[Aortic stenosis: An update]. / Rétrécissement aortique : mise au point.

Aortic stenosis remains one of the most frequent valvulopathy worldwide, burdened with great mortality and morbidity, and for which there is not yet an effective preventive approach, although the pathophysiological mechanisms involved in its development are better understood nowadays. Its cure, however, has been revolutionized in the last decade by the advent of transcatheter aortic valve implantation, or TAVI (also named transcatheter aortic valve replacement or TAVR). The technique of TAVI has been refined and its indications has been extended, following the publication of large randomized controlled trials where it was compared to surgical aortic valve replacement with favorable results. Consequently, transfemoral TAVR has become the first line of treatment in case of symptomatic severe aortic valve stenosis. In this review, we describe the pathophysiological mechanisms leading to severe aortic stenosis and the main ongoing randomized controlled trials targeting them. We describe the indication for surgical or percutaneous aortic valve replacement and the main complications following the procedure.

Epicardial adipose tissue volume is associated with left ventricular remodelling in calcific aortic valve stenosis.

BACKGROUND: The severity of left ventricular (LV) remodelling is only partially related to the severity of aortic valve stenosis; additional factors, including diabetes, insulin resistance, obesity and metabolic syndrome, may play important roles. Epicardial adipose tissue (EAT), now considered as a metabolically active organ, is also linked to these factors. AIM: To analyse the association between EAT volume measured using computed tomography and LV remodelling in a prospective cohort of patients with aortic stenosis. METHODS: Consecutive asymptomatic patients with at least mild degenerative aortic stenosis enrolled in a prospective cohort that aimed to assess the determinants of aortic stenosis occurrence and progression constituted our population. RESULTS: We enrolled 143 patients (78±5 years; 65% men). Mean LV mass and EAT volume were 219±64g and 134±56mL, respectively. LV hypertrophy was diagnosed in 86 patients (60%), and concentric hypertrophy (32%) was the main remodelling pattern. EAT was associated with body mass index (P<0.001) and body surface area (P<0.001), but not with age (P=0.33) or aortic stenosis severity (all P>0.10). EAT was correlated with LV mass (r=0.41; P<0.0001), and after adjustment for age, sex, body mass index/body surface area, hypertension, waist circumference, low-density lipoprotein cholesterol and aortic stenosis severity, EAT was independently associated with LV mass (P=0.01/P=0.02). Similar results were found when EAT and LV mass index (adjusted for body surface area) were considered instead of absolute values (P=0.04). CONCLUSIONS: In this prospective cohort of patients with aortic stenosis, EAT volume was independently associated with LV mass. Further studies are warranted to elucidate the underlying mechanisms of this link.