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Valvular Heart Disease: Difference between revisions
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The tricuspid valve is located at the junction between the right atrium and right ventricle. The tricuspid valve apparatus consists of 3 leaflets, chordae tendinae, anterior, posterior and often a third papillary muscle. The peripheral ends of the septal, anterosuperior and inferior or mural leaflets are referred to as commissures. The tricuspid valve has no well defined collagenous annulus. The three leaflets are attached to a fibrous elliptic shaped annulus. The direct attachment of the septal leaflet is a distinctive feature of the tricuspid valve. The prominent papillary muscles support the leaflets at the commissures. | The tricuspid valve is located at the junction between the right atrium and right ventricle. The tricuspid valve apparatus consists of 3 leaflets, chordae tendinae, anterior, posterior and often a third papillary muscle. The peripheral ends of the septal, anterosuperior and inferior or mural leaflets are referred to as commissures. The tricuspid valve has no well defined collagenous annulus. The three leaflets are attached to a fibrous elliptic shaped annulus. The direct attachment of the septal leaflet is a distinctive feature of the tricuspid valve. The prominent papillary muscles support the leaflets at the commissures. | ||
The anterior papillary muscle provides chords to the anterior and mural leaflets, the posterior papillary muscle provides chords to the mural and septal leaflets. | The anterior papillary muscle provides chords to the anterior and mural leaflets, the posterior papillary muscle provides chords to the mural and septal leaflets. | ||
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Valvular insufficiency is defined as reverse flow caused by failure of a valve to close completely, may result from either intrinsic disease of the valve cusps or from damage to or distortion of supporting structures without primary cuspal pathology. | Valvular insufficiency is defined as reverse flow caused by failure of a valve to close completely, may result from either intrinsic disease of the valve cusps or from damage to or distortion of supporting structures without primary cuspal pathology. | ||
=== Rheumatic valve disease === | |||
Chronic rheumatic valve disease is characterized by chronic, progressive deforming valvular disease. Anatomic lesions combine to varying degrees fibrous, or fibrocalcific distortion of leaflets or cusps, valve commissures and chordae tendineae, with or without annular or papillary muscle deformities. | |||
Stenosis results from fibrous leaflet and chordal thickening and commissural and chordal fusion with or without secondary calcification. Fusion of a commisure in an open position can cause regurgitation, as well as scarring induced retraction of chordae and leaflets. | |||
=== Aortic valve Stenosis === | |||
Obstruction of the left ventricle outflow can occur at subvalvular level (eg hypertrophic cardiomyopathy), supravalvular level or valvular level. Aortic valve stenosis is left ventricle outflow obstruction at valvular level. | |||
In industrialized countries, aortic stenosis is the most common lesion among patients referred for treatment of valvular disease <cite>Iung</cite>. Age-related degenerative calcified aortic stenosis is the most common cause of aortic stenosis in adults in North America and Western Europe. The second most common cause is calcification of a congenitally bicuspid aortic valve. Other rare causes of calcified aortic stenosis include Fabry disease, lupus erythematosus, Paget disease, and ochronosis with alkaptonuria. The most common etiology of aortic stenosis worldwide remains rheumatic heart disease. | |||
Prevalence of aortic valve abnormalities increases due to age-related pathology in the ageing population. | |||
The first detectable macroscopic modifications of the calcification process is named aortic valve sclerosis. <cite>Rajamannan</cite> Aortic sclerosis, seen as calcification or focal leaflet thickening with normal valve function, was detected in 25% of people at 65 years of age, this increases to 48% in people aged >75% in a population-based echocardiographic study. <cite>Otto</cite> <cite>Otto2</cite> | |||
The prevalence of calcified aortic stenosis is estimated at 2 % of people 65 years of age, increasing to 3-9% after the age of 80 years. <cite>Nkomo</cite> <cite>Otto</cite> | |||
Calcified degenerative aortic valve stenosis was previously considered to be the result of a passive degenerative process due to longterm mechanical stress in combination with calcium accumulation. Recently this concept is revised. Calcified degenerative aortic stenosis is considered an active pathobiological process, including proliferative and inflammatory changes, lipid accumulation, renin-angiotensin system activation, valular interstitial cell transformation, ultimately resulting in calcification of the aortic valve <cite>RajamannanGershBonow</cite><cite>Rajamannan2</cite> <cite>OBrien</cite> <cite>Mohler</cite>. Risk factors for development of calcific aortic stenosis are similar to those for vascular atherosclerosis such as diabetes, hypertension, and cholesterol levels. <cite>Stewart</cite> <cite>Stritzke</cite> Progressive calcification leads to immobilization of the cusps causing stenosis. | |||