Left ventricular haemodynamics in murine viral myocarditis.
In susceptible DBA/2 mice infection with coxsackievirus B3 leads to severe inflammatory and necrotic lesions in the heart. There is a temporal discrepancy of peak concentrations of replicative virus in the heart and maximal cardiac inflammation. Aims of this study were, first, to determine whether haemodynamic changes occur in coxsackievirus B3-induced murine myocarditis and, second, the time frame in which those alterations may be apparent. By puncture of the left ventricle, pressures and the first derivative dp/dt as parameters of left ventricular function could be obtained on several days of the infection. Haematoxylin-eosin stains of cross-sections of the heart showed the course of inflammatory lesions in the heart; a plaque forming assay assessed virus titres in the heart. Cardiac concentrations of replicative virus peaked on day 3, inflammatory lesions in the heart were maximal on day 7. Left ventricular function was almost preserved until day 5 of the infection, then dropped significantly until day 10. The study suggests that either a cumulative virus-mediated destruction of the myofibres or virally triggered immune reactions to heart cells lead to impairment of left ventricular function.
Herzum
M
M
Philipps University, Department of Internal Medicine, Marburg, Germany.
Mahr
P
P
Wietrzychowski
F
F
Jomaa
H
H
Weller
R
R
Spengler
D
D
Ruppert
V
V
Maisch
B
B
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D003384:Coxsackievirus Infections / Q000473:pathology / Q000503:physiopathology* / Q000821:virology; D029822:Enterovirus B, Human / Q000472:pathogenicity; D006439:Hemodynamics / Q000502:physiology*; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D009205:Myocarditis / Q000473:pathology / Q000503:physiopathology* / Q000821:virology; D016277:Ventricular Function, Left / Q000502:physiology*; D014779:Virus Replication / Q000502:physiology