HHV-6 in Myocarditis

Researchers at the Robert Bosch Medical Center in Stuttgart, Germany recently demonstrated that HHV-6 is far more common in myocarditis than was previously believed. Not only did they find 35% or 31 out of 87 biopsies positive for HHV-6, they determined that patients with HHV-6 involvement progressed more frequently toward chronic heart failure. Furthermore, unlike patients with parvovirus B-19 (the most common virus found), patients with HHV-6 had no chest pain and often did not seek treatment until the late stages of disease (Mahroldt, 2006)

Kuhl et al found in 2005 found HHV-6 in 23% of 172 myocarditis patient biopsies, and also found that when the virus cleared (which happened spontaneously in 44% of the cases) there was patient improvement in left ventricular ejection fraction, while in patients where the virus did not clear, there was progressive impairment. (Kuhl, 2005)

Infectious disease specialist Martin Lerner has found 24-hour Holter monitor abnormalities in Chronic Fatigue Syndrome patients with elevated antibody titers to EBV, CMV or HHV-6. Furthermore, he has demonstrated improvement in both fatigue levels and cardiac function in several small trials of antiviral therapy with ganciclovir and valacyclovir.  (Lerner 1993, Lerner 2001, Lerner 2002) Another group of CFS researchers found reduced cardiac output as measured by impedance cardiography in patients with chronic fatigue syndrome. (Peckerman 2003)

Caruso et al demonstrated that HHV-6 infects the aorta and endothelial cells in the heart, contributing to inflammation by producing proinflammatory cytokines. (Caruso 2002) 

HHV-6 infects endothelial cells of the aorta as well as veins and capillaries of the heart. Infection with HHV-6 appears to cause vascular endothelial damage that is worse than infection with CMV, and may cause thrombotic microangiopathy. (Takatsuka 2003)

There have been case reports of HHV-6 in large vessel arteritis (Toyabe 2002 and in fulminant myocarditis. (Fukae 2000)