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European Journal of Heart Failure 2003 5(6):741-749; doi:10.1016/S1388-9842(03)00152-1
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© 2003 European Society of Cardiology

The effects of acute afterload change on systolic ventricular function in conscious dogs with normal vs. failing hearts{star}

Richard B. Thompsona, Ewout J. van den Bosb, David J. Espositoa, Clarence H. Owena and Donald D. Glowera,c,*

a Departments of Thoracic Surgery Box 3851, Duke University Medical Center Durham, NC 27710, USA
b Departments of Cardiology Box 3851, Duke University Medical Center Durham, NC 27710, USA
c Departments of Biomedical Engineering Box 3851, Duke University Medical Center Durham, NC 27710, USA

* Corresponding author. Tel.: +1-919-681-5789; fax: +1-919-681-8912. E-mail address: glowe001{at}mc.duke.edu


  Abstract

Background: To date, no data exist on the linearity and, therefore, the usefulness of the preload recruitable stroke work (PRSW) and end-systolic pressure–volume (ESPVR) relationships during acute afterload changes in heart failure.

Aims: Our aim was, therefore, to characterize both relationships in a model of ventricular pacing induced heart failure at baseline and during acute changes in afterload.

Methods: Dynamic left ventricular volume and transmural pressure were measured in 10 conscious dogs using sonomicrometry and micromanometry under control conditions and during heart failure produced by 3 weeks of rapid right ventricular pacing. Afterload was varied from baseline with intravenous infusions of nitroprusside and phenylephrine. Left ventricular function was assessed using the PRSW and ESPVR relationships.

Results: Cardiac output demonstrated a linear inverse relationship with afterload in both normal and failing hearts (r2>0.5, P<0.001) with failure producing a parallel, downward shift of the afterload (x) vs. cardiac output (y) relationship (P<0.01). Yet, afterload variation did not affect PRSW or ESPVR relationships in either normal or failing hearts (r2<0.12, P>0.05).

Conclusion: Thus, the PRSW and ESPVR relationships are insensitive to acute afterload changes in both failing and normal hearts, and the failing left ventricle is no more afterload-sensitive than the normal heart.

Key Words: Ventricular function • Tachycardia • Pacing • Cardiomyopathy • Arterial resistance • Afterload

Received February 12, 2003; Revised April 28, 2003; Accepted July 17, 2003

{star} This work was supported by NIH grants HL46242 and HL17670.


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