Hi Doctor!
Hi Doctor!
OK, you mentioned, that you have aortic regurgitation (AR). You poste in the bicuspid valve section, so I understand, that you are a bicuspid valver. You have a stable aortic root dilation, which haven't changed for about 10 years. Since you don't have a progression in the root diameter (usually measured at the sinuses of valsalva), they will probably not put you under the knife. Currently, the aortic root sizes are indexed for the body surface area, so I am sure your cardiologists assume that and they are looking after it. Normaly, a healthy root (at the S. Vals.) is meaured between 20-37 mm. However, those numbers mean nothing, since there is the BSA/AoRo index.
Aortic regurgitation in the BAV valvers is commonly caused by a root dilation. Often, a change in the diameter and shape of the sinotubular junction may pull the valves comissures/leaflets to the point where they can not coapt well (insuficient closure). However, a dilatation in the S.Vals. doesn't nessecery means a STJ dilatation. It means more commonly an aortic annulus dilatation - the result of it is regurgitation. Regurgitation may also be caused by a leaflet restriction, when a fibrous thickening occures in result of the altered haemodynamics of the valve (you know, that if you are BAV, your valve has worked inproperly since your first heart beat). The aortic regurgitation is usually scaled from 0+ (trace reg.) to the great 4+ (where the valve almost doesn't close). Actualy, a reg. scaled at 2+, as yours is called "moderate" and is very well tolerated by the myocardium with different mechanisms, called cardiac reserve.
One of these mechanisms is eccentric hypertrophy (by aortic stenosis it is concentric). Then your heart muscle becomes thickener (stiffer) to take the overload of the regurgitant volume.
Even if the regurgitation becomes more severe and hit the 3 -> 3+, your myocardium still may have the tolerance. However with the time, the extra blood volume will make it "tired" and slowly it's abbility to pump sufficient all the blood will begin to fall down. Years ago, a surgery was admitted, when the ejection fraction falls under 46-49%. Nowadays, the echocardiography follows quite different values of the hearts work, like intramyocardial velocities, fibre-shortening, fractional shortening... and surgery may be warranted at an earlier stage, to prevent a myocardial damage.
As for the mitral valve prolapse. It is a common finding in hearts with very-long lasting regurgitation. The AR jet strikes thousend times a day the anterior mitral leaflet (AML) and its chordaes taendinae. Sometimes, depending on the jet shape and velocity, it causes damage of the leaflets/chordaes tissue, making it fibrous-thickened, elongating the chordaes (making them thinner) and as a result a prolapse of the AML appears besides the fluttering.
Sometimes, the bicuspid aortic valve is associated with a disorder of the connective tissue. However a culprit gene has not been found, so there may be a faulty gene-transcription, which in some patients may cause some more systemic signs of connective tissue disorder.
The mystery of the BAV disease is still very unclear. However some things are already known: from the genetics point of view BAV may be primary to deffective valvular genesis, or secondary to another cardio-disorder. Both have been found to have a percent of hereditarity: for the BAV, it is estimated about 10-30%, with an autosomal dominant (with reduced penetrance) pattern of inheritance in the familial cases.
Current hypotheses put 2 directions for researches of the appearance of a BAV: one is the genetic disorder, causing also the vascular effects of the disease, and the second is the haemodynamical. the second researches the hydraulic and mechanical forces, found in the valves with tho leaflets, and its effect on the aortic walls and structures.
I hope, I was clear with my "east european english"!
Best wishes,
Ivo
