each has a tell on CMR.
Acquire the study
- Cine SSFP in short-axis stack (base to apex), 2-, 3- and 4-chamber; native T1 mapping; LGE (PSIR) 10–15 min after gadolinium; ECV if a haematocrit is available; phase contrast or cine through the LVOT when obstruction is the question.
The manoeuvre
- Short-axis cine at end-diastole: measure the maximal wall thickness in mm per segment (17-segment model), perpendicular to the wall, excluding RV trabeculae and the moderator band.
- 3-chamber cine: systolic anterior motion (SAM) of the mitral leaflet and the dephasing jet in the LVOT; note mitral–septal contact.
- Vertical long axis: apical hypertrophy (spade cavity) and an apical aneurysm with a thin, scarred wall — easily missed on short axis alone.
- LGE (PSIR): patchy mid-wall enhancement in the hypertrophied segments and at the RV insertion points; estimate extent as % of LV mass (≥ 15% is a sudden-death risk marker — verify).
- Native T1 and ECV: raised in scarred HCM; LOW native T1 points to Fabry disease; very high ECV with diffuse subendocardial LGE points to amyloidosis.
- Report LV volumes, EF (often supranormal), mass index and left atrial size.
What confirms it
- Maximal end-diastolic thickness ≥ 15 mm (or ≥ 13 mm with family history/genotype) not explained by loading conditions, with the phenotype named and LGE extent quantified.
What licenses you to exclude it
- Normal wall thickness on a complete short-axis stack including the apex excludes HCM phenotype at this time — gene carriers may develop it later; say "no phenotypic HCM at present".
The classic misread
- Measuring through the RV trabeculae or an oblique short-axis slice — overestimates septal thickness.
- Missing apical HCM and apical aneurysm by reading only the basal and mid short-axis slices.
- Calling amyloidosis HCM because the wall is thick — look at the LGE pattern and the difficulty nulling myocardium.