Pericarditis caused by herpes zoster

Abstract

Infection with the varicella zoster virus (VZV) causes two distinct clinical syndromes, varicella and herpes zoster. Primary infection with VZV results in varicella, characterized by viremia with a diffuse rash and seeding of multiple sensory ganglia, where the virus establishes lifelong latency. Endogenous reactivation of latent VZV typically results in a localized skin infection known as herpes zoster. VZV may cause various complications such as secondary bacterial infection, pneumonia, acute cerebellar ataxia, meningitis, encephalitis, and Reye syndrome [1,2]. In contrast, the occurrence of myopericarditis is extremely rare [2]. The occurrence of concurrent myopericarditis with herpes zoster, as in the present case, is extremely rare [3-5]. This article describes a case of pericarditis caused by herpes zoster. Case report We report the case of a 53-year-old immunocompetent male who developed pericarditis caused by herpes zoster. The patient had no particular past history except for varicella in his childhood. Six hours prior to consultation, the patient suddenly noticed chest pain at rest without physical disorders before chest pain developed. At the time of consultation, the patient had a blood pressure of 134/92 mmHg, heart rate of 110 beats per minute, and body temperature of 37.6 C. There was no paradoxical pulse observed. Heart sounds were slightly distant and muffled with no sound of pericardial friction. The jugular venous distension was not observed, and there was no edema of the legs. No rash was observed on the body surface. However, the chest pain persisted. The 12-lead electrocardiography (ECG) revealed concave upward ST segment elevation in the leads of I, II, aVL, aVF, and V1-6 without mirror-image changes and PR segment depression (Fig. 1A). Blood tests revealed a white blood cell count of 11.5 Â 10 3 /mL [normal range (NR), 3.6-8.7 Â 103/mL] and C-reactive protein (CRP) of 1.27 mg/dL (NR, 0.00-0.17 mg/dL) both of which were slightly elevated. Myocardial enzyme was normal with the creatine kinase/ creatine kinase-myocardial band level of 158/80 IU/L (NR, 110-318/ 0-12 IU/L) and troponin I level of 0.02 ng/mL (NR, 0.00-0.04 ng/ mL). Renal function was normal with a creatinine level of 0.78 mg/ dL (NR, 0.65-1.07 mg/dL). The human immunodeficiency virus antibody (types 1, 2) and antigen (type p24) evaluated by chemiluminescent enzyme immunoassay test were negative (NR, negative). Transthoracic echocardiography (TTE) revealed left ventricular ejection fraction of 67%, indicating normal left

Transient constrictive pericarditis following coxsackievirus A4 infection as a rare cause of acute mediastinitis: A case report

“…Thus, routine viral serology is not currently recommended for cases of suspected pericarditis [ 33 ]. However, given that serological virus antibody titers usually increase 4-fold or more during acute infection [ 36 ], a significant increase in virus antibody titers may support the diagnosis of acute viral pericarditis in some cases [ 26 , 37 ]. Similarly, considering the increased virus antibody titers and the identification of coxsackievirus that prefers to infect the pericardium and myocardium, we believe that acute CVA4 monoinfection most likely might have caused the TCP in the present case.…”

Pericardial effusion and tamponade in the context of herpes zoster: a novel occurrence

“…Previous authors propose that re-activation of neurotropic latent VZV affecting the dermatomes described here-above may affect the pericardium, cause pericarditis, and result in an effusion. 4 The pathophysiology of primary VZV-induced myopericarditis is not well understood. It is postulated that VZV is directly cytotoxic and causes the release of inflammatory cytokines, which leads to T-cell-mediated lysis of cardiac myocytes.…”

“… 2 , 3 Varicella zoster virus (VZV) infection, in the form of chicken pox or herpes zoster (HZ), has been documented to be associated with acute myopericarditis. 4 …”