Automatic Detection of Mitral Regurgitation from Heart Sounds using SODP of Imperical Mode Decomposition

In this paper we discussed the heart valve disease. This heart valve disease occur throughout the world due to the more ethical estimation and grow curator of heart valve diseases use the diagnosis for this type of valve disease . Actually Phonocardiogram (PCG) signals are used because it having less price and acquire the signals. In this we learn five different kind of heart areas, Also typical are aortic stenosis, mitral valve prolapse, mitral stenosis and mitral regurgitation.

Correction of extensive mitral paravalvular leak with three occlusion devices via transapical access: a case report

Heart valve diseases account for a significant portion of hospitalizations due to cardiovascular diseases in Brazil. Prosthetic heart valves, which are often part of treatment, are susceptible to complications, such as paravalvular leak. Surgical intervention remains the treatment of choice for correcting this defect. However, transesophageal echocardiography-guided catheter correction has emerged as a less invasive alternative for paravalvular leak treatment in patients at high surgical risk. We report a case of extensive mitral paravalvular leak in a patient who had two previous cardiac surgeries and a high surgical risk, who underwent successful transcatheter closure with three prosthesis implantation by transapical access.

Dialdehyde pectin-crosslinked and hirudin-loaded decellularized porcine pericardium with improved matrix stability, enhanced anti-calcification and anticoagulant for bioprosthetic heart valves

To conveniently and effectively cure heart valve diseases or defects, combining with transcatheter valve technology, bioprosthetic heart valves (BHVs) originated from the decellularized porcine pericardium (D-PP) have been broadly used...

Abstract 319: Tnf-α and Il-1β Decrease Myofibroblast Differentiation in 3d-cultured Mitral Valve Interstitial Cells

Background: Fibrosis contributes to many heart valve diseases such as calcific aortic valve disease, rheumatic heart disease, and secondary mitral regurgitation. Heart valve leaflets are populated by quiescent, fibroblast-like valve interstitial cells (VICs). During fibrosis, VICs differentiate into activated, myofibroblast-like cells that adversely remodel the extracellular matrix. Activated VICs overexpress α-smooth muscle actin (ACTA2/αSMA) and smooth muscle 22-α (TAGLN/SM22α) and display increased contractility. Tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β) have been reported to either promote or inhibit fibrosis, depending on tissue type. Understanding how TNF-α and IL-1β affect VIC activation in the mitral valve of the heart could enable development of pharmaceutical treatments for heart valve diseases, which are currently managed surgically. Methods: To avoid artifactual activation on tissue culture plastic, VICs were encapsulated in biomimetic scaffolds consisting of polyethylene glycol (4% w/v) functionalized with protease-degradable (GGGPQGIWGQGK) and integrin-binding (RGDS) peptides. These 3D cultures were treated with 10 ng/ml TNF-α, 10 ng/ml IL-1β, or vehicle for 2 days in low-serum (1%) media. RNA and protein were measured via qRT-PCR, western blotting, and immunostaining. To measure contractility, VICs were encapsulated in collagen I (2.5 mg/ml) gels and allowed to contract freely for 2 days. Results: TNF-α and IL-1β significantly decreased RNA expression of ACTA2 (TNF-α: -91±6%, IL-1β: -99±1% change vs. vehicle) and TAGLN (TNF-α: -77±9%, IL-1β: -93±1% change). TNF-α and IL-1β also significantly decreased αSMA protein expression (TNF-α: -76±11%, IL-1β: -91±5% change) and the percentage of αSMA-positive cells (vehicle: 21±3%, TNF-α: 13±2%, IL-1β: 13±5% positive). Finally, TNF-α and IL-1β attenuated VIC-mediated collagen gel contraction (vehicle: 81±7%, TNF-α: 71±3%, IL-1β: 61±4% contraction). Conclusions: TNF-α and IL-1β decrease VIC activation in a 3D culture model of the mitral valve. These results reveal novel pathway targets for reducing fibrosis during mitral valve disease. Future work will use this model to study the downstream signaling events that drive VIC de-activation.