Meta-analysis of metabolic syndrome and its individual components with risk of atrial fibrillation in different populations.

BACKGROUND: Recent studies have reported the effects of metabolic syndrome (MetS) and its components on atrial fibrillation (AF), but the results remain controversial. Therefore, we performed a meta-analysis to evaluate the relationship between MetS and AF risk. METHODS: Studies were searched from the Cochrane library, PubMed, and Embase databases through May 2020. Adjusted hazard ratios (HRs) and its corresponding 95% confidence intervals (CIs) were extracted and then pooled by using a random effects model. RESULTS: A total of 6 observational cohort studies were finally included. In the pooled analysis, MetS was associated with an increased risk of AF (HR 1.57; 95% CI 1.40-1.77; P < 0.01). And the components of MetS including abdominal obesity (HR 1.37; 95% CI 1.36-1.38; P < 0.01), elevated blood pressure (HR 1.56; 95% CI 1.46-1.66; P < 0.01), elevated fasting glucose (HR 1.18; 95% CI 1.15-1.21; P < 0.01) and low high density cholesterol (HDL) (HR 1.18; 95% CI 1.06-1.32; P < 0.01) was also associated with an increased risk of AF, while high triglyceride (HR 0.99; 95% CI 0.87-1.11, P = 0.82) was not. CONCLUSIONS: Our present meta-analysis suggested that MetS, as well as its components including abdominal obesity, elevated blood pressure, elevated fasting glucose and low HDL cholesterol were associated with an increase in the risk of AF.

Association of the Triglyceride-Glucose Index With Risk of Alzheimer's Disease: A Prospective Cohort Study.

INTRODUCTION: Triglyceride-glucose index (TyG) is a reliable surrogate marker of insulin resistance, and insulin resistance has been implicated in Alzheimer's disease pathophysiology. However, the relationship between the TyG index and Alzheimer's disease remains unclear. This study aimed to evaluate the association of the TyG index with the risk of Alzheimer's disease. METHODS: This prospective study included 2,170 participants free of Alzheimer's disease from the Framingham Heart Study Offspring Cohort Exam 7 (1998-2001), whose follow-up data were collected until 2018. The TyG index was calculated as Ln(fasting triglyceride [mg/dL] × fasting glucose [mg/dL]/2). The association of the TyG index with Alzheimer's disease was evaluated by competing risk regression model. Statistical analyses were performed in 2023. RESULTS: During a median follow-up of 13.8 years, 163 (7.5%) participants developed Alzheimer's disease. When compared with the reference (TyG index ≤8.28), a significantly elevated risk of Alzheimer's disease was seen in the group with a triglyceride-glucose index of 8.68-9.09 (adjusted hazard ratio=1.69, 95% CI=1.02, 2.81). When the TyG index was considered as a continuous variable, each unit increment in the TyG index was not significantly associated with the risk of Alzheimer's disease (adjusted hazard ratio=1.32, 95% CI=0.98, 1.77). CONCLUSIONS: This study showed that moderately elevated TyG index was independently associated with a higher incidence of Alzheimer's disease. TheTyG index might be used to define a high-risk population of Alzheimer's disease.

Usefulness of CHADS2, R2CHADS2, and CHA2DS2-VASc scores for predicting incident atrial fibrillation in heart failure with preserved ejection fraction patients.

AIMS: Coexisting of atrial fibrillation (AF) in patients with heart failure with preserved ejection fraction (HFpEF) could increase the risk of mortality. In this study, we aimed to assess the values of the CHADS2, R2CHADS2, and CHA2DS2-VASc scores for AF prediction in HFpEF patients. METHODS AND RESULTS: We performed a retrospective analysis on symptomatic HFpEF patients in the TOPCAT (Treatment of Preserved Cardiac Function Heart Failure with an Aldosterone Antagonist) trial. Associations of the CHADS2, R2CHADS2, and CHA2DS2-VASc scores with the risk of incident AF in HFpEF patients without baseline AF (n = 2202) were assessed using the multivariable competing risk regression models. The discriminatory performances of these scores were calculated using the C-index. During a median follow-up of 3.3 years, the average incidence of AF was 1.80 per 100 patient-years in HFpEF patients. When score was analysed as a continuous variable, per 1-point increase in the CHADS2 (hazard ratio [HR] = 1.42, 95% confidence interval [CI]: 1.20-1.68, C-index: 0.71), R2CHADS2 (HR = 1.25, 95% CI: 1.10-1.42, C-index: 0.69), or CHA2DS2-VASc (HR = 1.30, 95% CI: 1.16-1.46, C-index: 0.70) scores was associated with an increased risk of incident AF. When score was analysed as a categorical variable, patients with CHADS2 ≥ 3 (HR = 2.62, 95% CI: 1.70-4.04), R2CHADS2 ≥ 3 (HR = 2.55, 95% CI: 1.56-4.17), or CHA2DS2-VASc ≥ 4 (HR = 2.54, 95% CI: 1.59-4.07) had a higher risk of incident AF compared with the corresponding controls. CONCLUSIONS: Our data first suggest that the CHADS2, R2CHADS2, and CHA2DS2-VASc scores could predict the risk of incident AF in HFpEF patients with modest predictive abilities.

Meta-analysis of type 1 diabetes mellitus and risk of cardiovascular disease.

BACKGROUND: Individuals with diabetes have a high risk of cardiovascular disease (CVD). However, the association between type 1 diabetes mellitus (T1DM) and the risk of CVD has not been well addressed. This meta-analysis aimed to investigate the association between T1DM and CVD. METHODS: We searched the PubMed and EMBASE for studies that examined the association between T1DM and CVD until October 2020. We calculated the pooled risk ratios (RRs) with confidence intervals (CIs) from individual studies based on a random-effects model. RESULTS: We included 10 observational studies involving 166,027 patients with T1DM, and individuals were matched controls from the general population. Among T1DM patients, the RR of CVD was 5.09 (95% CI, 3.72-6.96), of coronary heart disease (CHD) was 9.38 (95% CI, 5.56-15.82), and of myocardial infarction was 6.37 (95% CI, 3.81-10.66). The RR of heart failure was 4.29 (95% CI, 3.54-5.19), of atrial fibrillation was 1.36 (95% CI, 1.17-1.59), and of stroke was 4.08 (95% CI, 3.42-4.86). Moreover, there was an increased RR among females for CHD, CVD, myocardial infarction, and stroke associated with T1DM. CONCLUSIONS: This study suggests that T1DM is associated with an increased risk of several types of CVD. However, the possible mechanisms for the increased risk of CVD remain unclear.

Role of Exosomal miRNAs in Heart Failure.

Heart failure is the terminal outcome of the majority of cardiovascular diseases, which lacks specific diagnostic biomarkers and therapeutic targets. It contributes to most of cardiovascular hospitalizations and death despite of the current therapy. Therefore, it is important to explore potential molecules improving the diagnosis and treatment of heart failure. MicroRNAs (miRNAs) are small non-coding RNAs that have been reported to be involved in regulating processes of heart failure. After the discovery of miRNAs in exosomes, the subcellular distribution analysis of miRNAs is raising researchers' attention. Growing evidence demonstrates that exosomal miRNAs may be promising diagnostic and therapeutic molecules for heart failure. This review summarizes the role of exosomal miRNAs in heart failure in the prospect of molecular and clinical researches.

Hispidulin Attenuates Cardiac Hypertrophy by Improving Mitochondrial Dysfunction.

Cardiac hypertrophy is a pathophysiological response to harmful stimuli. The continued presence of cardiac hypertrophy will ultimately develop into heart failure. The mitochondrion is the primary organelle of energy production, and its dysfunction plays a crucial role in the progressive development of heart failure from cardiac hypertrophy. Hispidulin, a natural flavonoid, has been substantiated to improve energy metabolism and inhibit oxidative stress. However, how hispidulin regulates cardiac hypertrophy and its underlying mechanism remains unknown. We found that hispidulin significantly inhibited pressure overload-induced cardiac hypertrophy and improved cardiac function in vivo and blocked phenylephrine (PE)-induced cardiomyocyte hypertrophy in vitro. We further proved that hispidulin remarkably improved mitochondrial function, manifested by increased electron transport chain (ETC) subunits expression, elevated ATP production, increased oxygen consumption rates (OCR), normalized mitochondrial morphology, and reduced oxidative stress. Furthermore, we discovered that Sirt1, a well-recognized regulator of mitochondrial function, might be a target of hispidulin, as evidenced by its upregulation after hispidulin treatment. Cotreatment with EX527 (a Sirt1-specific inhibitor) and hispidulin nearly completely abolished the antihypertrophic and protective effects of hispidulin on mitochondrial function, providing further evidence that Sirt1 could be the pivotal downstream effector of hispidulin in regulating cardiac hypertrophy.