Abstract
Recent experimental studies have suggested that galectin-3 has an interaction with aldosterone, and modifies its adverse effects. We therefore aimed to elucidate whether the relationship between plasma aldosterone concentrations (PACs) and long-term fatal cardiovascular (CV) events would depend on plasma galectin-3 levels. A total of 2,457 patients (median age: 63.5 [interquartile range (IQR) = 56.3 to 70.6] years, 30.1% women) from the LUdwigshafen RIsk and Cardiovascular Health study, with a median follow-up of 9.9 (IQR = 8.5 to 10.7) years, were included. We tested the interaction between aldosterone and galectin-3 for CV-mortality using a multivariate Cox proportional hazard model, reporting hazard ratios (HRs) with 95% confidence intervals (95%CIs). Adjustments for multiple CV risk factors as well as medication use were included. Mean PAC was 79.0 (IQR = 48.0 to 124.0) pg/ml and there were 558 (16.8%) CV deaths. There was a significant interaction between PAC and galectin-3 (p = 0.021). When stratifying patients by the median galectin-3, there was a significant association between aldosterone and CV-mortality for those above (HR per 1 standard deviation = 1.14; 95%CI [1.01 to 1.30], p = 0.023), but not below the cut-off value (HR per 1 standard deviation = 1.00; 95%CI [0.87 to 1.15], p = 0.185). In conclusion, the current study demonstrates for the first time a modifying effect of galectin-3 on the association between aldosterone and CV-mortality risk in humans. These findings indicate that galectin-3 is an intermediate between aldosterone and adverse outcomes.
Highlights
No correlation between plasma aldosterone concentrations (PACs) and Gal-3 was observed in the spearman correlation (r = -0.009; p = 0.664), and in the linear regression analysis
Stability of the results was seen throughout the different models (Table 2)
We examined the relationship between PAC and CV mortality in each of the Gal-3 subgroups
Summary
The LUdwigshafen RIsk and Cardiovascular Health (LURIC) study is a prospective cohort study of consecutive patients referred to invasive coronary angiography. The baseline correlation between PAC and Gal-3 was tested by Spearman’s correlation and a multivariate linear regression analysis. We performed a Cox proportional hazard regression analysis investigating the association of Gal-3 and PAC with CV mortality with adjustments for established risk factors. After detecting the first order interaction between PAC and Gal-3 we included an interaction term in the Cox regression models. Coronary Artery Disease/Galectin 3, Aldosterone, and CV Mortality Risk mortality, we repeated the analyses by stratifying the cohort according to the median value of Gal-3. A two-sided p value of less than 0.05 was considered to indicate statistical significance
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