Valvular Heart Disease: Difference between revisions

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.

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!Aortic stenosis severity

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.  

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!Current Guidelines  

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.  

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|'''The current 4 different approaches are:'''

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.  

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!Causes of chronic aortic regurgitation 

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.   

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!Current Guidelines: Medical treatment of Aortic 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.

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!Current Guidelines