Background: Cardiac resynchronization therapy (CRT) is an established treatment for heart failure with reduced ejection fraction (HfrEF). Etiology may influence the outcome of patients undergoing CRT. Objective: to evaluate whether etiology (ischemic vs non-ischemic) influences the response to CRT and overall outcome. Methods: Our study included HFrEF patients undergoing CRT between January 2017-November 2019. We assessed right ventricle (RV) and left ventricle (LV) function using transthoracic echocardiography at baseline and one year after CRT. The response to CRT was defined by a decrease of more than 15% of left ventricle systolic volume. Patients were divided in two groups: ischemic and non-ischemic based on personal history. Adverse events (HF related hospitalizations and deaths) were tracked for 33± 12.8 months. Results: 52 patients undergoing CRT were included (64±13.5 years, 55.7% male, 70% non-ischemic etiology) The two groups were similar considering LV systolic baseline parameters and volumes. Ischemic etiology was associated with non-LBBB morphology on ECG (p=0.03), a more severe LV diastolic dysfunction using E/e ratio (p<0.05), and a more severe RV dysfunction using TAPSE (p=0.008) and RV fractional area change (FAC) (p<0.05). There was no significant difference in CRT response between ischemic and non-ischemic etiology. 14 (26.9%) patients had events (10 hospitalizations and 4 deaths) with a higher prevalence in the ischemic group (58.33% vs 25%, p=0.01). Univariate Cox regression analysis reported a higher risk of cardiovascular events for ischemic etiology (HR 2.4, 95% CI [0.8-8.1], p <0.05). In our cohort there was no significant difference in use of an implantable cardioverter-defibrillator in addition to CRT between ischemic and non-ischemic group (64.2% respectively 63.3%, p =0.3). Conclusion: Our study shows that ischemic and non-ischemic HF patients had similar response to CRT. However, ischemic etiology was associated with a higher risk of adverse cardiovascular events and a worse RV systolic dysfunction at baseline.

Background: Recent data suggest that the mechanisms contributing to ischaemic mitral regurgitation (IMR) in the setting of acute myocardial infarction (MI) are different compared to chronic IMR. However, little is known about the dynamic changes over time of mitral valve (MV) geometry after acute MI. Methods and results:Comprehensive three-dimensional (3D) assessment of the MV geometry was performed in 30 patients in the first 7 days after a first ST elevation myocardial infarction (STEMI), and after 4 years of follow-up. The MV annulus diameters and area remained unchanged over time, however the MA became progressively flatter (mean difference of annular height 0.19±0.33 cm, p<0.05), independently of the presence or severity of IMR. The posterior leaflet length and area got smaller over time (1.53±0.51 cm vs 1.27±0.33 cm; p<0.05 and 5.65±1.58 cm2 vs 4.88±1.65 cm2; p<0.05, respectively). The tenting height and area were smaller at follow-up (9.06±2.6 mm vs 7.84±2.61 mm, p<0.05; and 1.88±0.6 cm2 vs 1.57±0.5 cm2; p<0.05, respectively). A larger tenting at follow-up correlated with 3D left atrial (LA) volumes, but not with LV volumes and ejection fraction. Conclusions: MV geometry changes over time even in patients with non-severe IMR. The MV healing process consists in annulus flattening associated with improved tenting.