DISCUSSION
We hypothesize a chronic CMV infection leading to endothelial
dysfunction and a procoagulant state followed by reactivation leading to
acute occlusion and cardiotoxicity. It is postulated that CMV infection
induces the progression of atherosclerosis in CAD. A meta-analysis of 55
studies showed individuals with positive CMV IgM antibody by
enzyme-linked immunosorbent assay or positive PCR were 1.67 times more
likely to develop CAD, especially in Asian population.8 In a study of 105 patients who underwent coronary
artery bypass grafting surgical interventions, Izadi et al reported that
about 26% of these patients had positive testing of CMV-PCR in the
coronary artery plaques, the patients who had positive family history of
CAD or has suffered from acute coronary syndrome (ACS) before were more
likely to have positive CMV-PCR with statistical significance.9 The mechanism of this relation is still not fully
understood, but it was proposed that CMV can alter the cellular signal
transduction of second messengers to alter cellular functions.10 It also enhances the proliferation of smooth muscle
cell which might contributes to the etiology of CAD. Furthermore, CMV
infection can temporarily increase the level of anti-phospholipid
antibodies, thus increasing the risk of acute thrombosis.11
CMV can affect immune competent individuals with a variety of severe
clinical syndromes. While many case reports of CMV hepatitis, myelitis,
colitis and myo-pericarditis were described, 12 but to
the best of our knowledge, no reported case describing a young
immune-competent individual presenting with ACS possibly attributed to
CMV infection, and without known risk factors of CAD, has been described
previously.
Our patient’s coronary angiography showed a complete LAD coronary artery
occlusion which leads to the cascade of events. Although it is reported
that acute CMV infection is associated with acute thrombosis, most
common thrombosis sites, according to a meta-analysis, were deep vein
thrombosis/pulmonary embolism in immune compromised patients and
splanchnic vein thrombosis and splenic infarction in immune competent
individuals. 13 Considering the elevated IgG and IgM
CMV-antibodies in our patient, we propose a chronic CMV infection
leading to atherosclerosis followed by reactivation leading to acute
occlusion and myocardial infarction.
It is noteworthy that the histopathological examination of our patient’
resected colon segment showed active CMV colitis. Also of mark that the
patient’s liver enzymes were elevated on initial presentation even
before the cardiac arrest and didn’t improve till ganciclovir treatment
started which is against ischemic hepatitis and suggests probable CMV
hepatitis.
A wide panel of investigations to reveal if the patient was
immunocompromised were conducted, all of which reported back
unremarkable except for the positive ANA panel which its titer improved
after antiviral therapy. The patient had no other clinical or laboratory
features suggestive of systemic lupus erythematosus or any other
auto-immune diseases. Possible explanations of this finding include CMV
direct damage to endothelial cells and molecular mimicry, inducing
autoantibodies’ production. 14,15