Excess trabeculation is common and often benign (athletes, pregnancy, sickle cell); the diagnosis of a cardiomyopathy needs more than a ratio — LV dilatation or dysfunction, LGE, thin compacted myocardium, and family history.
Orient first
- The Petersen ratio (non-compacted/compacted > 2.3 in end-diastole — verify) is sensitive but not specific.
- Current thinking treats hypertrabeculation as a phenotype that may accompany other cardiomyopathies.
- Complications: heart failure, arrhythmia, thromboembolism (LV thrombus).
Acquire the study
- CMR: cine SSFP short-axis stack and long axes; LGE; native T1 if available.
The manoeuvre
- End-diastolic long-axis cine: maximal non-compacted/compacted ratio in the segment with the most trabeculation.
- Compacted myocardium thickness in mm.
- LV volumes and EF indexed to BSA.
- LGE: presence and pattern (adverse prognosis).
- LV thrombus on LGE with a long inversion time.
What confirms it
- Hypertrabeculation with LV dilatation/dysfunction, LGE or a family history — a cardiomyopathy phenotype.
What licenses you to exclude it
- Isolated hypertrabeculation with normal size, function and no LGE should be reported as a trait, not a disease.
The classic misread
- Labelling a healthy athlete with non-compaction cardiomyopathy.