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Valvular Heart Disease: Difference between revisions
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Life expectancy in adult patients with bicuspid aortic valve disease is not shortened when compared | Life expectancy in adult patients with bicuspid aortic valve disease is not shortened when compared | ||
with the general population. 10-year survival in asymptomatic adults with bicuspid aortic valve disease with a spectrum of valve function, was 96% <cite>Tzemos</cite>. In asymptomatic adults with bicuspid aortic valve disease without significant valve dysfunction the 20-year survival was 90%. <cite>Michelena</cite> | with the general population. 10-year survival in asymptomatic adults with bicuspid aortic valve disease with a spectrum of valve function, was 96% <cite>Tzemos</cite>. In asymptomatic adults with bicuspid aortic valve disease without significant valve dysfunction the 20-year survival was 90%. <cite>Michelena</cite> | ||
== Aortic Regurgitation == | |||
A variety of aetiologies can cause aortic regurgitation by preventing proper coaptation of the aortic valve leaflets with a subsequent diastolic reflux of blood from the aorta into the left ventricle. Etiology of aortic regurgitation can be primary valvular, or it can be primarily caused by aortic root or disease. | |||
The origin of primary valve disease may be calcific aortic disease, idiopathic degenerative disease, endocarditis, rheumatic disease, a biscuspid aortic valve, or myxomatous proliferation of valvular tissue. In the majority of patients the disease is caused by rheumatic disease. However, in Western countries the disease is most often of degenerative origin. In the Euro Heart Survey degenerative aortic regurgitation accounted for approximately half of the cases of aortic regurgitation, 15% of cases had a bicuspid aortic valve <cite>Iung</cite>. Accelerated degeneration of valve leaflets, resulting in regurgitation similar carcinoid syndrome related regurgitation, can be caused by certain anorectic medications, such as fenfluramine and phentermine <cite>Mihaljevic</cite>. | |||
Aortic annulus dilation, without primary involvement of the leaflets may result in aortic regurgitation due to leaflet separation. Aortic regurgitation of primary aortic root or annulus etiology includes idiopathic aortic root dilatation, aortic dissection, trauma, and chronic severe systemic hypertension. Aortitis representing less than 5% of the aetiologies of aortic regurgitation and may be due to inflammatory disease, such as giant cell, Takayasu and Behcet syndrome. Syphilis and ankylosing spondylitis may affect the aortic valve, but may also be associated with aortic dilatation. Other systemic arteritides and connective tissue disorders such as Marfan syndrome, Reiter disease, Ehlers-Danlos syndrome, osteogenesis imperfecta, and rheumatoid arthritis can lead to annular dilatation and valvular insufficiency. In patients without generalized tissue disease the same pattern of ascending aortic enlargement is known as annuloaortic ectasia. Chronic aortic regurgitation itself may lead to progressive aortic root dilatation. | |||
Aortic valve regurgitation is often accompanied by other valvular abnormalities. Aortic valvular insufficiency is most commonly seen in combination with aortic stenosis. | |||
Aortic insufficiency due to rheumatic etiology is often associated with mitral valve disease. The valve leaflets are retracted by fused commissures and fibrotic scarring of the leaflets itself. | |||
Aortic cusp prolapse can be isolated, or due to myxomatous degeneration, sometimes with associated mitral or tricuspid valve involvement. In 15% of patients with ventricular septum defect prolapse of an aortic cusp leads to aortic insufficiency. | |||
Isolated aortic regurgitation is often caused by a primary aortic annular etiology. Rheumatic origin is much less common in patients with pure aortic regurgitation. In approximately 10% of cases, aortic regurgitation results from infective endocarditis, with perforation or erosion of leaflets. | |||
It is of considerable clinical importance to distinguish between acute aortic regurgitation and chronic regurgitation, since acute aortic regurgitation can be life-threatening if not treated immediately, in contrast to chronic regurgitation which can be tolerated for years. | |||
=== Pathophysiology === | |||
In patients with aortic insufficiency the regurgitating volume increases total stroke volume. This volume might equal the effective forward stroke volume in patients with severe aortic regurgitation. In chronic aortic regurgitation, several compensatory mechanisms ensure cardiac output. | |||
==== Acute aortic regurgitation ==== | |||
Acute aortic regurgitation is a sudden hemodynamically significant aortic incompetence, which can often be catastrophic. An increase in left ventricular end diastolic volume with absence of ventricular remodelling may lead to elevated left atrial and pulmonary artery wedge pressure and decreased effective cardiac output, with compensatory tachycardia to maintain sufficient output. | |||
Acute severe aortic regurgitation typically occurs with infective endocarditis, trauma, and aortic dissection. The left ventricle cannot dilate sufficiently. The patient may present with chest pain due to increased myocardical oxygen consumption combined with decreased coronary bloodflow from changes in diastolic perfusion. Coronary bloodflow in acute aortic insufficiency occurs during stystolic cardiac phase. Other symptoms of acute aortic regurgitation are tachypnea, tachycardia and rapidly progressive pulmonary edema and/or cardiogenic shock. | |||
==== Chronic Aortic regurgitation ==== | |||
Aortic root dilatation, annular dilation and congenital bicuspid valve are, in developed countries, the most common causes of severe chronic Aorta regurgitation. | |||
The slow process of chronic aortic regurgitation allows adaptation of the ventricle to the increased preload and afterload. The left ventricular compensates to the regurgitant flow, the increased volume and pressure by enlargement. The left ventricle end diastolic pressure remains relatively low and does not approach the aortic diastolic pressure. The additional stroke volume is responsible for increased systolic pressure and eventually the wide pulse pressure. The systolic hypertension further increases left ventricle afterload. | |||
In contrast to the compensatory mechanism in mitral valve regurgitation, a modest concentric left ventricular hypertrophy accompanies the eccentric hypertrophy, with a normal mass-to-volume ratio(Feiring and Rumberger 1423-32). In a chronic state, progressive left ventricle dilatation leads to pre- and afterload mismatch. With gradually decompensation and deterioration of systolic function, the ventricle is not able to sustain perfusion. | |||