Valvular Heart Disease: Difference between revisions

no edit summary
No edit summary
Line 15: Line 15:


== Pathophysiology ==
== Pathophysiology ==
{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="100%"
|-
|align="center"|[[Image:Diagram of the human heart (valves improved).svg|400px]]
|-
|'''Diagram of the human heart (valves improved)'''
|}
{| border="0" cellpadding="1" cellspacing="1" width="100%"
{| border="0" cellpadding="1" cellspacing="1" width="100%"
|-
|-
Line 29: Line 36:


==== Aortic valve ====
==== Aortic valve ====
[[Image:Aortic_valve_(1).gif‎|Thumb|right|100px|This animation shows the aortic valve of a pig's heart.]]
The tricuspid aortic valve separates the left ventricle outflow tract from the aorta.  Behind the three semilunar shaped cusps of the aortic valve are dilated pockets of the aortic root, called sinuses of Valsalva. The right coronary sinus gives rise to the right coronary artery, the left coronary sinus gives rise to the left coronary artery. The commissures are the areas where attachments of two adjacent cusps to the aorta meet.  
The tricuspid aortic valve separates the left ventricle outflow tract from the aorta.  Behind the three semilunar shaped cusps of the aortic valve are dilated pockets of the aortic root, called sinuses of Valsalva. The right coronary sinus gives rise to the right coronary artery, the left coronary sinus gives rise to the left coronary artery. The commissures are the areas where attachments of two adjacent cusps to the aorta meet.  


Line 68: Line 77:
=== Aortic valve Stenosis ===
=== Aortic valve Stenosis ===
|}
|}
[[Image:Aortic stenosis rheumatic, gross pathology 20G0014 lores.jpg|thumb|400px|right|Gross pathology of rheumatic heart disease: aortic stenosis. Aorta has been removed to show thickened, fused aortic valve leaflets and opened coronary arteries from above. Autopsy, CDC/Dr. Edwin P. Ewing, Jr.]]
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.


Line 86: Line 98:
Aortic stenosis is assessed by estimating the mean systolic pressure gradient and aortic valve area (AVA). The normal aortic valve area is 3-4 cm2.  Mild aortic stenosis is defined as an aortic valve area 1.5 cm2, mean gradient less than 25 mm Hg, or jet velocity less than 3.0 m per second, moderate aortic stenosis as an area of 1.0 to 1.5 cm2, mean gradient 25 to 40 mmHg, or jet velocity 3.0 to 4.0 m per second. A valve area of <1 cm2,  a mean gradient greater than 40 mm Hg, or jet velocity greater than 4.0 m per second  implies severe aortic stenosis The valve area may decrease by as much as 0.12 ±  0.19cm2  per year.<cite>OttoBurwaskLegget</cite> In late stages of severe aortic stenosis, cardiac output declines due to systolic dysfunction of the left ventricle, with a decline in the transvalvular gradient.
Aortic stenosis is assessed by estimating the mean systolic pressure gradient and aortic valve area (AVA). The normal aortic valve area is 3-4 cm2.  Mild aortic stenosis is defined as an aortic valve area 1.5 cm2, mean gradient less than 25 mm Hg, or jet velocity less than 3.0 m per second, moderate aortic stenosis as an area of 1.0 to 1.5 cm2, mean gradient 25 to 40 mmHg, or jet velocity 3.0 to 4.0 m per second. A valve area of <1 cm2,  a mean gradient greater than 40 mm Hg, or jet velocity greater than 4.0 m per second  implies severe aortic stenosis The valve area may decrease by as much as 0.12 ±  0.19cm2  per year.<cite>OttoBurwaskLegget</cite> In late stages of severe aortic stenosis, cardiac output declines due to systolic dysfunction of the left ventricle, with a decline in the transvalvular gradient.


<div align="center">
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
|-
|-
Line 109: Line 120:
|greater than 4.0 m per second
|greater than 4.0 m per second
|}
|}
</div>


== Clinical Presentation ==
== Clinical Presentation ==
Line 180: Line 190:
No medical treatment has proven to delay the progression of aortic stenosis. Surgery is inevitable for symptomatic patients. Patients at prohibitive risk for intervention may benefit from medical treatment including digitalis, diuretics, ACE inhibitors, or angiotensin receptor blockers, if experiencing heart failure. Beta-blockers should be avoided in these circumstances.  
No medical treatment has proven to delay the progression of aortic stenosis. Surgery is inevitable for symptomatic patients. Patients at prohibitive risk for intervention may benefit from medical treatment including digitalis, diuretics, ACE inhibitors, or angiotensin receptor blockers, if experiencing heart failure. Beta-blockers should be avoided in these circumstances.  


<div align="center">
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
|-
|-
Line 205: Line 214:
AVR is not useful for the prevention of sudden death in asymptomatic patients with AS who have none of the findings listed under the Class IIa/IIb recommendations. (Level of Evidence: B)
AVR is not useful for the prevention of sudden death in asymptomatic patients with AS who have none of the findings listed under the Class IIa/IIb recommendations. (Level of Evidence: B)
|}
|}
</div>


{| border="0" cellpadding="1" cellspacing="1" width="100%"
{| border="0" cellpadding="1" cellspacing="1" width="100%"
Line 230: Line 238:
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.  
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.  


<div align="center">
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
|-
|-
Line 243: Line 250:
|Transsubclavian, retrograde
|Transsubclavian, retrograde
|}
|}
</div>


== Prognosis ==
== Prognosis ==
Line 249: Line 255:


== Bicuspid Aortic valve ==
== Bicuspid Aortic valve ==
[[Image:Heart bicuspid aortic valve.svg|thumb|right|400px|Heart bicuspid aortic valve anatomy by Patrick J. Lynch, medical illustrator, 2006]]
Bicuspid Aortic valve disease affects as many as 1-2% of the population, and is the most frequent congenital cardiovascular malformation in humans.<cite>Fedak</cite>  
Bicuspid Aortic valve disease affects as many as 1-2% of the population, and is the most frequent congenital cardiovascular malformation in humans.<cite>Fedak</cite>  


Line 319: Line 327:


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.  
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.  
{| border="0" cellpadding="1" cellspacing="1" width="80%"
{| border="0" cellpadding="1" cellspacing="1" width="100%"
|-
|-
|bgcolor="#FAF8CC"|
|bgcolor="#FAF8CC"|
Line 337: Line 345:


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.  
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.  
<div align="center">


{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
Line 354: Line 360:
|In association with other diseases
|In association with other diseases
|}
|}
</div>


{| border="0" cellpadding="1" cellspacing="1" width="100%"
{| border="0" cellpadding="1" cellspacing="1" width="100%"
Line 391: Line 396:
The relative reduction of myocardial blood supply due to increased demand and/or associated obstructive coronary artery disease may cause angina. Angina may be treated by reducing aortic regurgitation, reduction of myocardial demand of revascularization of the myocardium. Clinical heart failure is treated with traditional therapy, including digitalis, diuretics, and ACEI. In severe heart failure, parenteral inotropic and vasodilator therapy may be needed.   
The relative reduction of myocardial blood supply due to increased demand and/or associated obstructive coronary artery disease may cause angina. Angina may be treated by reducing aortic regurgitation, reduction of myocardial demand of revascularization of the myocardium. Clinical heart failure is treated with traditional therapy, including digitalis, diuretics, and ACEI. In severe heart failure, parenteral inotropic and vasodilator therapy may be needed.   


<div align="center">
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
|-
|-
Line 410: Line 414:
#Vasodilator therapy is not indicated for long-term therapy in symptomatic patients with either normal LV function or mild to moderate LV systolic dysfunction who are otherwise candidates for AVR. (Level of Evidence: C)
#Vasodilator therapy is not indicated for long-term therapy in symptomatic patients with either normal LV function or mild to moderate LV systolic dysfunction who are otherwise candidates for AVR. (Level of Evidence: C)
|}
|}
</div>


====Surgical treatment====
====Surgical treatment====
Line 419: Line 422:
Although the prosthetic valve replacement remains the standard for aortic valve regurgitation, aortic valve repair procedures are performed with a combination of different surgical techniques.  The quality of the cusps is essential for repair. The annulus and sinotubular junction can be surgically readapted to the cusps, eliminating the regurgitation.
Although the prosthetic valve replacement remains the standard for aortic valve regurgitation, aortic valve repair procedures are performed with a combination of different surgical techniques.  The quality of the cusps is essential for repair. The annulus and sinotubular junction can be surgically readapted to the cusps, eliminating the regurgitation.


<div align="center">
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
{| class="wikitable" border="1" cellpadding="0" cellspacing="0" width="80%"
|-
|-
Line 434: Line 436:
# An asymptomatic adolescent with chronic severe AR* with onset of ST depression or T-wave inversion over the left precordium on ECG at rest may be considered for aortic valve repair or replacement. (Level of Evidence: C)
# An asymptomatic adolescent with chronic severe AR* with onset of ST depression or T-wave inversion over the left precordium on ECG at rest may be considered for aortic valve repair or replacement. (Level of Evidence: C)
|}
|}
</div>


== Mitral Stenosis ==
== Mitral Stenosis ==
Line 646: Line 647:


==Pulmonary valve stenosis==
==Pulmonary valve stenosis==
{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="100%"
|-
|bgcolor="#FFFFFF" align="center"|[[Image:Pulmonary valve stenosis.svg|400px]]
|-
|'''The diagram shows a healthy heart and one suffering from Pulmonary valve stenosis.'''
|}
{| border="0" cellpadding="1" cellspacing="1" width="100%"
{| border="0" cellpadding="1" cellspacing="1" width="100%"
|-
|-
467

edits