Galectin‐3 Predicts Left Ventricular Remodeling of Hypertension

Abstract

Previous studies have suggested that galectin-3 is an important mediator of cardiac fibrosis. The aim of this study was to investigate the utility of galectin-3 in identifying early left ventricular remodeling (LVRM) in patients with hypertension. A total of 107 patients with hypertension and 108 controls were enrolled in this study. The levels of galectin-3 were significantly greater in hypertension patients with LVRM compared with those without LVRM. Multivariate regression analysis demonstrated that body mass index and galectin-3 were independent predictors of LVRM in the hypertension group. Only left ventricular mass was independently correlated with serum galectin-3 levels in patients with hypertension. The receiver operating characteristic analysis showed an area under the curve for galectin-3 of 0.698 (P<.001), with an optimal cutoff of 9.43 ng/mL. Therefore, galectin-3 is independently correlated with LVRM and can be regarded as a valuable biomarker of early cardiac remodeling of hypertension.

Icariside II prevents hypertensive heart disease by alleviating endoplasmic reticulum stress via the PERK/ATF-4/CHOP signalling pathway in spontaneously hypertensive rats

“…Hypertensive heart disease is one of the most common complications and can lead to death in hypertensive patients. Therefore, it is an important strategy to improve ventricular remodelling and to prevent hypertensive heart disease for the reduction of the morbidity and mortality of hypertensive patients …”

“…Therefore, it is an important strategy to improve ventricular remodelling and to prevent hypertensive heart disease for the reduction of the morbidity and mortality of hypertensive patients. [19,20] In this study, we examined the function of left ventricular at the 18, 22 and 26 weeks of age in SHRs. The results showed that the LVPW became thickened with age in the SHR group, while the EF and FS decreased, indicating that SHRs exhibited ventricular remodelling and dysfunction.…”

Galectin‐3 and Hypertensive Heart Disease

“…The identification of new biomarkers of subclinical cardiovascular (CV) damage allowing for improvement in CV risk estimation represents a challenging task for CV medicine. In this issue of the Journal, Yao and colleagues describe the results of a study designed to assess the role of circulating galectin‐3 (Gal‐3) in predicting abnormal left ventricular (LV) geometries (ie, concentric LV hypertrophy, eccentric LV hypertrophy, and concentric LV remodeling) in a group of essential hypertensive patients.…”

“…In the study by Yao and colleagues, a total of 107 uncomplicated essential hypertensive patients without comorbidities (mean age 58±11 years) and 108 age‐ and sex‐matched controls (58±4 years) underwent clinic BP measurement, NT‐pro‐BNP and Gal‐3 determinations, and standard echocardiography. The major findings of this report are summarized as follows: (1) a progressive increase in circulating Gal‐3 concentrations occurred across normotensive controls (5.6 ng/mL), hypertensive patients with normal LV mass/geometry (7.3 ng/mL), and hypertensive patients with LV remodeling (12.5 ng/mL); (2) in multivariate analysis, only Gal‐3 and body mass index (BMI) were independently correlated to LV remodeling; (3) NT‐pro‐BNP did not differ in hypertensive patients with (30 pg/mL) and without (30 pg/mL) LV remodeling; and (4) receiver operating characteristic curve analyses showed that Gal‐3 performed better than NT‐pro‐BNP in detecting LV remodeling as documented by a greater area under the curve (0.698 [ P <.001] vs 0.530 [ P =.347], respectively).…”

“…In the study by Yao and colleagues, the majority of patients with (82%) and without (73%) LV remodeling were taking antihypertensive drugs that interfered with the renin‐angiotensin‐aldosterone system and approximately half of them were taking calcium channel blockers. The impact of antihypertensive drugs on tissue and circulating levels of Gal‐3 is largely unknown and may have influenced the relationship between this marker with clinical and echocardiographic variables.…”