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Background Transcatheter aortic valve implantation (TAVI) results in an immediate and greater aortic pressure gradient improvement in patients with severe aortic valve stenosis (AS), and induces early left ventricular (LV) mass regression, which may be related to favorable effects on the mid to long term outcomes. However, the extent of LV mass regression after unloading of chronic pressure overload is varying, and its determinants are still unknown. Thus, the study aims to identify echocardiographic determinants of LV mass regression following TAVI. Methods We retrospectively screened all TAVI procedures in symptomatic AS from 2017 to 2019, and selected 74 successful TAVI cases that had serial echocardiographic studies both at the baseline and at the mid-term follow-up (4 to 6 months after the procedure). Through the digitalized medical records, clinical and echocardiographic data as well as angiographic grading (0-3) of post-procedure paravalvular leakage (PVL) were obtained. LV mass was calculated by using Cube formula. Thus, the extent of LV mass regression was defined as the differences of left ventricular mas index (LVMI) between at the baseline and at the follow-up (ΔLVMI). Quantification of the baseline mitral valve regurgitant volume was performed by stroke volume method with pulmonic site measurement on the assumption of no pre-existing intra/extra cardiac shunt. Cases with prior mitral valve replacement were excluded. Results At the post-procedure angiogram, only 3 cases had significant PVL (grade 2≤). At the mid-term follow–up, average LVMI decreased significantly from the baseline (165 ± 38 g/m2vs 140 ± 37 mg/ m2, P Conclusions Pre-existing mitral regurgitation has an impact on the mid–term left ventricular mass regression following TAVI. In severe AS, mitral regurgitation might be functioning as an afterload adjuster, and thus, produces protective effects on LV structure.

Radiation has been shown to enhance intercellular communication in the skin and lungs through an increase of connexin43 (Cx43) expression. If analogous Cx43 up-regulation is induced in the diseased heart, it would provide a new perspective in radiation therapy for arrhythmias. The aim of the present study is to test this hypothesis.Non-transmural myocardial infarction (MI) was created in 24 rabbits by microsphere injection into the coronary arteries. Twenty-four rabbits without MI were used as controls. Targeted external heavy ion beam irradiation (THIR; 15 Gy) was applied 2 weeks after MI with an accelerator (HIMAC, Chiba, Japan).The THIR was associated with an increase of Cx43 mRNA and protein levels in the left ventricle in control as well as in MI rabbits. THIR also increased lateralization of Cx43, which was no longer colocalized with cadherins. In MI hearts, immunoreactive Cx43 signals were reduced in the peri-infarct zone, and the reduction was reversed by THIR. In-vivo epicardial potential mapping on the free wall (64 unipolar electrodes to cover 7 x 7 mm) in MI hearts revealed reduced conduction velocity, whereas dispersion of the activation-recovery interval (ARI) was increased compared with controls, and these changes were reversed by THIR. The vulnerability for ventricular tachyarrhythmias (VT/VF), which was estimated by programmed stimulation, was increased in MI hearts, and this increased vulnerability to arrhythmias was reversed by THIR.THIR increases Cx43 expression, improves the conductivity, decreases the spatial heterogeneity of repolarization, and reduces the vulnerability of rabbit hearts to ventricular arrhythmias after MI. THIR could have an antiarrhythmic potential through an improvement of electrical coupling.