Background Despite revascularisation, a large proportion of acute coronary syndrome (ACS) patients continue to experience major adverse cardiovascular events (MACEs), which are worsened by diabetes mellitus (DM). Fibrinogen (FIB) is a risk factor for MACEs in coronary artery disease and often elevated in DM. However, the relationships between FIB, glucose metabolism (haemoglobin A1c [HbA1c] and fasting blood glucose [FBG]) and MACEs following percutaneous coronary intervention (PCI) in DM, non-DM or whole patients with ACS remains unknown. Methods A total of 411 ACS patients undergoing PCI were enrolled in this study. We compared baseline FIB levels between DM ( n = 103) and non-DM ( n = 308) patients and divided participants into three groups according to FIB level, i.e. FIB-L, FIB-M and FIB-H, to compare baseline characteristics and MACEs. Linear regression analysis of the relationship between glucose metabolism and FIB, Cox regression, survival and landmark analyses of MACEs were also performed over a median of 27.55 months of follow-up. Results Patients with DM had higher FIB levels than non-DM patients (3.56 ± 0.99 mg/dL vs. 3.34 ± 0.80 mg/dL, P < 0.05). HbA1c and FBG were significantly positively correlated with FIB in whole and DM patients but not in non-DM patients (all P < 0.05). Compared with the FIB-L group, the FIB-M (hazard ratio [HR] 1.797, 95% CI 1.117–2.892, P = 0.016) and FIB-H (HR 1.664, 95% CI 1.002–2.763, P = 0.049) groups were associated with higher MACEs in whole; the FIB-M (HR 7.783, 95% CI 1.012–59.854, P = 0.049) was associated with higher MACEs in DM patients. FIB was not associated with MACEs in non-DM patients. During landmark analysis, FIB showed better predictive value for MACEs after PCI in the first 30 months of follow up than in the subsequent period. Conclusion In this study from China, FIB was positively associated with glucose metabolism (HbA1c and FBG) in whole and DM populations with ACS. Moreover, elevated baseline FIB levels may be an important and independent predictor of MACEs following PCI, especially amongst those with DM. However, as the follow-up period increased, the baseline FIB levels lost their ability to predict MACEs.
Purpose: Anion gap (AG) is a valuable and easily obtained clinical tool for differentially diagnosis of acid-base disorders. Current understanding of the prognostic impact of AG on mortality after acute myocardial infarction (AMI) is limited. We aimed to investigate whether AG is a predictor of short-term and long-term all-cause mortality after AMI. Patients and Methods: We examined 1806 patients diagnosed with AMI in intensive care unit from the Medical Information Mart for Intensive Care III (MIMIC-III) database. We analyzed the association of AG with 30-day, 180-day and 1-year all-cause mortality on a continuous scale and in categories, using multivariable Cox regression. We utilized restricted cubic splines to evaluate the linearity between hazard ratio (HR) and AG concentrations.Results: AG was associated with a higher risk of 30-day, 180-day and 1-year all-cause mortality, with adjusted HRs of 1.083 (95% CI 1.051 to 1.117), 1.077 (95% CI 1.049 to 1.105), and 1.074 (95% CI 1.047 to 1.101), respectively. The results were consistent in subgroup analyses. The association between AG and all-cause mortality was linear for 180day and 1-year mortality, and near linear for 30-day mortality, as higher concentrations were associated with high all-cause mortality. When stratified according to quartiles, AG was associated with 30-day mortality (HR[95% CI]: second quartile, 2. 243[1.273, 3.955]; third quartile, 3.026 [1.763, 5.194]; top quartile, 4.402[2.573, 7.531]), 180-day mortality (HR[95% CI]: second quartile, 1. 719[1.118, 2.645]; third quartile, 2.362[1.575, 3.542]; top quartile, 3.116[2.077, 4.676]), and 1-year mortality (HR[95% CI]: second quartile, 1. 700[1.143, 2.528]; third quartile, 2.239[1.536, 3.264]; top quartile, 2.876[1.969, 4.201]) using bottom quartile as reference. Conclusion:We firstly demonstrated that higher AG was significantly associated with increased 30-day, 180-day and 1-year all-cause mortality in AMI patients. AG as an easily obtained marker is of strong and reliable predictive value for AMI mortality during follow-up.
Background. Emerging evidence demonstrates that the lipid metabolism in acute coronary syndrome (ACS) patients with type 2 diabetes mellitus (T2DM) differs from nondiabetic patients. However, the distinct lipid profiles and their relationships with the severity of coronary artery stenosis and prognosis in patients with T2DM remain elusive. Method and Result. This single-center, prospective cohort study enrolled 468 patients diagnosed with ACS undergoing coronary angiography, consisting of 314 non-DM and 154 DM patients. The HDL-C/apoA-I ratio was significantly higher in DM patients with a multivessel (≥3 affected vessels) lesion than a single-vessel (1-2 affected vessels) lesion. Regression analyses showed that the HDL-C/apoA-I ratio was positively correlated to the number of stenotic coronary arteries in DM patients but not non-DM patients. However, Kaplan-Meier survival analysis revealed no significant difference in the major adverse cardiovascular event rate regarding different HDL-C/apoA-I levels in DM or non-DM ACS patients at the end of the 2-year follow-up. Conclusion. A higher HDL-C/apoA-I ratio is associated with increased severity of coronary artery stenosis in DM patients with ACS but not with the rate of major adverse cardiovascular events at the end of the 2-year follow-up.
Background. Previous studies have shown that increased mean corpuscular volume (MCV) is an independent predictor for worse outcomes in coronary artery disease. However, as parameters to classify different types of anemia together with MCV, the relationship between mean corpuscular hemoglobin (MCH), mean corpuscular hemoglobin concentration (MCHC), and long-term outcomes in acute coronary syndrome (ACS) remains obscure. Moreover, few studies have compared the prognostic value of these red blood cell indices in anemic and nonanemic patients with ACS. Methods and Results. In this single-center observational cohort study, we enrolled 393 patients diagnosed with ACS, including 75 anemic and 318 nonanemic patients. The composite end points were defined as major adverse cardiovascular events (MACEs). After a median follow-up of 31.24 months, Kaplan–Meier survival analysis showed that higher MCV and MCH but not MCHC were significantly associated with increased MACEs in nonanemic ACS patients. Among the enrolled ACS patients without anemia, Cox regression analysis revealed that high MCV and MCH were correlated with increased MACEs after adjustment for cardiovascular risk factors, and receiver operating characteristic (ROC) curve analysis further confirmed the predictive value of high MCV and MCH. In bivariate correlation and linear regression analysis, plasma homocysteine was positively correlated with MCV and MCH but not MCHC in the nonanemic group even after adjusting for age, male sex, BMI, SBP, DBP, smoking, and diabetes. However, MCV, MCH, and MCHC showed no predictive value for MACEs, and no correlation was found between these red blood cell indices and homocysteine in ACS patients with anemia. Conclusion. After adjusting for cardiovascular risk factors, this study showed that higher admission MCV and MCH but not MCHC were independent predictors for long-term MACEs and positively correlated with homocysteine levels in the blood among the nonanemic but not anemic patients with ACS in China.
Life’s Simple 7 (LS7) is the American Heart Association’s (AHA) proposal for a healthy lifestyle, also known as cardiovascular health (CVH) metrics. However, the association between CVH metrics and the severity of hepatic steatosis and liver fibrosis detected by transient elastography is unknown. We performed a cross-sectional study using the data from the 2017–2018 National Health and Nutrition Examination Survey (NHANES) cycle. The controlled attenuation parameter (CAP) and liver stiffness measurement (LSM) were used to evaluate the severity of hepatic steatosis and liver fibrosis and to define NAFLD, advanced liver fibrosis, and cirrhosis. A total of 2679 participants were included. Multivariate linear regression analysis revealed that per 1-unit increase in the CVH metric, CAP and LSM decreased by 8.565 units and 0.274 units, respectively. In the multivariate logistic regression analysis, the risk of NAFLD, advanced liver fibrosis, and cirrhosis were 7, 10, and 6 times higher in the poor CVH group than in the ideal CVH group. Subgroup analysis indicated that CVD patients and non-Hispanic whites could benefit more from ideal CVH. In conclusion, adherence to ideal CVH metrics, as proposed by the AHA, can significantly reduce the risk of hepatic steatosis and liver fibrosis.
The effects of interferon-γ (IFN-γ ) on cholesterol accumulation and the development of foam cells are still unclear. In the present study, we found that IFN-γ promoted liver X receptor (LXR)-α degradation through the ubiquitin-proteasome system in macrophages. The process was dependent on its interactions with phosphorylated signal transducer and activator of transcription 1 (p-STAT1) and protein inhibitor of activated STAT 1 (PIAS1) because both fludarabine and PIAS1 shRNA reversed the decrease in LXR-α protein expression induced by IFN-γ . Additionally, IFN-γ enhanced the interactions of ubiquitin-conjugating enzyme 9 (UBC9), small ubiquitin-like modifier (SUMO)-1 and SUMO-2/3 with LXR-α. Moreover, treatment with shRNA specific for them not only reduced LXR-α polyubiquitination but also reversed the IFN-γ -induced decrease in its expression. Two specific sumoylation sites in LXR-α, K22 and K326, were indispensable for its IFN-γ -induced polyubiquitination because the K22R and K326R mutations inhibited the polyubiquitination and degradation of LXR-α in IFN-γ -treated macrophages. In addition, K22R or K326R mutation almost completely restored ATP-binding cassette subfamily G member 1 (ABCG1)mediated cholesterol efflux in IFN-γ -treated macrophages. Taken together, these findings indicate that IFN-γ promotes LXR-α degradation through a SUMO-ubiquitin-dependent pathway, which may inhibit cholesterol efflux mediated by ABCG1 from macrophages and promote the development of atherosclerosis.
Atrial fibrillation (AF) and heart failure (HF) coexistence is common of clinical significance. Although anemia is a well-recognized risk factor for adverse outcomes, the prognostic value of hemoglobin is controversial in AF and HF. We aimed to determine whether hemoglobin is associated with in-hospital outcomes in such patients.On the basis of the data from the CCC-AF (Improving Care for Cardiovascular Diseases in China-Atrial Fibrillation) project, 2367 inpatients with a definitive diagnosis of AF and HF and record of admission hemoglobin concentration were included. Logistic regression analysis was performed to investigate the relationship between hemoglobin and in-hospital outcomes.All patients were divided into 4 groups according to quartiles of hemoglobin values. Compared with patients with higher hemoglobin, patients with lower hemoglobin had higher proportion of males, heart rate (HR), and diastolic blood pressure (DBP). On the contrary, they had lower age, medical history, left ventricular ejection fraction (LVEF), and brain natriuretic peptide (P < .05). Spearman correlation showed that hemoglobin was negatively correlated with age, LVEF, international normalized ratio, and serum creatinine but positively correlated with HR, DBP, and blood urea nitrogen (P < .05). Multivariable logistic regression analysis revealed that increasing hemoglobin was an independent protective factor for in-hospital outcomes (odds ratio = 0.989; 95% confidence interval: 0.979–1.000; P = .046).Admission hemoglobin concentration was an independent protective factor for in-hospital outcomes in HF patients with AF. Our study indicated that increasing hemoglobin level and improving anemia degree might improve the prognosis of patients with AF and HF.
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