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The effects of acute afterload change on systolic ventricular function in conscious dogs with normal vs. failing hearts
Author(s) -
Thompson Richard B.,
Bos Ewout J.,
Esposito David J.,
Owen Clarence H.,
Glower Donald D.
Publication year - 2003
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/s1388-9842(03)00152-1
Subject(s) - afterload , preload , cardiology , medicine , heart failure , sonomicrometry , ventricle , frank–starling law of the heart , volume overload , systole , cardiac output , stroke volume , hemodynamics , anesthesia , blood pressure , diastole , ejection fraction
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 ( r 2 >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 ( r 2 <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.