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Galectin-1, a β-galactoside-binding lectin mediating inflammation and neovascularization, is reported to attenuate ventricular remodeling after myocardial infarction. But its role in stable coronary artery disease (CAD) has not been fully elucidated. This study aimed to identify the relationship between the circulating galectin-1 level and the severity of CAD in patients with suspected CAD. Pre-procedure galectin-1 and high-sensitivity C-reactive protein (hs-CRP) concentrations were measured in 834 subjects who underwent scheduled coronary angiography. Subjects were grouped into tertiles of the galectin-1 levels. SYNTAX scores were calculated to evaluate the severity of CAD. All patients were followed until January 2019 or the occurrence of major adverse cardiovascular events (MACE). Patients with higher galectin-1 concentrations were older; had greater prevalence of hypertension, diabetes, chronic kidney disease, and heart failure; and were more likely to present with higher hs-CRP levels and SYNTAX scores. During the follow-up period of 1.3 ± 1.1 years, patients in the highest tertile of galectin-1 were associated with a greater risk of MACE after adjustment for age, sex, comorbidities, co-medications, serum levels of hemoglobin, creatinine, hs-CRP, ejection fraction, SYNTAX scores, and revascularization modalities (adjusted hazard ratio 10.95, 95% confidence interval 2.29–52.47, p = 0.003). Galectin-1 showed better discriminatory performance than hs-CRP, and non-inferior performance to SYNTAX scores, in predicting the incidence of MACE.

Trimethylamine N-oxide (TMAO) is a metabolite originated from bacterial metabolism of choline-rich foods. Evidence suggests an association between TMAO and atherosclerosis, but the relationship between TMAO and endothelial progenitor cells (EPCs) remains unclear. This study aimed to identify the relationship between TMAO concentrations, circulating EPCs, and endothelial function in patients with stable angina. Eighty-one stable angina subjects who underwent coronary angiography were enrolled. The circulating EPCs and flow-mediated vasodilation (FMD) were measured to evaluate endothelial function. Plasma TMAO and inflammatory markers, such as hsCRP and IL-1β, were determined. Furthermore, the effect of TMAO on EPCs was assessed in vitro. Patients with lower FMD had significantly decreased circulating EPCs, elevated TMAO, hsCRP, and IL-1β concentrations. Plasma TMAO levels were negatively correlated with circulating EPC numbers and the FMD, and positively correlated with hsCRP, IL-1β concentrations. In in vitro studies, incubation of TMAO in cultured EPCs promoted cellular inflammation, elevated oxidative stress, and suppressed EPC functions. Enhanced plasma TMAO levels were associated with reduced circulating EPCs numbers, endothelial dysfunction, and more adverse cardiovascular events. These findings provided evidence of TMAO’s toxicity on EPCs, and delivered new insight into the mechanism of TMAO-mediated atherosclerosis, which could be derived from TMAO-downregulated EPC functions.

Fibroblast growth factor 21 (FGF21) is a regulator of glucose homeostasis, and is suggested to have protective effect on diabetic nephropathy. Its impact on non-diabetic kidney disease is unclear. To investigate the impact of FGF21 on contrast-induced nephropathy (CIN), 531 subjects underwent elective coronary angiography (CAG) were enrolled. Baseline creatinine and FGF21 were obtained before CAG. Patients were grouped into tertiles according to their FGF21 concentration. Creatinine was obtained 48 hours after CAG, and every 6 months in the follow-up period. Renal function decline was defined as >30% reduction of eGFR from baseline. All subjects were followed up till December 2016, or till the occurrence of major adverse cardiovascular events (MACE). Patients with higher FGF21 concentration were older, had higher incidence of hypertension, diabetes, chronic kidney disease, and heart failure. Thirty-four cases of CIN and 111 cases of renal function decline were identified during mean follow-up of 2.3 ± 1.3 years. Circulating FGF21 level was independently associated with CIN (aOR: 4.66, 95% CI: 1.29–16.86, p = 0.019) and renal function decline (aHR: 7.98, 95% CI: 4.07–15.66, p

Activin A and its binding protein follistatin may be crucial in glucose homeostasis, as multifunctional proteins mediating inflammatory and anti-inflammatory effects. However, clinical data on the activin A level in prediabetes, and the association between the circulating activin A level and carotid intima-media thickness (cIMT), are lacking. We aimed to investigate activin A and follistatin levels and their associations with cIMT. In total, 470 inhabitants of I-Lan county (235 men; mean age 69 ± 9 years) with measurements of serum activin A and follistatin levels were included. Patients with prediabetes and diabetes had significantly increased activin A concentrations compared with those in the normal glycemic group (both p rs = 0.264, p = 0.001). In conclusion, activin A level, but not follistatin, was elevated independent of demographic variables with borderline significance and was correlated positively with cIMT in prediabetes. Activin A and follistatin levels were elevated in diabetes. In addition, elevated activin A was an independent risk factor for prediabetes and diabetes.

Frailty is characterized by decreased physiological reserve and increased vulnerability to atherosclerosis and subsequent mortality. Recently, low-grade albuminuria has been proposed as an atherosclerotic risk factor. We aimed to investigate the relationship between low-grade albuminuria and frailty by using cross-sectional data among community-dwelling middle-aged and older people. Totally, 1,441 inhabitants of I-Lan County with normal urinary albumin excretion (urine albumin to urine creatinine ratio [UACR]

Fibroblast growth factor 21 (FGF21), a polypeptide ligand promoted glucose homeostasis and lipids metabolism, was recently reported to attenuate cardiac hypertrophy. The aim of this study was to investigate the impact of FGF21 in diastolic heart failure. Subjects admitted for coronary angiogram were screened for heart failure and those with left ventricular (LV) ejection fraction p = 0.012) or confirmed with LVEDP level (odds ratio: 3.73, p = 0.030). Both plasma FGF21 (log rank p p = 0.0057) showed good predictive power to the 1-year adverse cardiac events. This finding suggested FGF21 could be involved in the pathophysiology of diastolic heart failure.

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Although the association of hyperuricemia and cardiovascular diseases is well established by previous research studies, the relationship between gout and deep vein thrombosis (DVT) remains unclear. We conducted a nationwide longitudinal cohort study to investigate the relationship between gout and DVT. We used the Taiwan National Health Insurance Research Database to identify patients with gout diagnosed in Taiwan during 2000–2011, and we followed up these patients to determine the incidence of DVT among them. The association between gout and DVT was analyzed by cox proportional hazard model. The study cohort included 35,959 patients with history of gout attack and 35,959 matched controls without gout attack. During the median follow-up of 7.5 ± 3.6 years, the incidence rate of DVT was significantly higher in patients with gout than that in control group (13.48 versus 9.77 per 104 person-years, p