Valvular Heart Disease: Difference between revisions

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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.
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.
In industrialized countries, aortic stenosis is the most common lesion among patients referred for treatment of valvular disease.<cite>IungB</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.  
Prevalence of aortic valve abnormalities increases due to age-related pathology in the ageing population.  
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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 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>
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.
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.
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=== Transcatheter intervention ===
=== Transcatheter intervention ===
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In 2002, the first transcatheter aortic valve implantation was performed by Dr. Alain Cribier <cite>Cribier</cite>. A transcatheter aortic valve implantation is a less invasive treatment option for patients at prohibitive risk for conventional aortic valve replacement.  In this technique, the native valve is not excised. After balloon valvuloplasty, the prosthetic valve is implanted in the aortic position, with the frame of the prosthesis covering the native valve. The bioprosthesis can be implanted retrograde or antegrade. Currently 4 different approaches may be used in this technique. (table…). Transcatheter aortic valve implantation is assessed in randomized clinical trials and registries.
 
{| class="wikitable" border="1" cellpadding="0" cellspacing="0"
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! The current 4 different approaches are:
! The current 4 different approaches are:
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|Transsubclavian, retrograde
|Transsubclavian, retrograde
|}
|}
In 2002, the first transcatheter aortic valve implantation was performed by Dr. Alain Cribier <cite>Cribier</cite>. A transcatheter aortic valve implantation is a less invasive treatment option for patients at prohibitive risk for conventional aortic valve replacement.  In this technique, the native valve is not excised. After balloon valvuloplasty, the prosthetic valve is implanted in the aortic position, with the frame of the prosthesis covering the native valve. The bioprosthesis can be implanted retrograde or antegrade. Currently 4 different approaches may be used in this technique. (table…). Transcatheter aortic valve implantation is assessed in randomized clinical trials and registries.


== Prognosis ==
== Prognosis ==
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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.   
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>  
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>IungB</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 aetiology includes idiopathic aortic root dilatation, aortic dissection, trauma, and chronic severe systemic hypertension. Aortitis represents 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 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 aetiology includes idiopathic aortic root dilatation, aortic dissection, trauma, and chronic severe systemic hypertension. Aortitis represents 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.
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==== Chronic Aortic regurgitation ====
==== Chronic Aortic regurgitation ====
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Aortic root dilatation, annular dilation and congenital bicuspid valve are, in developed countries, the most common causes of severe chronic aortic valve 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.<cite>FeiringRumberger</cite> 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.
 
{| class="wikitable" border="1" cellpadding="0" cellspacing="0"
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!Causes of chronic aortic regurgitation 
!Causes of chronic aortic regurgitation 
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#In association with other diseases
#In association with other diseases
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|}
Aortic root dilatation, annular dilation and congenital bicuspid valve are, in developed countries, the most common causes of severe chronic aortic valve 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.<cite>FeiringRumberger</cite> 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.


=== Clinical presentation ===
=== Clinical presentation ===
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#Otto pmid=10403851
#Otto pmid=10403851
#Otto2 pmid=18815402
#Otto2 pmid=18815402
#OttoBurwaskLegget  
#OttoBurwaskLegget Otto CM, Burwash IG, Legget ME et al. Prospective study of asymptomatic valvular aortic stenosis. Clinical, echocardiographic, and exercise predictors of outcome. Circulation 1997 May 6;95(9):2262-70.
#PaderaSchoen Padera R Fi J r and Schoen F Ji. "Pathology of Cardiac Surgery." Cardiac Surgery in the Adult. Ed. Cohn L.H. New York: McGraw-Hill, 2012. 111-78.
#PaderaSchoen Padera R Fi J r and Schoen F Ji. "Pathology of Cardiac Surgery." Cardiac Surgery in the Adult. Ed. Cohn L.H. New York: McGraw-Hill, 2012. 111-78.
#Rajamannan pmid=22007101
#Rajamannan pmid=22007101
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#Harken HARKEN DE, ELLIS LB, . The surgical treatment of mitral stenosis; valvuloplasty. N Engl J Med 1948 November 25;239(22):801-9.
#Harken HARKEN DE, ELLIS LB, . The surgical treatment of mitral stenosis; valvuloplasty. N Engl J Med 1948 November 25;239(22):801-9.
#Antunes Antunes MJ, Vieira H, Ferrao de OJ. Open mitral commissurotomy: the 'golden standard'. J Heart Valve Dis 2000 July;9(4):472-7.
#Antunes Antunes MJ, Vieira H, Ferrao de OJ. Open mitral commissurotomy: the 'golden standard'. J Heart Valve Dis 2000 July;9(4):472-7.
#Capentier Carpentier A. Cardiac valve surgery--the "French correction". J Thorac Cardiovasc Surg 1983 September;86(3):323-37.
#Harrison Harrison MR, MacPhail B, Gurley JC et al. Usefulness of color Doppler flow imaging to distinguish ventricular septal defect from acute mitral regurgitation complicating acute myocardial infarction. Am J Cardiol 1989 October 1;64(12):697-701.
#Harrison Harrison MR, MacPhail B, Gurley JC et al. Usefulness of color Doppler flow imaging to distinguish ventricular septal defect from acute mitral regurgitation complicating acute myocardial infarction. Am J Cardiol 1989 October 1;64(12):697-701.
#Vahanian1 Vahanian A, Palacios IF. Percutaneous approaches to valvular disease. Circulation 2004 April 6;109(13):1572-9.
#Vahanian1 Vahanian A, Palacios IF. Percutaneous approaches to valvular disease. Circulation 2004 April 6;109(13):1572-9.
#Elizabeth Elisabeth Bédard, Michael A Gatzoulis. Adult congenital heart disease. In: S.Yusuf JACAJCELFaBJG, editor. evidence based cardiology. third ed. 2012.
#Elizabeth Elisabeth Bédard, Michael A Gatzoulis. Adult congenital heart disease. In: S.Yusuf JACAJCELFaBJG, editor. evidence based cardiology. third ed. 2012.
#IungB Iung B, Baron G, Tornos P, Gohlke-Barwolf C, Butchart EG, Vahanian A. Valvular heart disease in the community: a European experience. Curr Probl Cardiol 2007 November;32(11):609-61.
#Cribier Cribier A, Eltchaninoff H, Bash A et al. Percutaneous transcatheter implantation of an aortic valve prosthesis for calcific aortic stenosis: first human case description. Circulation 2002 December 10;106(24):3006-8.
</biblio>
</biblio>
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