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Treatment of aortic regurgitation

Aortic valve repair or aortic valve reconstruction is the reconstruction of both form and function of a dysfunctional aortic valve. Most frequently it is used for the treatment of aortic regurgitation. It can also become necessary for the treatment of aortic aneurysm, less frequently for congenital aortic stenosis.

The goal of the operation is the improvement of life expectancy and treatment of heart failure as the consequence of dysfunction of the aortic valve. The goal may also be to avert complications of the aorta (rupture or dissection) in the treatment of aneurysm. Repair is a more recent alternative to replacement; in many instances replacement will be the only realistic option because of severe destruction of the valve. While replacement of the aortic valve is a safe and reproducible procedure it may still be associated with the long term occurrence of so called valve related complications. The probability of these complications depends on the age of the patient and the type of operation. Typical complications are blood clot formation on the valve or dislodgment of thrombus (embolism); bleeding complications are commonly a consequence of "blood thinning" medication needed to prevent clots (anticoagulation). Biologic/tissue replacement valves have a tendency to degenerate, and there is also an increased risk of infections of valve prosthesis (prosthetic valve endocarditis). Compared to the results of valve replacement there will be a minimal tendency towards clot formation after aortic valve repair, and anticoagulation is commonly not necessary, thus minimizing the possibility of bleeding complications. The likelihood of infection of the repaired aortic valve is much lower compared to what is seen after aortic valve replacement. A repair procedure may not last forever, but in many instances the durability of an aortic valve repair will markedly exceed that of a biological prosthesis. are available. Using these parameters and a good transesophageal echocardiogram the precise mechanism of regurgitation can be determined in most cases.

Congenital aortic valve stenosis can be treated by aortic valve repair if there is no relevant calcification. The repair approach differs from commissurotomy mainly in that not only valve tissue is divided to improve opening, but also at least an additional commissure (suspension point of the valve) is created for the aortic valve. Thus, a bicuspid valve is created which results in near normal function of the aortic valve. The most reproducible concept is the creation of a bicuspid aortic valve with two normal commissures and two cusps. Tissue of the aortic valve is removed or detached from the aorta in places where it is clearly abnormal. The location of a second commissure of normal height is determined; using a patch or the original cusp tissue the cusps are then sutured to the aortic wall in order to create cusps of sufficient tissue and adequate form reaching the new commissure.

In tricuspid aortic valves the anatomy is principally normal; if there is an aneurysm of the ascending aorta the principles of aortic aneurysm will have to be applied. Without aneurysm, the cause of regurgitation is frequently stretching of one or two of the valve components (cusps). Such stretching can be combined with the presence of congenital tissue fenestrations. Additionally, enlargement of the aortic annulus can contribute to valve dysfunction. Shrinkage of the cusps is less frequent in industrial countries; this is currently not well treatable by repair. In surgical treatment, the extent of cusp stretching is exactly determined and then corrected by sutures. Enlargement of the annulus requires its size reduction and stabilization by an annuloplasty. In the case of annular dilatation, the annulus has to be reduced; currently, the largest experience exists with a strong suture that is placed around the annulus and tied to the desired size. Stretching is corrected by plicating sutures to the point that all cusps have a normal configuration. At the end of the operation, the cusp margins should be at an identical height.

In bicuspid aortic valve anatomy, there is congenital fusion of two cusps. This fused cusp is exposed to higher than normal stress and will stretch over time as a consequence. This results in aortic valve regurgitation. Annular enlargement is very frequent in this context, and it increases the tendency to leak. As a result of long standing dysfunction also the normal cusp may undergo deformation and stretch. In half of the affected individuals there is also an aneurysm of the ascending aorta which has to be treated appropriately. Since the bicuspid anatomy commonly has an almost normal valve function (unless deformed) it is left bicuspid; the repair procedure simply corrects the secondary deformations that led to regurgitation. Similar to tricuspid aortic valves, the cusps must be measured to rule out shrinkage. The annulus is commonly enlarged, it must be reduced and stabilized by an annuloplasty. Tissue redundancy through stretching is corrected by sutures.

The unicuspid aortic valve may not only result in relevant stenosis (narrowing), it may also primarily lead to regurgitation. In a proportion of the affected individuals, an aneurysm of the ascending aorta may be present which may need treatment as well. The repair procedure will change the configuration of the valve by creating at least one additional commissure. Commonly the unicuspid valve is changed into a bicuspid configuration; the resulting valve function will be close to normal. Cusp tissue is resected where it is grossly abnormal. Using patch tissue, the cusps are enlarged so they reach the second (new) commissure. If the annulus is enlarged it must be reduced and stabilized. In some cases a bicuspid configuration may be appropriate. In order to achieve this cusp, tissue is detached from the aorta and the valve is then brought into adequate form.

Contrary to valve replacement with mechanical prostheses inhibition of the blood clotting system (anticoagulation) is not necessary after aortic valve repair. Blood thinning may only be necessary if atrial fibrillation occurs or persists in order to prevent blood clot formation in the left atrium. Following aortic valve replacement, prophylactic administration of antibiotics is recommended for interventions involving mouth and throat (e. g. dental surgery). In those times, both surgeons and cardiologists had minimal information on the exact nature and severity of dysfunction of the aortic valve. This changed with the development of echocardiography by Inge Edler and Carl Hellmuth Hertz in the early 1950s. Nonetheless, the development of heart valve prostheses made replacement the standard approach because of its reproducibility. The first ball cage valve was implanted in 1961 by the American surgeons Albert Starr and Lowell Edwards, and in the next decades many mechanical and biological prostheses were developed and used. The positive results with the repair of the mitral valve stimulated surgeons in the 1980s and 1990s to develop surgical techniques that could be applied for the different causes of aortic regurgitation. Stepwise improvements were introduced in the subsequent years; today many regurgitant aortic valves can be treated by repair.