Fibroblast Growth Factor 21 Correlates with the Prognosis of Dilated Cardiomyopathy.

OBJECTIVES: The goal of this study was to evaluate whether serum fibroblast growth factor 21 (FGF21) levels can be used to predict the prognosis of dilated cardiomyopathy (DCM). METHODS: 241 patients with DCM and 80 control subjects were recruited and followed up for an average of 16.12 months. A 2-dimensional (2-D) echocardiography technique was performed to calculate the left ventricular end-diastolic diameter (LVEDD) and left ventricular ejection fraction (LVEF) percentages. The levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and creatinine were measured in routine clinical laboratory tests. Serum FGF21 levels were measured by enzyme-linked immunosorbent assay (ELISA). RESULTS: The levels of serum FGF21 were significantly higher in the DCM groups than in the control groups (225.85 ± 32.57 vs. 145.36 ± 30.57, p < 0.001). Serum FGF21 levels were positively correlated with the NYHA functional classification of heart failure (HF) (r = 0.610, p < 0.001) and NT-proBNP levels (r = 0.741, p < 0.001). Moreover, a negative correlation was observed between the serum FGF21 levels and the LVEF (r = -0.402, p < 0.001). FGF21, NT-proBNP, the LVEF and a history of atrial fibrillation (AF) correlated significantly with NYHA class IV (p < 0.05). The AUC of NT-proBNP for predicting NYHA class IV in DCM patients was greater than that of FGF21 (0.830 vs. 0.772, p < 0.001). Overall, 133 patients with DCM were recorded at the end point. Kaplan-Meier analysis results showed that the survival probability of those individuals with high levels of FGF21 and NT-proBNP was significantly lower than of those with low levels of these factors (p < 0.001). In the multivariate Cox analysis, FGF21 (HR 2.561; 95% CI 1.705-3.849) and NT-proBNP (HR 4.458; 95% CI 2.645-7.513) were independent predictors of a poor prognosis in DCM patients. CONCLUSIONS: Serum FGF21 levels were associated with the risk factors, severity, and prognosis of DCM. Therefore, FGF21 may serve as a novel biomarker for the prognosis of DCM.

Correlations and Prognostic Roles of the Nutritional Status and Neutrophil-to-lymphocyte Ratio in Elderly Patients with Acute Myocardial Infarction Undergoing Primary Coronary Intervention.

The prognostic capacities of nutritional status and inflammation in patients with acute myocardial infarction (AMI) have attracted increasing interest. However, the combined usefulness of the Controlling Nutritional Status (CONUT) score and neutrophil-to-lymphocyte ratio (NLR) in predicting adverse outcomes has not been investigated. The aim of our study was to investigate the relationship between the CONUT score and the NLR in patients with AMI and assessing the potential of these factors as prognostic markers.In this retrospective study, we reviewed the medical records of consecutive patients aged 65 years or older who were diagnosed with AMI and who underwent primary coronary intervention. We assessed the nutritional and inflammatory statuses using the CONUT score and the NLR, respectively. The NLR and CONUT score in the major adverse cardiovascular event (MACE) (+) patients were significantly higher than those in the MACE (-) patients. The areas under the receiver operating characteristic curves of the NLR and CONUT score were 0.71 and 0.77, respectively. The Kaplan-Meier analysis showed that patients with a high NLR (≥6.07) and CONUT score (≥3.5) had the worst prognoses. The multivariate Cox proportional hazards analyses suggested that the CONUT score was an independent predictor.The CONUT score was proven to be a significant prognostic factor of clinical outcomes in patients with AMI. However, further research in this area is needed to more fully understand the relationship among nutritional status, inflammation, and cardiovascular diseases, which might help reduce MACEs in patients with AMI.

Sugar-sweetened beverages and risk of hypertension and CVD: a dose-response meta-analysis.

A number of prospective cohort studies have investigated the associations between consumption of sugar-sweetened beverages (SSB) and the risk of hypertension, CHD and stroke, but revealed mixed results. In the present study, we aimed to perform a dose-response meta-analysis of these prospective studies to clarify these associations. A systematic literature search was conducted using the PubMed and Embase databases up to 5 May 2014. Random- or fixed-effects models were used to calculate the pooled relative risks (RR) with 95 % CI for the highest compared with the lowest category of SSB consumption, and to conduct a dose-response analysis. A total of six prospective studies (240 726 participants and 80 411 incident cases of hypertension) from four publications on hypertension were identified. A total of four prospective studies (194 664 participants and 7396 incident cases of CHD) from four publications on CHD were identified. A total of four prospective studies (259 176 participants and 10 011 incident cases of stroke) from four publications on stroke were identified. The summary RR for incident hypertension was 1·08 (95 % CI 1·04, 1·12) for every additional one serving/d increase in SSB consumption. The summary RR for incident CHD was 1·17 (95 % CI 1·10, 1·24) for every serving/d increase in SSB consumption. There was no significant association between SSB consumption and total stroke (summary RR 1·06, 95 % CI 0·97, 1·15) for every serving/d increase in SSB consumption. The present meta-analysis suggested that a higher consumption of SSB was associated with a higher risk of hypertension and CHD, but not with a higher risk of stroke.

[A multi-center survey on the therapeutic status of patients with acute myocardial infarction in Wuxi city of China].

OBJECTIVE: To explore the characteristics and therapies of patients with acute myocardial infarction (AMI) in Wuxi city, China. METHODS: A network was established to obtain information of patients with AMI who were admitted to 9 designated hospitals between 2011 and 2012. A total of 1 714 patients were enrolled (1 334 males, 754 smokers, 1 076 hypertension, 270 hyperlipidemia and 398 diabetes) including 1 410 patients with acute ST-segment elevation myocardial infarction (STEMI) and 304 patients with acute non ST-segment elevation myocardial infarction (NSTEMI). Patients' characteristics, therapies, the incidence of major adverse cardiovascular events (MACEs) and all-cause mortality were analyzed. RESULTS: (1) Medication therapy was as follows: antiplatelet therapy 98.3% (1 685 cases) , beta-blockers 59.1% (1 013 cases) , ACEI or ARB 67.6% (1 159 cases) , statins 98.1% (1 682 cases) , and nitrates 71.1% (1 218 cases) . Of the patients, 7.1% (132 cases) received temporary pacemakers, 34.0% (480 cases) with acute STEMI underwent reperfusion [direct PCI 18.4% (260 cases) and thrombolysis 15.6% (220 cases)]. (2) According to the hospital admission data, patients were divided into three groups: group A, transported to the hospital by ambulance (n = 361); group B, transported to the hospital by private vehicles (n = 1 318); and group C, AMI occurred in the hospital (n = 35). The median time of AMI onset to physician contact of the 3 groups was 178 min, 368 min, and 9 min, respectively. The median time from AMI onset to the first ECG was 181 min, 379 min, and 10 min, respectively. The median time from AMI onset to cardiology specialist consultation was 187 min, 431 min, and 69 min, respectively. AMI onset-to-physician contact, AMI onset-to-first ECG, and AMI onset-to-specialized treatment time was the shortest in group C, followed by group A and group B. For patients with STEMI underwent reperfusion therapy, the median AMI onset-to-reperfusion therapy time was significantly shorter in group A patients than group B patients [thrombolysis group: 224(171, 514) min vs. 378 (158, 785) min, PCI group: 318 (154, 674) min vs. 489 (143, 816) min, all P < 0.05]. (3) The total incidence of MACEs was 16.3% (279/1 714), the all-cause in-hospital mortality rate was 13.1% (224/1 714). According to the AMI onset-to-physician contact, patients were divided into 4 groups: <3 h, 3-6 h, 6-12 h, and >12 h. The incidence of MACEs [4.4% (23/517), 13.3% (60/451), 19.1% (77/404) and 34.8% (119/342),χ(2) = 114.36, P < 0.01] and all-cause in-hospital mortality rate [4.1% (21/517) , 10.4% (47/451), 18.6% (75/404), 23.7% (81/342), χ(2) = 84.36, P < 0.01] increased in proportion to the time of AMI onset-to-physician contact. Among STEMI patients, the incidence of MACEs [5.8% (15/260) , 12.3% (27/220) , 20.9% (194/930) ,χ(2) = 39.93, P < 0.01] and all-cause in-hospital mortality [1.5% (4/260) , 10.0% (22/220) , 18.2% (170/930) ,χ(2) = 50.90, P < 0.01] was the lowest in the primary PCI group, followed by thrombolysis group and was the highest in the early conservative treatment group. CONCLUSIONS: Guideline is well followed in terms of drug treatments of AMI in this cohort, but only a small proportion of AMI patients in Wuxi received reperfusion therapy. There is a considerable out-of-hospital time delay for AMI patients in this cohort which is shorter in group A than in group B. All-cause in-hospital mortality and MACEs is the lowest in AMI patients underwent primary PCI.

Olmesartan attenuates the impairment of endothelial cells induced by oxidized low density lipoprotein through downregulating expression of LOX-1.

Oxidized low density lipoprotein (ox-LDL) and its receptor, lectin-Like ox-LDL receptor-1 (LOX-1), play important roles in the development of endothelial injuries. Olmesartan can protect endothelial cells from the impairment caused by various pathological stimulations. In the present study we investigated whether olmesartan decreased the impairment of endothelial cells induced by ox-LDL by exerting its effects on LOX-1 both in vitro and in vivo. Incubation of cultured endothelial cells of neonatal rats with ox-LDL for 24 h or infusion of ox-LDL in mice for 3 weeks led to the remarkable impairment of endothelial cells, including increased lactate dehydrogenase synthesis, phosphorylation of p38 mitogen-activated protein kinases (p38 MAPK) and expression of apoptotic genes such as B-cell leukemia/lymphoma 2 (Bcl-2)-associated X protein (Bax) and caspase-3. Simultaneously, the cell vitality and expression of Bcl-2 gene were greatly reduced. All these effects, however, were significantly suppressed by the treatment with olmesartan. Furthermore, ox-LDL promoted up-regulation of LOX-1 expression either in cultured endothelial cells or in the aortas of mice, which was reversed with the administration of olmesartan. Our data indicated that olmesartan may attenuate the impairment of endothelial cell via down-regulation of the increased LOX-1 expression induced by ox-LDL.

[Metalloproteinase Tolloid-like 1 gene mutation in Chinese patients with sporadic congenital heart diseases].

OBJECTIVE: To explore whether there are gene mutations of Tolloid-like 1 (TLL-1) gene in Chinese patients with sporadic congenital heart disease (CHD). METHODS: One hundred and fifteen patients with sporadic CHD were selected as CHD group. One hundred and two age and gender-matched healthy people were recruited as control group. After amplifying the exon 10 of the TLL-1 gene by polymerase chain reaction, the polymerase chain reaction products were purified, sequenced and analyzed in order to investigate the TLL-1 gene mutation. RESULTS: An insertion mutation of base A in the exon 10 of TLL-1 gene was identified in 7 out of 115 CHD patients, including 3 patients with atrial septal defect, 2 patients with ventricular septal defect, 1 patients with patent ductus arteriosus and 1 patients with complex CHD, the total mutation rate was 6.1% in CHD group and 0 in control group (P < 0.01). CONCLUSIONS: TLL-1 gene mutation with an insertion mutation of base A in exon 10 is often in Chinese patients with various CHD. The underlying pathogenesis between TLL-1 gene mutation and occurrence of congenital heart disease in Chinese people remains unclear and warrants further investigations.

Elevated serum FGF21 predicts the major adverse cardiovascular events in STEMI patients after emergency percutaneous coronary intervention.

BACKGROUND: Although there have been several studies related to serum fibroblast growth factor 21 (FGF21) levels and acute myocardial infarction, the value of serum FGF21 levels in ST-segment elevation myocardial infarction (STEMI) patients after emergency percutaneous coronary intervention (PCI) has not been previously investigated. METHODS: A total of 348 STEMI patients who underwent emergency PCI were enrolled from January 2016 to December 2018. The primary endpoint was the occurrence of major adverse cardiovascular events (MACEs), with a median follow-up of 24 months. Eighty patients with stable angina (SA) who underwent selective PCI served as the control group. Serum FGF21 levels were measured by ELISA. RESULTS: Serum FGF21 levels were significantly higher in the STEMI group than in the SA group (225.03 ± 37.98 vs. 135.51 ±  34.48, P < 0.001). Multiple linear regression analysis revealed that serum FGF21 levels were correlated with NT-proBNP (P < 0.001). According to receiver operating characteristic (ROC) analysis, the areas under the ROC curve (AUCs) of FGF21 and NT-proBNP were 0.812 and 0.865, respectively. The Kaplan-Meier curves showed that STEMI patients with lower FGF21 levels had an increased MACE-free survival rate. Cox analysis revealed that high FGF21 levels (HR: 2.011, 95% CI: [1.160-3.489]) proved to be a powerful tool in predicting the risk of MACEs among STEMI patients after emergency PCI. CONCLUSION: Elevated FGF21 levels on admission have been shown to be a powerful predictor of MACEs for STEMI patients after emergency PCI.

Tumor necrosis factor-alpha 308G>A polymorphism and risk of rheumatic heart disease: a meta-analysis.

Rheumatic heart disease (RHD) remains a serious cardiovascular disorder across the world. Tumor necrosis factor alpha (TNF-α) codifies a potent immunomodulator and pro-inflammatory cytokine that mediates diverse pathological processes. A promoter 308G>A polymorphism in TNF-α has been implicated in RHD risk. However, the results remain controversial. Therefore, to evaluate more precise estimations of the relationship, a meta-analysis was performed. A total of 7 studies including 735 RHD cases and 926 controls were involved in this meta-analysis. Overall, our results revealed that there was a significant association with RHD risk in three genetic models (homozygous model: OR = 3.06, 95%CI = 1.22-10.60, P = 0.020; dominant model, OR = 2.03, 95%CI = 1.01-4.07, P = 0.048; and recessive model, OR = 4.26, 95%CI = 2.41-7.55, P < 0.001). Further ethnic population analysis found a significantly increased risk of RHD among Asians and Europeans. Interestingly, similar results were found among hospital-based studies. Begg's funnel plot and Egger's test did not reveal any publication bias. Taken together, this meta-analysis demonstrates that the TNF-α 308G>A polymorphism is associated with RHD susceptibility, and it contributes to the increased risk of RHD. However, additional well-designed studies with larger samples are warranted to confirm these findings.