Galectin 3 and Galectin 3 Binding Protein Improve the Risk Stratification after Myocardial Infarction

Abstract

Background: Acute myocardial infarction (AMI) survivors are at risk of major adverse cardiac events and their risk stratification is a prerequisite to tailored therapeutic approaches. Biomarkers could be of great utility in this setting. Methods: We sought to evaluate the utility of the combined assessment of Galectin 3 (Gal-3) and Galectin 3 binding protein (Gal-3bp) for post-AMI risk stratification in a large, consecutive population of AMI patients. The primary outcomes were: Recurrent angina/AMI and all-cause mortality at 12 months after the index event. Results: In total, 469 patients were included. The median Gal-3bp was 9.1 μg/mL (IQR 5.8–13.5 μg/mL), while median Gal-3 was 9.8 ng/mL (IQR 7.8–12.8 ng/mL). During the 12 month follow-up, 34 patients died and 41 had angina pectoris/reinfarction. Gal-3 was associated with all-cause mortality, while Gal-3bp correlated with the risk of angina/myocardial infarction even when corrected for other significant covariates. The final multivariable model for mortality prediction included patients’ age, left ventricular ejection fraction (LVEF), Gal-3, and renal function. The ROC curve estimated for this model has an area under the curve (AUC) of 0.84 (95%CI 0.78–0.9), which was similar to the area under the ROC curve obtained using the GRACE score 1-year mortality. Conclusions: The integrated assessment of Gal-3 and Gal-3bp could be helpful in risk stratification after AMI.

Low levels of soluble TWEAK, indicating on-going inflammation, were associated with depression in type 1 diabetes: a cross-sectional study

“…Three independent risk factors or risk markers for cardiovascular disease were demonstrated in these depressed patients with T1DM. Low sTWEAK levels [12][13][14] and high galectin-3 levels [22][23][24][25]27] have previously been linked to the development of cardiovascular disease and increased mortality. HDL-cholesterol levels decrease in inflammatory states [28,29].…”

“…Galectin-3 is a beta-galactoside-binding lectin involved in several inflammatory processes [ 21 ]. Increased galectin-3 levels have been linked to coronary artery disease [ 22 , 23 ], heart failure [ 24 , 25 ], prolonged inflammatory responses in the brain [ 26 ], and to cardiovascular and all-cause mortality [ 25 , 27 ]. Systemic inflammation causes decreased high-density lipoprotein (HDL)-cholesterol levels which contribute both to reduced capacity for reverse cholesterol transport, and to reduced capacity to protect low-density lipoprotein (LDL)-cholesterol from oxidation [ 28 ].…”

Low levels of soluble TWEAK, indicating on-going inflammation, were associated with depression in type 1 diabetes: a cross-sectional study

“…Three independent risk factors or risk markers for cardiovascular disease were demonstrated in these depressed patients with T1DM. Low sTWEAK levels [12][13][14] and high galectin-3 levels [22][23][24][25]27] have previously been linked to the development of cardiovascular disease and increased mortality. HDL-cholesterol levels decrease in in ammatory states [28,29].…”

“…Galectin-3 is a beta-galactoside-binding lectin involved in several in ammatory processes [21]. Increased galectin-3 levels have been linked to coronary artery disease [22,23], heart failure [24,25], prolonged in ammatory responses in the brain [26], and to cardiovascular and all-cause mortality [25,27]. Systemic in ammation causes decreased high-density lipoprotein (HDL)cholesterol levels which contribute both to reduced capacity for reverse cholesterol transport, and to reduced capacity to protect low-density lipoprotein (LDL)-cholesterol from oxidation [28].…”

Galectin-3 Binding Protein, Depression, and Younger Age Were Independently Associated With Alexithymia in Adult Patients With Type 1 Diabetes

“…It has been suggested that alexithymia impacts the function of the human immune system both through the sympathetic overreactivity and the activation of the HPA axis (2,3). Disturbances of the immune system, involving monocytes and macrophages, contribute to the development of atherosclerosis and cardiovascular disease (19)(20)(21)(22)(23)(24)(25). Galectin-3 binding protein (Gal3BP) is a macrophage scavenger receptor which, while activated, induces a number of pro-inflammatory cytokines (21).…”