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EXPERIMENTAL STUDY

Left ventricular pressure-volume relationship in a murine model of congestive heart failure due to acute viral myocarditis

^* Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, Kyoto, Japan

Manuscript received January 23, 2002; revised manuscript received May 29, 2002, accepted June 7, 2002.

^* Reprint requests and correspondence: Dr. Akira Matsumori, Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, 54 Kawahara-cho, Shogoin, Sakyo-ku, Kyoto 606-8397, Japan.
amat{at}kuhp.kyoto-u.ac.jp

OBJECTIVES: 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.

Abbreviations and Acronyms   AOmean   mean aortic pressure   dP/dtmax   maximum derivative of change in systolic pressure over time   dP/dtmin   minimum derivative of change in diastolic pressure over time   Ea   elastance of artery   EDPVR   end-diastolic pressure volume relationship   EMCV   encephalomyocarditis virus   ESPVR   end-systolic pressure volume relationship   NL Eed   normalized end-diastolic volume elastance   NL Ees   normalized end-systolic volume elastance   PRSW   preload recruitable stroke work   PVA      RAmean   mean right atrial pressure   SVI   stroke volume index   SVRI   systemic vascular resistance index   SWI   stroke work index   SW/PVA   efficiency   Vp   parallel volume

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