Role of galectin-3 in subclinical myocardial impairment in psoriasis.

BACKGROUND: Psoriasis has been shown to increase cardiovascular risk, and a contributor to this might be enhanced myocardial fibrosis promoted by the disease-associated pro-inflammatory milieu. OBJECTIVE: We sought to investigate the relationship of galectin-3 (Gal-3) - a recognized mediator of fibrosis with inflammatory activation and left ventricular (LV) systolic and diastolic function in patients with psoriasis. METHODS: We enrolled 102 psoriatic patients (mean age: 52.5 ± 12.6 years). Sixty-five age- and sex-matched healthy subjects served as controls. Echocardiographic assessment of myocardial function included estimation of LV longitudinal systolic deformation (GLS) and diastolic indices: tissue e' velocity and E/e' ratio. Laboratory measurements encompassed blood Gal-3, creatinine, glucose, insulin, CRP and erythrocyte sedimentation rate (ESR). RESULTS: Patients with psoriasis were characterized by elevated Gal-3 (12.3 [9.3-13.4] vs. 6.3 [5.5-9.4] ng/mL in healthy controls, P < 0.001), ESR (17.0 [11.0-29.0] vs. 8.5 [6.0-13.0] mm, respectively, P < 0.001) and CRP (3.1 [1.7-10.6] vs. 1.9 [1.5-4.0] mg/L, respectively, P < 0.001), and reduced GLS (19.9 ± 3.7 vs. 22.0 ± 3.0%, respectively, P < 0.001). Progressive deterioration of GLS was demonstrated across Gal-3 tertiles. Significant associations between GLS and age (beta = -0.21, P < 0.04), Gal-3 (beta = -0.27, P < 0.01), CRP (beta = -0.22, P < 0.03), ESR (beta = -0.25, P < 0.01), waist circumference (beta = -0.22, P < 0.03) and waist-to-hip ratio (beta = -0.20, P < 0.05) were found. Stepwise multiple regression analysis revealed that the independent determinants of GLS in psoriatic patients were Gal-3 (beta = -0.24, P < 0.01) and ESR (beta = -0.21, P < 0.03). Regression-based mediation analysis demonstrated that the relationship between ESR and GLS was partially mediated by Gal-3. CONCLUSIONS: Subclinical left ventricular systolic dysfunction in psoriasis, as evidenced by reduced GLS, is linked with the inflammatory upregulation, and enhanced profibrotic activity (as reflected by elevated serum Gal-3) may be involved in this process. These putative mechanisms may be responsible for the observed higher incidence of heart failure in this disease condition and should be considered as a potential target for preventive and therapeutic measures.

[Biochemical indicators of coronary arteriosclerosis]. / Biochemiczne wskazniki miazdzycy tetnic wiencowych.

In 251 patients undergoing cardiac catheterization, plasma levels of lipids, lipoproteins, apoproteins and nonlipid risk factors as fibrinogen, fibrinolysis time, glucose and uric acid in blood were correlated with the incidence and severity of coronary artery disease (CAD). There were significant differences between CAD group and controls and between men and women with CAD with respect to the mean lipid values. Among the nonlipid risk factors fibrinogen concentration in CAD patients was significantly higher than in controls. In univariate analysis in men, score for the severity of atherosclerosis was strongly related to the apoB and LDL concentration, less to the HDL and fibrinogen levels and to ratios of total cholesterol/HDL and LDL/HDL. In women severity of the disease correlated with apoB, fibrinolysis time, fibrinogen and triglyceride levels. By stepwise multivariate analysis, in both men and women, apoB was selected as the best discriminator between CAD patients and controls. The results of the study indicate that the levels of apoB may be a more accurate predictor of the severity of CAD than the other biochemical risk factors. The presented data also suggests an association between increased fibrinogen concentration, reduced fibrinolytic capacity and CAD. The values of apoB and fibrinogen as indicators of cardiovascular risk should be assessed in prospective studies.

[Does chronic therapy of hypertension with acebutolol or hydrochlorothiazide effect coronary risk factors?]. / Czy leczenie nadcisnienia tetniczego acebutololem lub hydrochlorotiazydem nasila biochemiczne czynniki zagrozenia choroba wiencowa?

In 78 patients with mild or moderate hypertension, effect of acebutolol and hydrochlorothiazide on plasma lipids, lipoproteins, fibrinogen and plasma fibrinolysis time were investigated. 42 patients were treated with acebutolol for 18 months and 36 with hydrochlorothiazide for 24 months. It was shown that neither acebutolol nor hydrochlorothiazide induced significant alterations in investigated biochemical risk factors. The possible causes of controversy encountered in literature and analysis of factors which may influence the character and severity of metabolic disorders resulting from antihypertensive therapy were discussed.

[Effect of long-term treatment with propranolol or hydrochlorothiazide on biochemical risk factors of coronary disease in patients with hypertension]. / Wplyw prezewleklego leczenia propranololem lub hydrochlorotiazydem na biochemiczne czynniki zagrozenia choroba wiencowa u chorych na nadcisnienie tetnicze krwi.

In 59 patients with mild or moderate essential hypertension effects of propranolol and hydrochlorothiazide on serum lipids, fibrynogen, glucose and uric acid concentrations as well as serum euglobulins fibrynolysis time were studied. 36 patients received propranolol and 23 subjects hydrochlorothiazide. Follow-up time was 1 year. Statistically significant increases of serum triglycerides, fibrynogen, levels and total cholesterol/HDL cholesterol LDH/HDL indices in comparison with their initial values were stated in a propranolol group. Significant serum cholesterol increase after 6 month therapy was the most substantial metabolic change in a hydrochlorothiazide group. Alterations of lipids indices in both groups were especially intensive in patients with pretreatment stated disturbances of lipids metabolism.