Left ventricular hemodynamic parameters in the course of acute experimental coxsackievirus B 3 myocarditis.
In susceptible DBA/2 mice coxsackievirus B 3-induced myocarditis leads to inflammatory and necrotic lesions in the myocardium 7-10 days after virus inoculation. The purpose of this study was to determine whether hemodynamic changes occur in murine coxsackievirus B 3 myocarditis and whether they are correlated to histological cardiac lesions throughout the infection. Left ventricular function was determined by open chest puncture of the left ventricle in the course of acute coxsackievirus B 3 infection. Histological cross sections of the heart were stained with hematoxylin/eosin and scored blindly for myocarditic lesions. Left ventricular function was preserved until day 7 post-virus inoculation Left ventricular systolic pressure, +dP/dtmax and -dP/dtmax and heart rate declined significantly from day 7 to day 10. The decrease in these parameters did not correlate with viral concentrations in the heart on the day of hemodynamic measurements. The decrease was related to histological changes on day 10, but not on day 7 of the infection. The data suggest (a) that a cumulative loss of cardiac myofibers, induced either by the virus and/or by immune reactions to the heart, is likely to lead to a late depression of cardiac function, and (b) that there is a weak and only temporary structure-function relationship in the heart in coxsackievirus B 3 myocarditis. Therefore, in addition to an analysis of histological changes, the measurement of cardiac function appears to be very important in order to completely evaluate the severity of myocarditis and the usefulness of any therapy.
Division of Cardiology, Philipps University, Marburg, FRG.
M
M
Herzum
R
R
Weller
H
H
Jomaa
F
F
Wietrzychowski
S
S
Pankuweit
P
P
Mahr
B
B
Maisch
D000818:Animals; D003384:Coxsackievirus Infections / Q000503:physiopathology*; D003971:Diastole; D004562:Electrocardiography; D029822:Enterovirus B, Human / Q000302:isolation & purification; D006321:Heart / Q000821:virology; D006439:Hemodynamics; D007249:Inflammation; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D009205:Myocarditis / Q000473:pathology / Q000503:physiopathology* / Q000821:virology; D009206:Myocardium / Q000473:pathology; D013599:Systole; D016277:Ventricular Function, Left