Compared with tricuspid AS, TAVR in bicuspid AS was associated with a similar prognosis, but lower device success rate. Procedural differences were observed in patients treated with the early-generation devices, whereas no differences were observed with the new-generation devices.
Clinical transcatheter heart valve thrombosis is more common than previously considered, characterized by imaging abnormalities and increased gradients and N-terminal pro-brain natriuretic peptide levels. It occurred more commonly after balloon-expandable transcatheter aortic valve replacement and valve-in-valve procedures. OAC appeared to be effective in the prevention and treatment of valve thrombosis. Randomized control trials are needed to define optimal antithrombotic therapy after transcatheter aortic valve replacement.
The clinical outcomes of TAVR in patients with bicuspid AS were favorable. New-generation devices were associated with less paravalvular leak and, hence, a higher device success rate than early-generation devices. (The Bicuspid Aortic Stenosis Following Transcatheter Aortic Valve Replacement Registry [Bicuspid TAVR]; NCT02394184).
Carbamylation of LDL induces endothelial dysfunction via LOX-1 activation and increased ROS production leading to eNOS uncoupling. This indicates a novel mechanism in the pathogenesis of atherosclerotic disease which may be pathogenic and prognostic in patients with CKD and high plasma levels of cLDL.
We provide pharmacological and genetic evidence that Sirt1 inhibition enhances TF expression and activity by increasing NFκB/p65 activation in human endothelial cells. Furthermore, Sirt1 inhibition induces arterial thrombus formation in vivo. Hence, modulation of Sirt1 may offer novel therapeutic options for targeting thrombosis.
Objective-Plant-derived ␣-linolenic acid (ALA) may constitute an attractive cardioprotective alternative to fish-derived n-3 fatty acids. However, the effect of dietary ALA on arterial thrombus formation remains unknown. Methods and Results-Male C57Bl/6 mice were fed a high-ALA or low-ALA diet for 2 weeks. Arterial thrombus formation was delayed in mice fed a high-ALA diet compared with those on a low-ALA diet (nϭ7; PϽ0.005). Dietary ALA impaired platelet aggregation to collagen and thrombin (nϭ5; PϽ0.005) and decreased p38 mitogen-activated protein kinase activation in platelets. Dietary ALA impaired arterial tissue factor (TF) expression, TF activity, and nuclear factor-B activity (nϭ7; PϽ0.05); plasma clotting times and plasma thrombin generation did not differ (nϭ5; Pϭnot significant). In cultured human vascular smooth muscle and endothelial cells, ALA inhibited TF expression and activity (nϭ4; PϽ0.01). Inhibition of TF expression occurred at the transcriptional level via the mitogen-activated protein kinase p38 in smooth muscle cells and p38, extracellular signal-regulated kinases 1 and 2, and c-Jun N-terminal kinases 1 and 2 in endothelial cells.
Conclusion
Patients without conduction disorders post-TAVR did not develop delayed high-degree AVB. Such patients may not require telemetry monitoring. All other patients should be monitored until the ECG remains stable for at least 2 days. This algorithm should be validated in a separate patient population.
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