BACKGROUND: Lack of increase in left ventricular (LV) stroke volume (SV) during low-dose dobutamine stress (LDD) is attributed to exhausted cardiac contractile reserve in failing heart. However, the role of the afterload and preload in SV changes is underestimated. The aim of the study was to investigate the effects of LDD on preload reserve and afterload in patients with non-ischemic heart failure. METHODS: 58 patients (age 62years) underwent LDD (up to 20μg/kg/min) using cardiac magnetic resonance. RESULTS: LV-SV increased by 27% in 24 patients (p<0.001) (SV+), while decreased by 19% in 22 patients (p<0.001) (SV-). The LDD-to-rest reduction in preload, as defined by LV end-diastolic volume (EDV), was more pronounced in SV- than SV+ (24% and 8% respectively, p<0.05). The LLD-to-rest increase in systolic blood pressure to LV end systolic volume ratio, an index of LV contractility, was higher but not statistically different in SV+ in comparison to SV- (70% vs 48%, p=ns). Systemic vascular resistance during LDD tended to be higher in SV- (23%, p=ns), while it was significantly reduced in SV+ (9.5%, p<0.011), whereas arterial elastance (Ea) increased in SV- (30%, p<0.001) but decreased in SV+ (0.5%, p=0.04). At multivariable regression models LV-EF, LV-EDV and Ea significantly contributed to LV-SV changes in all patients. Also among SV+ and SV- LV-EDV and Ea revealed significant contribution to LV-SV change. CONCLUSIONS: At similar contractile reserve response, the lack of LDD-induced increase in LV-SV, can be related to reduced preload reserve as well as to increased afterload.

Influence of preload and afterload on stroke volume response to low-dose dobutamine stress in patients with non-ischemic heart failure: A cardiac MR study

LORENZONI, VALENTINA;PASSINO, Claudio;EMDIN, MICHELE;LIONETTI, Vincenzo;L'ABBATE, ANTONIO
2013-01-01

Abstract

BACKGROUND: Lack of increase in left ventricular (LV) stroke volume (SV) during low-dose dobutamine stress (LDD) is attributed to exhausted cardiac contractile reserve in failing heart. However, the role of the afterload and preload in SV changes is underestimated. The aim of the study was to investigate the effects of LDD on preload reserve and afterload in patients with non-ischemic heart failure. METHODS: 58 patients (age 62years) underwent LDD (up to 20μg/kg/min) using cardiac magnetic resonance. RESULTS: LV-SV increased by 27% in 24 patients (p<0.001) (SV+), while decreased by 19% in 22 patients (p<0.001) (SV-). The LDD-to-rest reduction in preload, as defined by LV end-diastolic volume (EDV), was more pronounced in SV- than SV+ (24% and 8% respectively, p<0.05). The LLD-to-rest increase in systolic blood pressure to LV end systolic volume ratio, an index of LV contractility, was higher but not statistically different in SV+ in comparison to SV- (70% vs 48%, p=ns). Systemic vascular resistance during LDD tended to be higher in SV- (23%, p=ns), while it was significantly reduced in SV+ (9.5%, p<0.011), whereas arterial elastance (Ea) increased in SV- (30%, p<0.001) but decreased in SV+ (0.5%, p=0.04). At multivariable regression models LV-EF, LV-EDV and Ea significantly contributed to LV-SV changes in all patients. Also among SV+ and SV- LV-EDV and Ea revealed significant contribution to LV-SV change. CONCLUSIONS: At similar contractile reserve response, the lack of LDD-induced increase in LV-SV, can be related to reduced preload reserve as well as to increased afterload.
2013
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11382/347377
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