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