Heart valve disease (mitral valve disease): mitral regurgitation

Author(s):  
Patrizio Lancellotti ◽  
Raluca Dulgheru ◽  
Mani Vannan ◽  
Kiyoshi Yoshida

Mitral regurgitation (MR) is increasingly prevalent in Europe. Echocardiography has a key role in the diagnosis and management of patients with MR. Each echocardiographic study in patients with MR should aim to characterize mitral valve morphology, identify the mechanism of valve dysfunction, quantify the severity of MR, and give hints regarding the aetiology of the disease affecting the valve. Assessment of MR severity should be based on a step-wise approach including two-dimensional-derived Doppler data and, when available, data derived from three-dimensional echocardiography. MR assessment by quantitative methods should be implemented in each patient when possible. It is imperative not only to quantify the MR severity, but also to assess its consequences on the left ventricle, left atrium, and pulmonary vascular bed and to put everything into the clinical context (presence of symptoms, individual risk assessment, etc.) before taking any decision to correct the valvular incompetence. A rigorous echocardiographic study and a correct interpretation in the individual clinical context are needed to decide if the patient should be operated on or followed up closely. Exercise stress echocardiography, when appropriate, should be part of the evaluation algorithm in patients with both primary and secondary MR, as it has proved to be useful in individual risk stratification.

Author(s):  
Gabbar Jadhav

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.


Author(s):  
Giovanni La Canna

The mitral valve is a complex anatomical structure that includes the valve tissue (leaflets), the left atrioventricular junction (annulus), and the valve suspension system (chordae tendineae, papillary muscles, and left ventricle). Its functional anatomy can be analysed using two- and three-dimensional transthoracic and transoesophageal echocardiography. Based on certain hallmarks (commissures, clefts), in vivo mitral valve tissue anatomy can be accurately categorized. In addition, three-dimensional reconstruction provides a quantitative model for comprehensive valve analysis. This chapter describes the anatomy and morphology of the mitral valve, including the subvalvular suspension system and functional anatomy and dynamics of the mitral annulus.


Author(s):  
Bogdan A. Popescu ◽  
Shantanu P. Sengupta ◽  
Niloufar Samiei ◽  
Anca D. Mateescu

The most common cause of mitral stenosis (MS) is rheumatic fever followed by degenerative MS. Echocardiography is the key method to diagnose and evaluate MS. Echocardiographic findings are closely related to aetiology. In rheumatic disease echocardiography shows thickening of leaflet tips with restricted opening caused by commissural fusion resulting in ‘doming’ of the mitral valve in diastole. Quantitation of MS severity includes measuring mitral valve area (MVA) by planimetry (anatomical area, by two-/three-dimensional echo), or by the pressure half-time (PHT) method (functional area, by Doppler), and the mean pressure gradient. Planimetry is considered the reference method to determine MVA as it is relatively load independent. The PHT method is widely used due to its simplicity, but different factors influence the relationship between PHT and MVA. Other indices of MS severity are rarely used in clinical practice. Echocardiography also helps in the assessment of consequences of MS, and of associated valvular lesions. Exercise Doppler is recommended when there is discrepancy between the resting echocardiography findings and the clinical picture. Echocardiography is crucial in determining the timing and type of intervention in patients with MS. When considering percutaneous mitral commissurotomy (PMC) valve morphology should be comprehensively evaluated for mobility, thickness, calcifications, and subvalvular apparatus. The echo findings may determine the suitability for PMC, guide the procedure, and assess its results.


2020 ◽  
Author(s):  
Robert J Levy ◽  
Emmett Fitzpatrick ◽  
Estibaliz Castillero ◽  
Halley J Shukla ◽  
Vaishali V Inamdar ◽  
...  

AbstractAimsHeart valve disease attributed to serotonin (5HT) has been observed with 5HT-secreting carcinoid tumors and in association with medications, such as the diet drug, Dexfenfluoramine, a serotonin transporter (SLC6A4) inhibitor and 5HT receptor (HTR) 2B agonist. HTR2B signaling upregulates TGFβ-1 resulting in increased production of extracellular matrix proteins. SLC6A4 internalizes 5HT, limiting HTR signaling. Selective 5HT reuptake inhibitors (SSRI), widely used antidepressants, target SLC6A4, thus enhancing HTR signaling. However, 5HT and SLC6A4 mechanisms have not been previously associated with degenerative mitral regurgitation (MR). The present studies investigated the hypothesis that both dysregulation of SLC6A4 and inhibition of SLC6A4 contribute to the pathophysiology of MR.Methods and ResultsHere we report SLC6A4 related studies of 225 patients with MR requiring surgery. A multivariate analysis showed that SSRI use in MR patients was associated with surgery at a younger age, indicating more rapidly progressive MR (p=0.0183); this was confirmed in a national dataset (p<0.001). Aspirin use by MR patients was associated with surgery at an older age (p=0.0055). Quantitative reverse transcriptase PCR of MR leaflet RNA from 44 patients, and 20 normal mitral leaflets from heart transplant recipients, demonstrated down regulation in MR of both SLC6A4 and vesicular monoamine transporter-2 (SLC18A2), that packages 5HT (p<0.001). Human mitral valve interstitial cells cultivated with Fluoxetine, a SSRI, demonstrated down regulation of SLC6A4 and upregulation of HTR2B, compared to untreated, in cells from both normal and MR leaflets. Platelet 5HT studies in healthy subjects without heart disease used ADP-induced activation to model MR-associated activation. Fluoxetine significantly increased platelet activation and plasma 5HT levels, while Aspirin inhibited ADP platelet activation.ConclusionsDown regulation and inhibition of SLC6A4 influences MR through enhanced HTR signaling. SSRI may further influence MR through inhibition and down regulation of SLC6A4, upregulation of HTR2B, and increased platelet release of 5HT.Translational PerspectiveDegenerative mitral valve regurgitation (MR) affects millions, and there is no medical therapy for this disease. MR becomes progressively worse, and for severe MR, the only option is cardiac surgery. Serotonin (5HT) is best known as a neurotransmitter. However, 5HT secreting carcinoid tumors cause a cardiac valve disorder in many cases, and 5HT related medications, such as the diet drug Fenfluoramine, have been associated with the development of cardiac valve disease. The present paper presents evidence that diminished serotonin transporter (SLC6A4) expression and inhibition, lead to increased 5HT receptor signaling, contributing to the progression of MR.


2021 ◽  
Vol 8 (2) ◽  
pp. 23
Author(s):  
Aniek L. van Wijngaarden ◽  
Boudewijn P. T. Kruithof ◽  
Tommaso Vinella ◽  
Daniela Q. C. M. Barge-Schaapveld ◽  
Nina Ajmone Marsan

Degenerative mitral valve disease causing mitral valve prolapse is the most common cause of primary mitral regurgitation, with two distinct phenotypes generally recognized with some major differences, i.e., fibroelastic deficiency (FED) and Barlow’s disease. The aim of this review was to describe the main histological, clinical and echocardiographic features of patients with FED and Barlow’s disease, highlighting the differences in diagnosis, risk stratification and patient management, but also the still significant gaps in understanding the exact pathophysiology of these two phenotypes.


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