Asymmetrical septal hypertrophy and anterior motion of mitral valve.

[aspiringmd1015]

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can someone explain the anterior motion of the mitral valve. on wiki, they kinda confused me with adding the venturi effect, with some high pressure low pressure stuff. help!

 

[Instatewaiter]

can someone explain the anterior motion of the mitral valve. on wiki, they kinda confused me with adding the venturi effect, with some high pressure low pressure stuff. help!

There are a couple mechanisms- one is that there is an abnormal insertion of the papillary muscle others are reduntant tissue. One way or another, there is abnormal motion of the mitral valve.

Normally, during systole, the mitral valve does not move toward the septum. This allows the LV to eject blood through the LVOT and then the aortic valve. However, when there is SAM, the anterior leaflet (most commonly) contacts the septum (or comes close) and creates a stenotic area which causes LVOT obstruction and restricts ejection of blood from the LV.

SAM is most commonly seen in HoCM and so there is also hypertrophy of the septum. This too narrows the LVOT making the systolic anteiror motion of the mitral valve in HoCM more deleterious. Thus you have a narrowed LVOT already in HoCM and then you have abnormal motion of the mitral valve which narrows the LVOT in a dynamic fashion and causes dynamic LVOT obstruction.

 

[Daitong]

So in the text it states that:

• Increased after load due to LVOT leads to worsening diastolic dysfunction
• Incr LA and pulm venous pressure leads to worsening pulm vascular congestion

But why would this happen? What would afterload have to do with ventricular filling or pulm congestion? Is it due to the higher filling pressures required during filling? But why would something that occurs during diastole affect something that happens during systole (LVOT)?

 

[Instatewaiter]

So in the text it states that:

• Increased after load due to LVOT leads to worsening diastolic dysfunction
• Incr LA and pulm venous pressure leads to worsening pulm vascular congestion

But why would this happen? What would afterload have to do with ventricular filling or pulm congestion? Is it due to the higher filling pressures required during filling? But why would something that occurs during diastole affect something that happens during systole (LVOT)?

The diastolic dysfunction is from a number of things. First the myocyte disarray prevents normal relaxation. Second the LVOT obstruction, just like AS, will cause some hypertrophy. This subsequently causes a stiffer ventricle and diastolic dysfunction. This in turn causes LAP and pulmonary edema.

Increased afterload is almost always associated with pulmonary congestion. When someone with systolic heart failure comes in with pulmonary edema, the treatment is diuretic and AFTERLOAD reduction. Hell this is the mechanism of flash pulmonary edema- afterload goes up, fluid backs up into the lungs. So the pulmonary edema in HoCM is due to the underlying diastolic dysfunction AND the problem with ejection d/t LVOT obstruction.