title: Left ventricular pressure-volume relationship in a murine model of congestive heart failure due to acute viral myocarditis.
abstract: OBJECTIVE
  This study, performed in a murine model of encephalomyocarditis virus myocarditis, used a new Millar 1.4F conductance-micromanometer system for the in vivo determination of the left ventricular (LV) pressure-volume relationship (PVR).
  
  
  BACKGROUND
  Viral myocarditis is an important cause of congestive heart failure and may lead to dilated cardiomyopathy. However, the hemodynamic changes associated with its acute phase have not been analyzed in detail.
  
  
  METHODS
  Four-week-old DBA/2 mice were inoculated with EMCV (day 0). Serial hemodynamic measurements, compared with uninfected control mice were made on days 0, 1, 3, 4, 5, 7, 9, 12, and 14.
  
  
  RESULTS
  On day 1, the hearts of infected mice manifested enhanced contractile function, decreased LV compliance, and abnormal diastolic function with increased LV end-diastolic pressure (EDP). Mean stroke index, ejection fraction (EF), and cardiac index (CI) were significantly higher than in uninfected control mice (p < 0.05). Contractile function decreased from days 4 to 14. On day 7, when hemodynamic abnormalities consistent with heart failure culminated, end-diastolic volume (EDV), EDP, and EDPVR were significantly higher, and CI, EF, end-systolic pressure (ESP), and ESPVR significantly lower in the infected than in control mice. Heart rate remained comparable in both groups. Although heart failure receded between day 9 and day 14, ESPVR, ESP, and EF remained significantly depressed up to day 14, and EDV and EDP remained significantly higher.
  
  
  CONCLUSIONS
  These hemodynamic data provide new insights into the pathophysiology of acute viral myocarditis and may be useful in the development of therapeutic interventions.
authors.affiliation: Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan.
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Nishio
authors.forename: Shigetake
authors.initials: S
authors.lastname: Sasayama
authors.forename: Akira
authors.initials: A
authors.lastname: Matsumori
mesh_terms: D000818:Animals; D016280:Atrial Function, Right; D002306:Cardiac Volume / Q000502:physiology*; D004553:Electric Conductivity; D006333:Heart Failure / Q000503:physiopathology* / Q000821:virology; D051379:Mice; D023421:Models, Animal; D009200:Myocardial Contraction / Q000502:physiology; D009205:Myocarditis / Q000150:complications / Q000503:physiopathology*; D012815:Signal Processing, Computer-Assisted; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology*; D017725:Ventricular Pressure