Valvular Disease from a Clinical Perspective

What are we going to cover?

1. Anatomy of the valves
2. General aspects of Valvular Disease (Most important part

Will go over generalities that can be applied to all diseases.

3. Specific valvular diseases.

 So now onto the anatomy

There are left side valves (mitral and aortic), which are under higher pressure, about 120 mmHg systolic, and right side valves (pulmonic and tricuspid), which are under lower pressure about 20 mmHg at systole.  So the ratio is about 5:1 or 6:1.

 The two “inlet” valves are the mitral and the tricuspid as illustrated by Netter.  He was an American surgeon and Belleview Hospital, until he was discovered to be a better illustrator than a surgeon.  So now he is our God of Anatomy.

But the “bread and butter” study is a 2D image of the human heart.   Its perty.

Now we talk about the exit valves, the pulmonic and aortic valve.  They are actually anatomically indistinguishable, except for the presence or absence of the coronary arteries, which originate at the sides of the leaflets of the aortic valve. 

This image is not correct, the valves are at 90º from each other.
 

Now we move onto the general aspects of valvular disease.

• In general there are 2 types
  • Stenosis-inability of a valve to open completely
  • Regurgitation (insufficiency)-improper closure of a cardiac valve.
• Both problems impose an increased load onto the UPSTEAM chamber, for example, mitral stenosis will affect the left atria.

So how do we study the valves?

• Echo cardiography-can be done transthoracic, or transesophageal (the patient swallows the camera and the images are taken from inside the body.
• Cardiac Catheter-venous or arterial access lets us put catheters into the chambers of the heart and pressures can be measured. 
  • The importance of pressure differences will be discussed later. 
  • Also, we can inject radiographic, iodine containing dyes, and then a series of x-rays will be taken. 
  • It can show the dye going into improper chambers, such as dye injected into the left ventricle, going into the left atria with mitral valve regurgitation. 
• Pathoanatomy-we can take surgical samples or done on autopsy. 

  
   

  • Here is a diseased heart valve (had endocarditis), but this person is still alive and has a replacement valve. 
     

So what about valvular stenosis?

• As mentioned before, this is the narrowing of the valvular orifice which creates impeded antegrade flow. 
• So the body compensates by increasing pressure to increase antegrade flow. 
• But you get a pressure overload in the upstream chamber. 
• So how do you access how serious it is? 
  • Look at valve area, the less the area, the more stenosis. 
  • Also, look at the pressure difference, the higher the difference, the more severe the stenosis. 
  • Normally there should be almost no pressure difference. 
• Also, we can look at the anatomical changes in the upstream chamber.
• These aspects apply to all stenotic valves.

So we talked about normal valves for cross sectional area, so what are the normal cross sectional areas?

• Aortic-2-4 cm², about the size of a nickel  Severe stenosis is less than .8 cm3 (loss of ¾ of area)
  • The severe stenosis will cause a pressure gradient of over 50 mmHg
• Mitral valve-4-6cm², about the size of a quarter.  Severe stenosis is about 1.0 cm2 (loss of over 75% of area)
  • Severe stenosis will cause a pressure gradient of over 10 mmHg.
• Mitral stenosis-you will see left atrial dilatation (normally dilation, not hypertrophy happens in atria)
• Aortic stenosis-you will see left ventricular hypertrophy.
  • Also, you will see the effects propagated upstream, as the atria now has to pump against a stronger left ventricle, so you will also see left atrial dilatation in aortic stenosis.

Now we go to valvular regurgitation

• Causes unimpeded retrograde flow
• Then causes a volume overload of the upstream chamber (constrast to stenosis which is pressure overload of upstream chamber)
• This leads to increased compliance of the upsteam chamber and dilatation of the upstream chamber. 
• So how do we access this?
  • How big the opening is when the valve is regurgitating.
  • How much volume goes back through the valve
  • The anatomical changes in the valve.

So how much blood is ejected from the heart into circulation?

• 70 mL (70cc), not much at all, only 1/3 of a can of coke.
• If you have regurgitation, you might eject up to 140 mL.
• 70 will go out into circulation, then the other 70 regurgitates back into the ventricle. 
• So this will cause the heart to have more blood in it (increased preload) and cause dilation to compensate for the extra volume.
• Dr. Saric mentioned that you get dilatation of both ventricle and atria with either aortic or mitral valve regurge. 
• Another complication that can happen from either is as you get upstream changes, it can cause pulmonary edema, due to a backup of blood into the pulmonary circulation, and this will cause shortness of breath in these patients.

So how do we treat them?

Well a damaged valve, either stenotic or insufficient can get infected (endocarditis)

It is a 3 stage process

1. Valve damage
2. Thrombus formation
3. Superinfection with microorganism (normally bacteria, but sometimes fungus, causing infectious endocarditis)

• If you stop it at stage 2, before infection, in someone with a chronic wasting disease, like cancer, it is called Marantic endocarditis.
• If it is stopped there in an immunological disease, like lupus, it is called Libman-Sacks disease
   

So how do you prevent stage 3? 

• By prophylaxis antibiotics
• People with diseases are normally given antibiotics for many procedures, most commonly teeth cleaning or a dental procedure.
• The most common antibiotic used is amoxicillin

So what about the disease itself, the valve problem?

• Unless symptomatic, stenosis is not treated.
  • The risks of the treatment are just as problematic as the problem in its current state.
• Regurtitant valves may be treated even before they become symptomatic to try to preserve LV function, but normally onliy is the regurgitation gets pretty bad

So what about the role of severity in these lesions?

• Well normally valvular lesions are not symptomatic unless severe.
• And the lesions are not treated unless severe, so therefore, they are not treated unless symptomatic (our original point).
• So while, we may give prophylactic therapy, we will generally not do much to the valve itself.

But if we do decide to do something, what treatments do we have?

• Most medical treatment is palliative and treats symptoms but it in principle does not improve survival.
• For stenosis, we treat if it is symptomatic.
  • For mitral stenosis we give medical therapy: diuretics and heart rate controlling agents, or we can do surgery is severe enough.
  • For aortic stenosis, we have no medical therapy and refer to surgery.
• For regurgitations, treat only if it is severe
  • For a mitral regurgitation, we have no medical therapy and send them directly to surgery.
  • For aortic regurgitation, we can give them vasodilators (nifedipine) which can delay the surgery, but eventually they will need surgery to correct the problem
     

So what surgical treatments do we have?

• We can do balloon valvuloplasty
  • We take the catheter we talked about before and instead now put a balloon which we can then inflate at the valve to “crack it open.”  This works very well for stenotic valves and is often done in pregnant women who have mitral stenosis
  • Remember, this is still considered an invasive procedure, but is much less invasive than an open surgery.
• We can also do valvular repair.
  • In this case, we can put in an anuloplasty ring, as seen below. It can be used to tighten a loose, floppy valve.

  
   

• We also have valvular replacement.
  • There are 2 types of valves we can put in.
  • The 1^st is a bioprosthetic valve.
  • Most commonly we use the porcine valve.  It is from a pig, normally the aortic valve.  It is sown in, with the coronary arteries attached onto it, so it functions like the normal healthy human valve.  It is used for both the aortic and mitral valve.  This makes sense with the aortic valve, but since we do not have a natural replacement for the mitral valve right now, we just invert the aortic valve, and sow it in.  These valves last for about 10-15 years and also (this is from small group from IHR) you do not need to take anticoagulants to have it.
  • The other valve is a mechanical valve (like the one seen in lab).
  • It is normally made from polycarbonate and you sow it in, just like the bioprosthetic for either the aortic or mitral.  They give a little click when auscultated on a heart exam. These can last forever but (again from small group IHR) you need to take anticoagulants chronically to have one, which makes you a borderline hemophiliac.  The esteemed governor of California has one in his heart.

  And some words about mortality

  Due to advanced studies and techniques, valvular disease mortality is extremely low, but ischemic heart disease is very high still.

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