Effects of 12 Weeks of Atorvastatin Therapy on Myocardial Fibrosis and Circulating Fibrosis Biomarkers in Statin-NaïVe Patients with Hypertension with Atherosclerosis

Chang, Yuan‐Jen; Wu, Yen‐Wen; Lee, Jen‐Kuang; Lin, Yu‐Min; Lin, Yen‐Ting; Kao, Hsien‐Li; Hung, Chi‐Sheng; Lin, Hung‐Ju; Lin, Yen‐Hung

doi:10.1136/jim-2016-000092

Cited by 12 publications

(6 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…McKinnon et al (46) showed that deletion of galectin-3 in the apolipoprotein E (−/−) knockout mice resulted in a markedly reduced volume of atherosclerotic plaques, and the authors concluded that strategies that inhibit galectin-3 may be a new approach in the treatment of atherosclerotic diseases. In a small study, 15 statin-naive patients with atherosclerosis were given atorvastatin 40 mg/day for 12 weeks, and at the end of study, galectin-3 levels decreased non-significantly (47). But in our study, atorvastatin 80 mg/day seems to have no effects on galectin-3 levels in patients with AMI at the end of 4-week therapy.…”

Section: Discussioncontrasting

confidence: 73%

Comparative Effects of Atorvastatin 80 mg and Rosuvastatin 40 mg On The Levels of Serum Endocan, Galectin-3 and Chemerin in Patients With Acute Myocardial Infarction

et al. 2019

View full text Add to dashboard Cite

Comparative effects of atorvastatin 80 mg and rosuvastatin 40 mg on the levels of serum endocan, chemerin, and galectin-3 in patients with acute myocardial infarction Introduction Myocardial infarction remains the leading cause of morbidity and mortality worldwide. In 2015, more than 8.75 million people lost their lives due to coronary artery disease (CAD), accounting for 15.5% of all deaths (1). Endothelial dysfunction, inflammation, and disruption-rupture of atherosclerotic plaques play a critical role in the pathogenesis of atherosclerosis and acute myocardial infarction (AMI) (2-5). Endothelial specific molecule-1 (ESM-1) or endocan, is a soluble dermatan sulfate proteoglycan, secreted and expressed by human vascular endothelial cells (6). The elevated levels of the endocan in patients with tumor progression or in patients with sepsis suggest that endocan may be a probable biomarker for endothelial dysfunction or endothelial activation (7, 8). A previous study showed that endocan levels have been significantly increased in patients with acute coronary syndrome (ACS) (9). In another study, admission endocan levels were found to be associated with in-hospital mortality and the CAD severity index in patients with ST segment elevation myocardial infarction (STEMI) (10). Adipose tissue is an active endocrine organ and regulates energy homeostasis and metabolism by communicating with Objective: Endocan, chemerin, and galectin-3 are discrete biomarkers associated with cardiovascular diseases and acting through different pathophysiological pathways. The aim of this study is to investigate and compare the effects of high doses of atorvastatin and rosuvastatin on serum endocan, chemerin, and galectin-3 levels in patients with acute myocardial infarction (AMI). Methods: Sixty-three patients with AMI were randomized to receive atorvastatin (80 mg/day) or rosuvastatin (40 mg/day) after percutaneous revascularization. Serum levels of endocan, chemerin, and galectin-3 were evaluated at baseline and after 4-week therapy. Results: Endocan levels were not decreased statistically significantly with atorvastatin 80 mg, but rosuvastatin 40 mg markedly decreased the levels of endocan according to baseline [from 110.27 (86.03-143.69) pg/mL to 99.22 (78.30-122.87) pg/mL with atorvastatin 80 mg and from 110.73 (77.28-165.22) pg/mL to 93.40 (70.48-115.13) pg/mL with rosuvastatin 40 mg, p=0.242 for atorvastatin 80 mg and p=0.014 for rosuvastatin 40 mg]. Chemerin levels significantly decreased in both groups according to baseline [from 264.90 (196.00-525.95) ng/mL to 135.00 (105.95-225.65) ng/ mL with atorvastatin 80 mg and from 309.95 (168.87-701.27) ng/mL to 121.25 (86.60-212.65) ng/mL with rosuvastatin 40 mg, p<0.001, respectively, for both groups]. Galectin-3 levels did not change markedly with atorvastatin 80 mg, but they decreased with rosuvastatin 40 mg [from 17.00 (13.10-22.25) ng/mL to 19.30 (15.25-23.45) ng/mL with atorvastatin 80 mg, p=0.721, and from 18.25 (12.82-23.82) ng/mL to 16.60 (10.60-20.15) ng/ mL with rosuvastatin 4...

show abstract

Section: Discussioncontrasting

confidence: 73%

Comparative Effects of Atorvastatin 80 mg and Rosuvastatin 40 mg On The Levels of Serum Endocan, Galectin-3 and Chemerin in Patients With Acute Myocardial Infarction

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Hence, changes in treatment and progression of disease were not taken into account. It has been reported that statin, ACEI, and ARB have no significant effect on galectin‐3 levels, but there are so far no data on the effect of diabetes medications on galectin‐3 levels. Furthermore, since our hospital is a secondary/tertiary referral centre, our cohort of patients are likely to be more complex than those in the general population or primary care, and the relationship between serum galectin‐3 levels and adverse cardiovascular outcome may not be generalizable to other patient populations.…”

Section: Discussionmentioning

confidence: 99%

Galectin‐3 and risk of cardiovascular events and all‐cause mortality in type 2 diabetes

Tan

Cheung

Lee

et al. 2018

Diabetes Metabolism Res

View full text Add to dashboard Cite

Aims Recent clinical studies have shown that galectin‐3 is a prognostic indicator in patients with coronary heart disease and in patients with heart failure. Experimental data suggest that galectin‐3 may play a role in atherogenesis. We have evaluated whether serum galectin‐3 level is associated with cardiovascular outcome in type 2 diabetes. Materials and methods Galectin‐3 was measured in baseline samples in 1495 persons with type 2 diabetes. The primary cardiovascular outcome, incident cardiovascular events, was defined as first non‐fatal myocardial infarction, non‐fatal stroke, coronary revascularization, or death from cardiovascular cause. The secondary outcome was all‐cause mortality. Results At baseline, 12% of the subjects had prevalent cardiovascular disease. Serum galectin‐3 was increased in the group with incident cardiovascular events compared with those who remained free of events during follow up (9.03 ± 2.98 ng/mL vs 8.15 ± 2.76, P < 0.01). Serum galectin‐3 was also significantly increased in those subjects with a fatal outcome. The hazard ratios (HR) for cardiovascular events and all‐cause mortality for individuals in the top quartile were 2.50 (95% CI 1.87, 3.36, P < 0.001) and 3.92 (95%CI 2.55, 6.01, P < 0.001), respectively. In a multivariate Cox regression analysis including traditional risk factors, log (eGFR), baseline albuminuria, and cardiovascular disease status, the HR per standard deviation change in galectin‐3 was 1.13 (95% CI 1.02, 1.26, P = 0.02) for cardiovascular events and 1.17 (95% CI 1.01, 1.35, P = 0.04) for all‐cause mortality. Conclusions Serum galectin‐3 is associated with adverse cardiovascular outcomes in persons with type 2 diabetes independent of traditional risk factors.

show abstract

“…Zhang et al [4] demonstrated that Ato ameliorates radiation-induced cardiac fibrosis in Sprague-Dawley rats. Similarly, Chang et al [5] showed that medium-dose Ato treatment for 12 weeks resulted in a significant reduction in myocardial fibrosis in patients. However, the specific mechanisms are not fully understood.…”

Section: Introductionmentioning

confidence: 96%

Atorvastatin Prevents Myocardial Fibrosis in Spontaneous Hypertension via Interleukin-6 (IL-6)/Signal Transducer and Activator of Transcription 3 (STAT3)/Endothelin-1 (ET-1) Pathway

et al. 2019

View full text Add to dashboard Cite

BackgroundHypertension is a leading global disease, and myocardial fibrosis is an important adverse effect of hypertension, seriously threatening human health. The IL-6/STAT3 pathway and endothelin-1 (ET-1) were previously suggested to play a part in myocardial fibrosis.Material/MethodsTo investigate the role of Atorvastatin (Ato) in spontaneous hypertension, systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured, and Masson trichrome staining was performed. Furthermore, the relative protein levels of the IL-6/STAT3/ET-1 pathway were tested.ResultsAto prevented myocardial fibrosis in spontaneous hypertension rats, especially at the dosage of 50 mg/kg/d. The IL-6/STAT3 pathway was observed to be suppressed by Ato, and ET-1 level in myocardial tissues was also downregulated by Ato. The phosphorylation status of STAT3 was tested after Ato treatment, showing that Ato mainly stimulated the tyr-705 phosphorylation of STAT3.ConclusionsResults of this study may help promote myocardial fibrosis therapy and provide insights into the IL-6/STAT3/ET-1-mediated mechanism in Ato-induced myocardial fibrosis inhibition.

show abstract

Effects of 12 Weeks of Atorvastatin Therapy on Myocardial Fibrosis and Circulating Fibrosis Biomarkers in Statin-NaïVe Patients with Hypertension with Atherosclerosis

Abstract: NTC00172419; results.

Cited by 12 publications

References 52 publications

Comparative Effects of Atorvastatin 80 mg and Rosuvastatin 40 mg On The Levels of Serum Endocan, Galectin-3 and Chemerin in Patients With Acute Myocardial Infarction

Comparative Effects of Atorvastatin 80 mg and Rosuvastatin 40 mg On The Levels of Serum Endocan, Galectin-3 and Chemerin in Patients With Acute Myocardial Infarction

Galectin‐3 and risk of cardiovascular events and all‐cause mortality in type 2 diabetes

Atorvastatin Prevents Myocardial Fibrosis in Spontaneous Hypertension via Interleukin-6 (IL-6)/Signal Transducer and Activator of Transcription 3 (STAT3)/Endothelin-1 (ET-1) Pathway

Contact Info

Product

Resources

About