Generally, in immunocompetent adults, CMV infection is either asymptomatic or involves a typical disease course similar to a self-limited mononucleosis-like syndrome. The infection rarely causes severe complications of specific organs; however, acute gastrointestinal, cardiovascular, neurological, and/or liver disorders have been reported [1].
Evidence of cardiac events, particularly acute pericarditis or myocarditis due to CMV infection, is uncommon in immunocompetent patients without any associated risk factor [4]. Normally, these changes occur asymptomatically and, in most cases, are diagnosed as incidental findings during the typical course of mononucleosis-like syndrome [4, 5]. However, there may occasionally be serious complications associated with infection, such as cardiogenic shock, tamponed, or acute cardiac insufficiency [5].
The diagnosis of myocarditis is a constant challenge in medical practice because of high clinical variability and high risk of sudden death, which can progress to dilated cardiomyopathy in approximately 10 % of these patients [6]. Myocarditis is defined as inflammation of the heart muscle and may involve the myocytes, interstitium, vascular elements, and pericardium [6]. Infectious agents, especially viral agents, are the most important etiologic agents [7].
Owing to their risks and high costs, use of endomyocardial biopsies for making diagnoses remains controversial. The incremental diagnostic, prognostic, and therapeutic values of risks associated with such an invasive procedure must be evaluated. Particularly, such an evaluation must be conducted when the aetiology of myocarditis, based on positive results of CMV serological tests, is very strongly suspected. An excellent clinical outcome after ganciclovir therapy that included >100 % EF increase confirmed the initial diagnosis made by using a non-invasive test [8].
Enteroviruses are widely associated with myocarditis and dilated cardiomyopathy, and CMV has sporadically been implicated in this process. In a survey of etiologic agents in cases of ventricular dysfunction designated as “idiopathic,” expression of the CMV genome was detected in only 0.8 % of the cases [7].
In a study based on myocardial autopsy, the CMV DNA was found in 38 % of the patients with myocarditis as the death cause; in contrast, no CMV DNA was found in the control subjects. The authors suggested that an anti-viral therapy could be potentially effective for treating CMV infection in patients with severe acute myocarditis; our study findings are similar to that of this study. We observed an excellent clinical outcome after ganciclovir therapy [9].
The pathophysiology of viral myocarditis involves a complex process characterized by three distinct phases: infection of myocytes, production of toxins, and immune-mediated cytotoxicity. Thus, injury occurs because of the direct cytotoxic effect of the causative agent, the secondary immune response caused by the infectious agent, cytokine expression in the myocardium, and the aberrant induction of apoptosis. It is believed that the progression to dilation and contractile dysfunction occurs in a linear manner and that the manifestation of symptoms may occur at any of the three phases [6].
The prognosis appears to be favourable in patients who survive the initial critical phase. Certain studies have shown a 50–80 % chance of resolving dilated cardiomyopathy within the first 2 years of the clinical onset [6]. In the present case, satisfactory progress was seen that included the recovery of ventricular function and decreased dilation of the cardiac chambers.
Abnormalities based on liver function tests are often reported in immunocompetent adults with clinically significant primary CMV infection. The blood levels of transaminases frequently increase slightly or moderately; however, the levels rarely exceed five times the reference values; in addition, the alanine transaminase (ALT) levels are more affected than the aspartate transaminase (AST) levels are. Increase in ALP, GGT, and total bilirubin levels are uncommon [1].
In this case, minimal change was detected in the AST and ALT levels, whereas the GGT and ALP levels increased significantly, which was expected during viral infection. These findings led to a hypothesis of asymptomatic viral cholangitis with a self-limited course due to anti-viral therapy. These enzymes decreased during therapy, and the abdominal ultrasound examination performed during the patient follow-up revealed no signs of gallstones or liver changes.
Additionally, petechiae and ecchymotic spots were observed on the lower limbs, which had appeared during the course of infection and disappeared a few days after the completion of the drug therapy. This trend suggested the possible evolution of infectious purpura fulminans caused by CMV infection. Vascular involvement by CMV has been reported; this virus induces vascular changes and triggers a cascade of events that can generate perivascular inflammation and even thrombosis [10].
The role of anti-viral therapy in the management of visceral diseases caused by CMV in immunocompromised patients, particularly transplant recipients, has been well established. However, the use of these agents in immunocompetent individuals is not well established, and no definitive conclusion has been established regarding their indication [4]. Nevertheless, several studies indicate the benefits of using anti-viral therapy, particularly during the acute phase of viral infection and in severe cases [6].
In the present case, the acute nature of the viral infection and the severity of the clinical situation prompted us specifically to provide ganciclovir therapy. The outcome was favourable and included the resolution of symptoms and a marked improvement of the cardiac, respiratory, and liver manifestations after specific anti-viral therapy.
