Abstract 2408: Lack of Gadolinium Late Enhancement in Non Compaction Cardiomyopathy
Introduction: Isolated ventricular non-compaction (IVNC) is an idiopathic form of cardiomyopathy. Little is known about the pathogenesis of this cardiomyopathy. Many cardiomyopathies have late enhancement with gadolinium in cardiovascular magentic resonance (CMR) scans that suggests the presence of fibrosis, necrosis or infiltration of the myocardium. The aim of this study was to assess if late enhancement gadolinium CMR technique identify potential pathogenic mechanisms of IVNC.
Methods: Patients with suspected IVNC by Doppler echocardiography were referred to a CMR scan to confirm diagnosis. CMR scans were performed in 1.5 Tesla scanners (Vision or Avanto, Siemens). Morphology was assessed by T1, T2 and Haste sequences, ventricular function and volumes by cines sequences, and late enhancement gadolinium by inversion recovery sequences. Diagnosis of non-compaction was confirmed by a ratio of non compacted /compacted myocardium >2.3 in the left ventricle at end-diastole. A 17-segment model was used for location of non-compacted myocardium.
Results: We studied 22 patients that had criteria for non-compaction by Doppler echocardiography and CMR. The mean age was 34 ± 11 years, 56% were male, the mean left ventricle ejection fraction was 53 ± 13 %, left ventricle end-diastolic volume was 180 ± 49 ml and left ventricle end-systolic volume was 86 ± 45 ml. The mean non-compacted / compacted ratio was 3.1 ± 0.52. The most frequently involved segments were lateral apical (76%), mid anterolateral (76%), mid inferolateral (64%) and apical inferior (54%). None of these patients had late enhancement after gadolinium injection. Only one patient has intramyocardium gadolinium late enhancement in a remote area from the non-compacted myocardium.
Conclusions: Late enhancement with gadolinium is commonly seen in diverse forms cardiomyopathies that have fibrosis, necrosis or infiltration of the myocardium. The lack of late enhancement suggests that necrosis, fibrosis or infiltration of the affected myocardium may not play a role in the pathogenesis of this idiopathic form of cardiomyopathy.