Cardiomyopathy and Myocarditis
- Notes from European Society of Cardiology Congress, 2008
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Notes from the European SOciety of Cardiology Congress, 2008
Myocarditis- ESC 2008
Review
Myocarditis can be due to:
- infection- viral and non-viral
- allergens
- autoimmune reactions
- drugs and toxins
Manifestations vary. But note 10% of SCD in young persons has been
found to be due to myocarditis.
Classification: could on basis of etiology, on temporal pattern (acute
fulminant, acute, chronic etc), on histological appearances.
Note the Dallas criteria for myocarditis do have limitations esp since
have better immunohistology and PCR.
European Heart J 2007;28:1326- histology can influence prognosis, those
that are PCR positive for virus have a worse prognosis.
Note not all with virus in myocardium actually get myocarditis. In
those with myocarditis, genetic susceptibility can influence prognosis.
review in Euro Heart J 2008, Dennert R et al
sensitivity of biopsy will increase if use CMR guided biopsy in area of
Gd enhancement.
serological evidence for viral infection is not sensitive at all, need
PCR on myocardial biopsy.
Role of Echo in diagnosis of myocarditis
Good review of available information. Yield of biopsy varies in
studies.
May see wall motion abnormalities, increased wall thickness due to
odema, systolic and diastolic dysfunction, increased sphericity of the
LV and increased LV volume.
CMR in myocarditis
May see evidence for odema on CMR but this is not always associated
with regional wall motion abnormality ie systolic function of the
affected segment may be normal or severely impaired.
Late enhancement with Gadolinium- what does this signify in the acute setting?
Possible capillary leakage and not myocardial injury. The degree of
enhancement decreases with time. There is some published data on the
value of CMR guided biopsy in myocaditis- presented a case in which
there was no RV enhancement but instead there was enhancement of the
lateral wall and it is likely that LV biopsy in this setting would be
required.
CMR in not always positive in terms of late enhancement- so still
consider myocardial biopsy if clinical suspicion is high.
Experimental anti-viral therapy
- Not much data on immunoglobulins
- Interferon may have a role in some instances with viral
persistence and with a TH2 cytokine pattern.
- Ganciclovir/Foscavir for HHV6 virus infection
Some say parvovirus affects the posterolateral wall most- the mechanism
behind this is not known- one speaker did dispute this finding and
thinks this pattern will not be reproducible. Note other infections are
also said to be more likely to show enhancement of the posterolateral
wall.
Borrelia is endemic in Germany and can cause myocarditis.
The role of inflammation and viral persistence
There is no correlation between symptoms and viral persistence.
Immunohistology is important- can not rely on histology alone.
Kuhl et
in Circulation report on viral persistence-
State that 40-60% of cases of acute myocarditis or dilated
cardiomyopathy will have evidence of viral presence with PCR. The type
of viruses found in acute myocarditis and dilated cardiomyopathy is
also the same ie found in similar frequency and this strongly suggests
that the dilated cardiomyopathy in these instances is due to viral
infection.
If perform serial biopsies will find that those that clear the virus
are the ones that show improvement of ejection fraction.
Coxsackie virus is found within myocardial cells and parvovirus is
found in endothelial cells. This author said to those with viral
persistence do not respond to immunosuppression- some will actually get
worse with this treatment. Immunosuppression may have role in those
with evidence of inflammation and with viral persistence.
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