Any experienced Echocardiographer who has been around since the Eighties (old aren’t we?), knows that just about every female with a murmur back in those olden days was almost automatically diagnosed with MVP. Therefore, you probably spend some amount of time with adult female patients who come into your lab with an old diagnosis of MVP. Upon examination however, you usually find no evidence of MVP.
Well, why is this?
When these patients come into my lab, I always have to tell them the (short version) history of MVP and why they are not likely to be diagnosed with it now in preparation for the cardiologist who will tell them they no longer have MVP.
In the pre-historic days of echocardiography, the experts claimed that up to one third of the population, especially females, had MVP. Nowadays, after a trillion hours of research and especially with the advent of 3D technology, there is really only about a 3% rate of “true†MVP.
Mitral valve prolapse is actually a congenital heart defect, very often associated with Marfans syndrome, but there is also an acquired form of this defect. It is often familial, and is highly associated to a defect in chromosome 16.
Further, a highly experienced adult and pediatric echo tech will find that MVP is extremely rare in neonates, more often found in young adults, but seems to almost disappear in the elderly population. Isn’t that strange? I have pondered that question often.
I only diagnose MVP in those people who have the truly congenital form in which the valve is myxomatous, and either the anterior or posterior leaflet is an almost “flail†in appearance, with moderate to severe mitral regurgitation (MR). The MR is usually aberrant, going off in either a posterior or anterior direction depending on which leaflet is involved.
If the posterior leaflet is involved, the MR will be anterior, and if the anterior leaflet is involved (most common) the MR will be posteriorly directed.
The acquired form develops after years of stress on the MV annulus wherein it can develop high of low spots in its anatomy, which will cause the leaflets to coapt incorrectly. Hence, this type is not seen in neonates, develops in adolescence but can also go away with time.
Another type of acquired MVP can develop as a result of a ruptured chordae, or in the case of a myocardial infarction the papillary muscle may be damaged.
There is another type of MV abnormality that should be discussed, and one that every echo tech has seen, but is not usually considered MVP.
This type is often seen in tall, thin, long boned “gangly†type of people, especially young women, in which the anterior leaflet presents as a long, stiff, hinge like anterior MV leaflet with a small posterior leaflet. This is not MVP, but it is a kind of anomaly that every echocardiographer has noticed.
If one does have “true†MVP, it is generally corrected surgically. A new mitral valve is generally not recommended unless the valve is a lost cause.
Ken Heiden RDCS