Echocardiography and global longitudinal strain in prediction for myocardial fibrosis in patients with left ventricle hypertrophy and hypertrophic cardiomyopathy

Background Late gadolinium enhancement (LGE) is the major imaging risk factor of ventricular arrhythmia, left ventricle (LV) dysfunction and sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). Purpose The aim of our study was to evaluate the diagnostic value of transthoracic echocardiography (TTE) with 2D global longitudinal strain (GLS) to detect myocardial fibrosis (LGE) in patients with LV hypertrophy (LVH). Methods A total of 95 consecutive patients scheduled for CMR due to suspected HCM were screened for the eligibility criteria. Both contrast-enhanced CMR and TTE with speckle-tracking echocardiography (GLS) were performed within 1 month in all the patients. Afterwards, 12 patients were excluded from the study due to alternative diagnosis and/or ischemic scar in CMR and 83 individuals were included in the study group. The presence, severity and the total rate (LGE%LV) of LGE in LV were assessed in CMR. Results The study group included 83 patients (57.5±13 y.o.; 55% males) with mild hypertension (42%), obesity (23%) or diabetes (10%). CMR confirmed HCM in 58 (70%) patients, including 23 individuals with LV outflow track obstruction. Meanwhile, the rest of the study group (n=23) had a lower degrees of LVH. Only 3 patients had LV systolic dysfunction (LVEF<50%) and 77% of patients had LV hyperkinesis (LVEF>60%). Regional wall motion abnormalities were found in 19 (22%) patients and a maximum thickness of LV wall of 15-18mm were found in 62% of patients and 10 individuals had a severe LVH (>20mm; 1 case with apical aneurysm). Most CMR studies (58 cases; 69%) showed a non-ischemic LGE in LV myocardium. The rate of LV segments with LGE was 23% (mostly segment 2 and 3; 84% intramyocardial) and the median number of LV segments with LGE was 2 (0-4). Among 58 patients with LGE, the median total LGE in LV was 2.95% (0-5.9%) with 14 cases found to have a significant LGE (>10% of LV mass). Global longitudinal strain in patients with LGE was significantly lower than that without LGE (-13.9±3.6 vs. -15.9±2.7%, P=0.01). The CMR LV mass (r=0.35; p<0.05), LVEF (r=-0.3; p<0.01) and TTE GLS (r=0.45; p,0.01) were associated with LGE%LV. The mean TTE GLS was -14.52±3.5% and it was associated with LGE%LV (r=0.45; p,0.01), which was confirmed in the multivariable regression analysis (standard coefficient=0.683; p<0.05). Moreover, the TTE GLS showed a significant prediction for LV LGE (-14.3%; AUC 0,658; p=0.01, sensitivity 39%, specificity 90%) with a better prediction for LGE in more than 4 LV segments (-12.1%; AUC 0,867; p<0.001, sensitivity 72%, specificity 87%). Conclusion Most of the patients with LVH revealed a myocardial fibrosis in CMR. TTE GLS showed a moderate or significant predictive value for any LGE or advanced LGE in LV (>4 segments) obtained in CMR.