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Am J Physiol Heart Circ Physiol (October 14, 2004). doi:10.1152/ajpheart.00465.2004
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Submitted on May 18, 2004
Accepted on September 30, 2004

Levosimendan Improves Left Ventricular Systolic and Diastolic Performance at Rest and During Exercise after Heart Failure

Hideo Tachibana1, Heng-Jie Cheng1, Tomohiko Ukai1, Akihiko Igawa1, Zhu-Shan Zhang1, William C. Little1, and Che-Ping Cheng1*

1 Internal Medicine-Cardiology, Wake Forest University School of Medicine, School of Medicine, Winston-Salem, NC, USA

* To whom correspondence should be addressed. E-mail: ccheng{at}wfubmc.edu.

Background. The new myofilament Ca2+ sensitizer, levosimendan (LSM), is a positive inotropic and vasodilatory agent. Its beneficial effects have been demonstrated at rest in heart failure (CHF). However, its effect during exercise (Ex) in CHF is unknown. Methods and Results. We assessed the effect of LSM on left ventricular (LV) dynamics at rest and during Ex in 8 conscious, instrumented dogs with pacing-induced CHF. After CHF, at rest, LSM decreased arterial elastance (EA) and increased LV contractile performance assessed by the slopes of LV pressure (P)-volume (V) relations. LSM caused more than a 60% increase in the peak rate of mitral flow (dV/dtmax) due to decreased minimal LVP (Pmin) and the time constant of LV relaxation ({tau}). LV-arterial coupling, quantified as EES/EA, was increased from 0.47 to 0.85%. LV mechanical efficiency, determined as the ratio of stroke work (SW) to total P-V area was improved from 0.54±0.09 to 0.61±0.07. These beneficial effects persisted during Ex after CHF. Compared with CHF Ex, treatment with LSM prevented Ex-induced abnormal increases in mean LAP, PED, and a decrease in EES/EA. With LSM, during CHF Ex, the early diastolic portion of LV P-V loop was shifted downward with decreased LVPmin<, {tau}, and further augmented dV/dtmax. EES/EA improved, and mechanical efficiency further increased from 0.61±0.07 to 0.67±0.07, which was close to the value reached during normal Ex. Conclusions. After CHF, LSM produces arterial vasodilatation, improving LV relaxation and diastolic filling; increases contractility, LV arterial coupling, and mechanical efficiency; and normalizes the response to Ex.




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