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ObjectiveLeft ventricular (LV) twist is a major component of ventricular mechanics reflecting the helical orientation of cardiac fibres and compensating for afterload mismatch. However, it is not known whether it determines outcome after transcatheter aortic valve implantation (TAVI). This study sought to investigate TAVI-induced short-term changes of LV twist and to define its role in outcome prediction.MethodsA total of 146 patients (median age 81.78 years, 50.7% male) undergoing TAVI for severe aortic stenosis were included. LV rotation and twist were determined by speckle tracking echocardiography within 3 months before and 2 weeks after TAVI. All-cause mortality at 2 years was defined as primary end point.ResultsPatients who survived exhibited a higher apical peak systolic rotation (APSR) (pConclusionAPSR, twist and torsion pre-TAVI as well as their change within 2 weeks after TAVI predict 2-year all-cause mortality after TAVI, adding incremental prognostic value to LVEF and GLS.

Isolated perfused rat liver was used to characterize the choleretic action of 4-[4-chloro-N-(4-methoxyphenyl)-benzamido]-butyric acid (clanobutin). The dose-dependent increase of the bile flow was associated with an increase of the Na+ secretion. In in vitro studies the drug inhibited the Na+-K+-ATPase of the sinusoidal membrane more than that of the canalicular membrane in a dose-dependent manner. The following hypothesis was proposed to explain the choleretic action of clanobutin. The intracellular Na+ concentration increased due to the inhibition of the sinusoidal Na+-K+-ATPase. This is then compensated by transporting the extra Na+ into the bile. However, it cannot be ruled out that Na+ is transported as counterion during hepatobiliary transport of clanobutin or else its metabolites. The effect of the drug seems to be non-specific since other enzymes of the plasma membrane were also inhibited.