Search

Aims: How the underlying etiology and pathophysiology of left ventricular (LV) hypertrophy affects LA remodeling and function remains unexplored. The present study aims to investigate the influence of various hypertrophic phenotypes on LA remodeling and function., Methods and Results: Patients with LV hypertrophy who underwent cardiac magnetic resonance (CMR) were compared to a control group. CMR data were analyzed retrospectively to assess LA strain, volume, sphericity and left atrioventricular coupling index (LACI). Independent clinical associates of LA strain were assessed using multivariable linear regression analysis.A total of 375 individuals were included: 148 hypertrophic cardiomyopathy (HCM), 35 cardiac amyloidosis (CA), 41 hypertensive heart disease (HTN), 97 severe asymptomatic aortic stenosis (AS) and 54 with normal CMR. Indexed LA end-systolic (iLVmax), diastolic volumes and LA sphericity were the largest in patients with CA (59.1±16.9ml/m2, 46.8±16.4ml/m2 and 83.2±2.1%, respectively). CA patients presented higher LACI when compared to other groups (58±2% vs 42±2% in HCM, 39±2% in HTN, 37±2% in AS and 22±1% in normal), while no differences were observed across others. CA patients showed the lowest LA reservoir (9.6%[0.6-18.6%]) and booster strain (9.1±5.4%), whereas no differences were observed across other groups. LACI and iLAVmax were independently correlated to LA reservoir (β=0.15 and β=-39.33, respectively), LA conduit (β=0.08 and β =-17.08, respectively) and LA booster strains (β=0.1 and β=-28.69, respectively). LA sphericity was independently correlated with LA reservoir strain (β=-0.51). Finally, LV global longitudinal strain was independently correlated with LA reservoir (β=-0.43), conduit (β=-0.20) and booster strain (β=-0.24)., Conclusions: LA characteristics differ among LV hypertrophic phenotypes. LACI and iLAVmax are independently correlated with LA function while LA sphericity correlates independently with LA reservoir strain., (© The Author(s) 2025. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Aims: To investigate the distribution of left atrioventricular coupling index (LACI) among patients with heart failure and left ventricular ejection fraction (LVEF)<50% and to explore its association with the combined endpoint of all-cause death or HF hospitalization at long term follow-up., Methods and Results: Patients with HF and LVEF<50% undergoing cardiac magnetic resonance (CMR) were evaluated. Patients with atrial fibrillation or flutter were excluded. LACI was measured as the ratio between the left atrial (LA) and the LV end-diastolic volumes. Patient population was divided according to LACI tertiles and followed-up. Total of 478 patients (mean age 62±12 years, 78% male) were included. The median value of LACI was 27.1% (interquartile range 19.9-34.5). Patients within the worst LACI tertile (≥30.9%) showed smaller LV volumes and larger LA volumes as compared to patients in the first or second tertile (LACI 6.2-22.2 and LACI 22.3-30.9; respectively). LACI was significantly associated with the combined endpoint (hazard ratio [HR] 1.87, p=0.01). After adjusting for sex, age, ischemic HF aetiology, LVEF, LA reservoir strain, diabetes mellitus, LV scar, mitral regurgitation and LVEDVi, LACI remained significantly associated with the combined endpoint (HR 1.77, p=0.02). Patients with highest LACI values had worse outcomes compared to patients in first and second tertiles (HR 1.69, p=0.02 and HR 1.77, p=0.02; respectively)., Conclusion: In patients with HF and LVEF <50%, LACI is independently associated with adverse events. Patients with most impaired left atrioventricular coupling have the worst clinical outcomes., (© The Author(s) 2025. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)