R I Lala1,2, D Lungeanu3, D Darabantiu4,5, L Pilat3, M Puschita4,5. 1. "Vasile Goldis" West University Arad, Arad, Romania. radu_lala@yahoo.com. 2. Department of Cardiology, Arad County Emergency Clinical Hospital, Arad, Romania. radu_lala@yahoo.com. 3. Department of Functional Sciences, "Victor Babes" University of Medicine and Pharmacy, Timisoara, Romania. 4. "Vasile Goldis" West University Arad, Arad, Romania. 5. Department of Cardiology, Arad County Emergency Clinical Hospital, Arad, Romania.
Abstract
BACKGROUND: Galectin-3 has been reported as a mediator of heart failure (HF) development and progression. Most studies, however, have been conducted on patients with chronic HF rather than acute HF (AHF). The aim of this study was to confirm galectin-3 as a prognostic marker in subjects with AHF and to investigate its possible relationship with left ventricular (LV) remodeling. METHODS: A total of 69 patients hospitalized with a primary diagnosis of AHF were followed up for 18 months. Galectin-3 and echocardiographic parameters were measured at baseline and after 6 months. Survival analysis and exploratory analysis of LV remodeling were performed. RESULTS: Patients with high baseline galectin-3 values (>16.5 ng/ml) had a significantly worse survival profile over the 18-month follow-up (log-rank test, p = 0.017), with Cox proportional hazards modeling showing a crude hazard ratio (HR) of 4.66 (95% CI = 1.16-18.67; likelihood-ratio test, p = 0.037) for all-cause mortality. Changes in galectin-3 levels (1 SD increase over 6 months) proved to be a significant explanatory factor for HF hospital re-admission in the short term when compared with quasi-stationary galectin-3 levels: worse Kaplan-Meier survival curves (log-rank test, p = 0.001) and a crude HR of 4.44 (95% CI = 1.76-11.18; likelihood-ratio test, p = 0.004). A significant association was found between the pathological evolution of relative wall thickness, LV end-diastolic diameter, LV end-diastolic volume, and increasing levels of galectin-3 in the short term (Cochran-Mantel-Haenszel test, p < 0.01). CONCLUSION: Galectin-3 can predict long-term mortality in patients with AHF. The results of our study suggest a possible relation between left ventricular remodeling and increasing galectin-3 levels.
BACKGROUND:Galectin-3 has been reported as a mediator of heart failure (HF) development and progression. Most studies, however, have been conducted on patients with chronic HF rather than acute HF (AHF). The aim of this study was to confirm galectin-3 as a prognostic marker in subjects with AHF and to investigate its possible relationship with left ventricular (LV) remodeling. METHODS: A total of 69 patients hospitalized with a primary diagnosis of AHF were followed up for 18 months. Galectin-3 and echocardiographic parameters were measured at baseline and after 6 months. Survival analysis and exploratory analysis of LV remodeling were performed. RESULTS:Patients with high baseline galectin-3 values (>16.5 ng/ml) had a significantly worse survival profile over the 18-month follow-up (log-rank test, p = 0.017), with Cox proportional hazards modeling showing a crude hazard ratio (HR) of 4.66 (95% CI = 1.16-18.67; likelihood-ratio test, p = 0.037) for all-cause mortality. Changes in galectin-3 levels (1 SD increase over 6 months) proved to be a significant explanatory factor for HF hospital re-admission in the short term when compared with quasi-stationary galectin-3 levels: worse Kaplan-Meier survival curves (log-rank test, p = 0.001) and a crude HR of 4.44 (95% CI = 1.76-11.18; likelihood-ratio test, p = 0.004). A significant association was found between the pathological evolution of relative wall thickness, LV end-diastolic diameter, LV end-diastolic volume, and increasing levels of galectin-3 in the short term (Cochran-Mantel-Haenszel test, p < 0.01). CONCLUSION:Galectin-3 can predict long-term mortality in patients with AHF. The results of our study suggest a possible relation between left ventricular remodeling and increasing galectin-3 levels.
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