Preload Reserve Is Restored in Patients With Decompensated Chronic Heart Failure Who Respond to Treatment
Article first published online: 1 AUG 2013
© 2013 Wiley Periodicals, Inc.
Congestive Heart Failure
Volume 19, Issue 4, pages 207–213, July/August 2013
How to Cite
Squara, P., Estagnasie, P., Belliard, O., Squara, F. and Dib, J. C. (2013), Preload Reserve Is Restored in Patients With Decompensated Chronic Heart Failure Who Respond to Treatment. Congestive Heart Failure, 19: 207–213. doi: 10.1111/chf.12033
- Issue published online: 1 AUG 2013
- Article first published online: 1 AUG 2013
- Manuscript Accepted: 18 APR 2013
- Manuscript Revised: 3 APR 2013
- Manuscript Received: 16 NOV 2012
The authors designed this prospective study to show the relationship between preload reserve and treatment effectiveness of chronic heart failure (CHF). Fifty patients, aged 77±24 years, with decompensated CHF (B-type brain natriuretic peptide [BNP] >1000 pg/mL) were included. Preload reserve was assessed by the changes in contraction indices during a passive leg raise (PLR). Contraction indices were assessed noninvasively using Bioreactance technology. After 4 days of optimized therapy, the same variables were reassessed and treatment-induced differences were calculated. Treatment effectiveness was assessed by the 4-day changes in BNP, body weight, and thoracic fluid content. The authors then compared treatment-induced changes in preload reserve with treatment effectiveness. Therapy was associated with an overall decrease in heart rate, blood pressure, and cardiac power index (CPi) and with an increase in all preload reserve indices. Treatment effectiveness correlated well with changes in preload reserve. The best correlation was found between treatment-induced changes in BNP and in PLR-induced changes of CPi (R=0.63, P<.001). The PLR-induced changes in CPi increased from 21±48 to 51±48 in BNP responders and decreased from 34±34 to 5±19 mW/m2 in BNP nonresponders (P<.0001). Hence, effective treatment, as indexed by a decrease in BNP, restores the preload reserve in patients with decompensated CHF.