Continuing our discussion of cardiovascular infections, we turn now to myocarditis.
Myocarditis is a clinical syndrome due to myocardial injury and inflammation. It can be caused
by a wide variety of infectious microorganisms. I’m showing you sort of the end stage
of a dilated cardiomyopathy. This is caused in about 10% of the cases by viruses.
So, this is what you would expect in patients who don’t recover from viral myocarditis.
The incidence of myocarditis is uncertain but the disease certainly is rare. It’s very difficult
to make a specific microbiological diagnosis for the same reason that viruses, many viruses
can do this and figuring out which virus did it is very, very difficult. Viral cultures are not often done.
It’s just a difficult problem. Males are affected more than females. It actually is the most common
cause of unexpected exercise-related death in the US air force recruits. So, that’s still going to be rare.
Unexpected death in a recruit is rare. But that’s where viral myocarditis explains many of the cases.
So, if you take home the message that viruses most commonly do this and there’s an entire
laundry list of them. There’s enteroviruses, adenovirus, parvovirus B 19, human herpesvirus 6,
dengue viruses, cytomegalovirus, coxsackie virus which is notorious, poliovirus, and even HIV
has been associated with myocarditis. Unfortunately, there’s not very much that we can do
about viral myocarditis except to support the patient. Bacterial infections are only occasionally
associated with myocarditis and usually result from either bacteremia, direct extension
from a contiguous focus say, in the lung or mediastinum somewhere, or from the effects
of a bacterial toxin. The leading parasite to cause this problem is Trypanosoma cruzi which causes
what we call Chagas disease. There are a variety of miscellaneous noninfectious causes
such as chemotherapy for cancer, a variety of drugs. Ethanol, unfortunately is still a pretty common
cause of dilated cardiomyopathy, allergic reactions, post-transplant rejection explains a fair amount
of this problem in cardiac transplants, and autoimmune diseases. In discussing the pathogenesis,
I’m showing you essentially two panels. On the left, you see the effects of viral myocarditis.
I think you can see the myocardial cells are infiltrated with enumerable round cells, both lymphocytes
of the T cell variety and B cell variety. It is these cells which injure the cardiac myocytes.
On the right panel, you’re looking at the infiltration of the parasite into the myocardial fibers.
These are the amastigotes of Trypanosoma cruzi causing a similar process as viral myocarditis.
First of all, the pathogenesis would involve invasion of the myocardium from the bloodstream
by the virus or by a toxin and direct myocyte death from viral damage itself from cytolytic T cells
or from apoptosis. As part of the immune system process, you end up with decreased regulatory
T cell function, activation of cytolytic T cells, and an increased influx of Th1 and Th2 cytokines.
The cytokines actually further damage the cells. Moreover, the antigen-presenting cells
stimulate a pathogenic response from T cells and antibodies so the pathogens may cross react
with endogenous epitopes. You get epitopes spreading between endogenous myocardial epitopes.
So, you can either resolve the infection and clear the virus and down regulate the immune response
or alternatively, you have ongoing injury because you have persistent viral infection
or you’ve got a damaging immune response. So, it’s hard to distinguish whether the virus is still active
or whether it’s the immune system that’s further damaging the cardiac myocytes.