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The cause of a dilated left ventricle on cardiac MRI

MRI

Draft this report · MRI
First and second year — the floor first, then every step

A dilated, poorly contracting LV is the phenotype, not the diagnosis: the LGE pattern separates ischaemic from non-ischaemic, and a mid-wall septal stripe is both a clue and a risk marker.

Orient first

  • Dilated cardiomyopathy is LV dilatation with systolic dysfunction not explained by coronary disease or abnormal loading (valve disease, hypertension).
  • LGE location is the key: subendocardial or transmural in a coronary territory = ischaemic; mid-wall (septal stripe) or subepicardial = non-ischaemic.
  • No LGE at all is common in idiopathic DCM and is prognostically favourable; mid-wall septal LGE predicts arrhythmia and death.

Acquire the study

  • Cine short-axis stack for volumes and EF (indexed to BSA); native T1/T2 mapping; LGE (PSIR) in short axis and long axes; ECV where available.

The manoeuvre

  • Short-axis stack: LV end-diastolic volume index and EF against sex- and age-specific normal ranges; RV volumes and EF too.
  • Wall thickness: thinned segments in a coronary territory suggest old infarction; uniform thinning suggests DCM.
  • LGE: subendocardial/transmural in a territory (ischaemic) vs mid-wall septal stripe or subepicardial (non-ischaemic); note extent.
  • T2 mapping/STIR: raised T2 suggests active inflammation (myocarditis evolving to DCM).
  • Non-compaction: compacted vs trabeculated layer on end-diastolic long axes; a ratio > 2.3 alone overcalls in dilated hearts — report as hypertrabeculation unless the clinical picture fits.
  • Thrombus: LV apex on LGE with long inversion time (thrombus stays dark).

What confirms it

  • LV dilatation with reduced EF, no ischaemic-pattern LGE, and no loading cause — with the presence and pattern of non-ischaemic LGE stated.

What licenses you to exclude it

  • Ischaemic cardiomyopathy is made unlikely, not excluded, by absent subendocardial LGE — balanced multivessel disease and hibernation can leave no scar.

The classic misread

  • Calling excessive trabeculation "LV non-compaction" in a dilated ventricle.
  • Missing LV apical thrombus because a standard inversion time was used.

Reference values

Each value carries the caveat that keeps it from being misused. Normal limits and diagnostic criteria are kept apart on purpose: a disease cut-off read as a normal range is the more dangerous mistake.

Normal limits

  • Left ventricle · End-diastolic wall thickness, normal adult

    commonly around 6–10 mm at end-diastole in a non-athletic adult; 11–12 mm is a grey zone and 15 mm is the HCM conversation (see that entry)

    Must be end-diastole and perpendicular to the wall. This entry is the NORMAL range; the HCM entry is the diagnostic threshold — do not collapse them.

    CT · MRI

Diagnostic criteria

  • Left ventricle · End-diastolic wall thickness for hypertrophic cardiomyopathy

    a wall thickness of 15 mm or more in any segment (13 mm or more with a family history or positive genotype) meets the conventional HCM criterion in adults

    Must be measured at END-DIASTOLE perpendicular to the wall — an oblique or systolic measurement over-reads. Hypertensive heart disease and athletic remodelling overlap the 13–15 mm range; the pattern of hypertrophy and the clinical context decide. Versioned criterion — verify against the current edition before clinical use.

    MRI · CT

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