Let's talk about non-infectious causes of endocarditis.
So, there is nonbacterial thrombotic endocarditis or NBTE.
Bad name because this is not endocarditis.
This is not -itis of the endocardium.
This is not inflammation of the endocardium.
And yet, the term persists, and so we just have to live with
The point about this is it's nonbacterial, it's nonfungal,
it is a thrombotic diathesis.
It is a predisposition to being hypercoagulable.
And in that setting, the valves, which are opening and
and have local areas of turbulence and have local areas of
because they're slapping up against each other, will, in a
develop little, tiny thrombi along the lines of closure.
That's the NBTE.
It's also called marantic endocarditis.
It comes from the root word marasmus relating to
and one of the causes of NBTE can be malnutrition with
These are sterile. Can't emphasize that enough, sterile
that deposit on the leaflets of the cardiac valves,
and most commonly, it's going to affect the mitral valve,
secondarily will affect the aortic valve,
and thirdly, will affect the tricuspid valve. It rarely
affects the pulmonic valve.
It occurs with hypercoagulable states.
So, anything that will lead to hypercoagulability.
Malignancy, pregnancy, oral contraception, and thrombophilic
the tendency to be hypercoagulable
because you don't make anticoagulants quite so well
or you make too much of the pro-coagulant factors.
The little bullet point there is really important.
These valvular lesions are loosely attached to the
They actually don't cause any damage.
They don't cause any injury to the valve, but they're
loosely attached, and they can embolize.
So, they can cause embolic disease throughout the body.
So, they're non-destructive, there's no inflammatory
But their size and the fact there are a lot of them
and they're on a valve that's flapping in the breeze 60, 70
times a minute,
they do tend to embolize and fragment,
and they can go to the brain causing stroke they can go to
to the coronary arteries causing a myocardial infarct.
It can go to systemic organs causing a renal infarct or what
A slightly different version of this, a different kind of
is due to immune complex deposition, and particularly in the
setting of lupus.
So, we can get the same sort of disease any time you get
immune complex deposition,
but SLE, systemic lupus erythematosus is most common.
When we see it in the setting of lupus, we refer to this as
And it's due to immune complex deposition.
So, we've talked about immune complex deposition that can
cause other valvular abnormalities.
Now, this is just an example with lupus.
Location of vegetations, they can be on the mural
endocardium of the atrium,
both side of the valve leaflets, they can be on the chordae,
they can be on the ventrical wall.
So, they can be wherever they want to attach,
and those valvular immune complexes then will activate
and recruit and activate Ets-1 receptor bearing cells.
So, because of the inflammation that occurs, you can get
They become scarred and you then will tend to get stenosis.
One entity that we need to be aware of, although it's a rare
is carcinoid valvular disease or carcinoid heart disease.
So, what is carcinoid? So, carcinoid is a slow-growing
indolent tumor neuroendocrine cells.
Those cells can cause a systemic disorder by virtue of their
elaboration of a variety of mediators,
including serotonin, bradykinin, and others.
Those mediators cause systemic syndrome, carcinoid syndrome,
that's characterized by flushing, it's a facial flushing,
bright red, diarrhea, dermatitis, and bronchoconstriction
that kind of mimics asthma.
And it is caused by the bioactive compounds.
And although we say that serotonin can be causal, that's has
not been proven.
In carcinoid heart disease, the final kind of manifestation
of carcinoid syndrome,
those same mediators that are causing all those other
flushing, diarrhea, dermatitis, bronchoconstriction,
can act on the endothelial cells and the smooth muscle cells
that sit beneath them,
and induce smooth muscle cell proliferation and matrix
So, in the heart, the way that this plays out is that we get
valvular disease for the most part.
Carcinoid heart disease really can't happen
unless we have massive hepatic disease, massive hepatic
Because typical carcinoid in the GI tract,
whatever mediators are being developed or secreted
are metabolites going through the liver and nothing happens
They're metabolized to go away.
But if you have massive hepatic metastases of this carcinoid
then it can dump its contents directly into the hepatic
vein, into the inferior vena cava,
and the first endocardium or valves that it will touch are
going to be on the right side of the heart.
So, in massive hepatic metastases, you can get this disease.
The mediators, again, include serotonin, bradykinin,
substance P, there are a whole variety.
We don't yet know exactly which one is causal for giving
rise to the valvular disease.
But what will happen is in the right side of the heart,
typically, in these patients because that's the first
endocardium that is encountered,
you will get thickening of the valves,
and the major manifestation is going to be tricuspid
So, the valve won't close because it's so stiff.
And pulmonic stenosis, it won't open because it's so stiff.
So, it's tricuspid insufficiency pulmonic stenosis.
And this is one of the few diseases that actually affects
the pulmonic valve
more than the mitral valve, interestingly enough.
The left side of the heart is usually spared
because whatever those mediators are, as they go through the
lungs, they get metabolized.
So, they're sparing of all the structures in the left side
of the heart.
There are exceptions, however.
So, if you have an atrial septal defect or a ventricular
and you have right to left flow, that will allow the same
to get onto the left-sided valves. Or if you have a primary
which does happen, that tumor can directly secrete its
contents into the pulmonary veins,
which will then hit predominantly the left side of the
So, it's just an interesting entity.