CARDIOVASCULAR JOURNAL OF AFRICA • Vol 24, No 6, July 2013
200
AFRICA
One weakness of the study is that a few putative cardiotropic
viruses, such as human herpes virus 6, hepatitis C and
varicella virus, were not tested. If the cardiotropic virus panel
investigated in this study had been more complete, the presence
of cardiotropic viruses among the patients in this study may
have been even higher than reported. Another weakness, as the
authors rightly point out, is the small sample size, which limits
the generalisability of the findings in this study.
Observations by Towbin
et al
.
11
in children who underwent
heart transplantation revealed that the presence of viral genomes
in the allograft heart predicts a subsequent risk of allograft
rejection. In the setting of HIV-associated cardiomyopathy where
viral infection is also present in immunocompromised hosts,
there may be a similar risk of progressive cardiomyopathy and
end-stage heart failure as a result of viral co-infections. The
hypothesis that opportunistic viral infection leads to end-stage
cardiomyopathy in patients with untreated HIV could be tested in
a prospective observational study performed in locations where
HAART is currently not available.
There are a number of unmeasured variables that may
have contributed to the development of cardiomyopathy and
myocarditis in the populations assessed in Shaboodien’s study,
including exposure to heavy metals and malnutrition. Exposure
to low doses of mercury has been shown to increase chronic
myocarditis and DCM in a murine model.
12
Deficiencies of
trace elements such as copper and selenium result in increased
oxidative stress and foster active virus replication, while
malnutrition results in increased oxidative stress as well as
increased virulence of cardiotropic viruses. Any of these factors
could contribute to a higher rate of myocarditis or viral infection
among the patients included in the current study.
Myocarditis is not infrequently associated with other
immunocompromised states such as rheumatological and
inflammatory bowel diseases. Usually the pathogenesis is
assumed to be related to epitope spreading or molecular mimicry
from the original inflammatory response and the treatment is
therefore augmented immunosuppression. However, there are no
outcome data regarding the benefit of such a strategy, and the
role of viral infection in the cardiomyopathies associated with
these disorders has yet to be explored.
Shaboodien and co-workers’ observations on the association
of viral genomes, myocarditis and cardiomyopathy should be
extended to include longer term outcome data such as risk of
death and recurrent heart failure in their population. We still
do not know whether the cardiomyopathy associated with
untreated HIV will improve with antiretroviral therapy. As
antiretroviral agents are most likely now available to this cohort,
the impact of these medications on left ventricular function,
inflammation and infection should be prospectively assessed.
In addition, an investigation of the cardiovascular effects of
treating opportunistic viral infections in patients with established
HIV-associated cardiomyopathy is warranted.
LORI A BLAUWET, MD,
LESLIE T COOPER (jun), MD
Division of Cardiovascular Diseases, Mayo Clinic, Rochester,
USA
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