Identification of High-Risk Chronic Heart Failure Patients in Clinical Practice: Role of Changes in Left Ventricular Function
Article first published online: 15 JUN 2012
© 2012 Wiley Periodicals, Inc.
Volume 35, Issue 9, pages 580–584, September 2012
How to Cite
Cicoira, M., Rossi, A., Chiampan, A., Frigo, G., Bergamini, C., Rigolli, M., Zanolla, L. and Vassanelli, C. (2012), Identification of High-Risk Chronic Heart Failure Patients in Clinical Practice: Role of Changes in Left Ventricular Function. Clin Cardiol, 35: 580–584. doi: 10.1002/clc.22024
- Issue published online: 10 SEP 2012
- Article first published online: 15 JUN 2012
- Manuscript Revised: 27 APR 2012
- Manuscript Received: 6 MAR 2012
Left ventricular (LV) dysfunction and remodeling are key pathophysiological features underlying disease progression in chronic heart failure (CHF).
To describe the course of LV dysfunction and identify predictors and prognostic impact of changes in LV volumes and function in stable CHF patients under optimal therapy.
There were 318 consecutive CHF outpatients who underwent a repeated echocardiographic evaluation at baseline and at 1 year and subsequently followed-up for at least 12 months. The end point of the study was all-cause mortality.
Mean LV ejection fraction (LVEF) was 33 ± 7% at baseline and 36 ± 9% at follow-up. Twenty-four percent of patients had an improvement of LVEF >5 absolute points (group 1); 58% remained stable (group 2), 17% worsened at >5 absolute points (group 3). Age, New York Heart Association class, diuretic dose, renal function, and baseline LVEF were independent predictors of LVEF improvement at 1 year. At the Cox analysis, patients in group 3 had a 4-fold higher risk of death when compared with group 1 (hazard ratio: 3.99, 95% confidence interval: 1.6-9.9, P = 0.002), independently of age, etiology, and symptoms severity.
In stable CHF outpatients, LV function improves in 24% of cases; a modest decrease in LV systolic function is associated with a significantly higher risk of all-cause mortality, independent of other markers of disease severity. Clin. Cardiol. 2012 doi: 10.1002/clc.22024
The authors have no funding, financial relationships, or conflicts of interest to disclose.