ABSTRACT
BACKGROUND: The interplay between diabetes mellitus (DM), glycemic traits, and vascular and valvular calcifications is intricate and multifactorial. Exploring potential mediators may illuminate underlying pathways and identify novel therapeutic targets. METHODS: We utilized univariable and multivariable Mendelian randomization (MR) analyses to investigate associations and mediation effects. Additionally, the multivariable MR analyses incorporated cardiometabolic risk factors, allowing us to account for potential confounders. RESULTS: Type 2 diabetes mellitus (T2DM) and glycated hemoglobin (HbA1c) were positively associated with both coronary artery calcification (CAC) and calcific aortic valvular stenosis (CAVS). However, fasting glucose (FG) was only linked to CAVS and showed no association with CAC. Additionally, CAVS demonstrated a causal effect on FG. Calcium levels partially mediated the impact of T2DM on both types of calcifications. Specifically, serum calcium was positively associated with both CAC and CAVS. The mediation effects of calcium levels on the impact of T2DM on CAC and CAVS were 6.063% and 3.939%, respectively. The associations between T2DM and HbA1c with calcifications were influenced by body mass index (BMI) and smoking status. However, these associations were generally reduced after adjusting for hypertension. CONCLUSION: Our findings suggest a genetically supported causal relationship between DM, glycemic traits, and vascular and valvular calcifications, with serum calcium playing a critical mediating role.
ABSTRACT
This study represents a case of idiopathic left posterior fascicle ventricular tachycardia (LPF-VT), which is intriguing due to regular alternation of short-long RR intervals and QRS morphology. Transthoracic echocardiogram analysis did not detect any structural heart disease. A baseline electrophysiological study was performed. Intracardiac recording during tachycardia showed V-A dissociation, confirming the final diagnosis of idiopathic LPF-VT. No regularity in the monomorphic VT was recorded. Previous relevant studies suggested that a single focus with two exits in distal branches of the left posterior fascicle or two different foci localized in the Purkinje-myocardial network of the left posterior fascicle can clarify the mechanisms. Our team proposed an additional explanation that combines the physiological refractory period with the Ashman phenomenon in individual reentrant LPF-VT circuit.
Subject(s)
Catheter Ablation , Tachycardia, Ventricular , Bundle of His , Electrocardiography , Humans , Myocardium , Tachycardia, Ventricular/diagnosis , Tachycardia, Ventricular/surgeryABSTRACT
OBJECTIVE: To investigate the association of ATP binding cassette transporter A1 (ABCA1) gene R219K polymorphisms with atrial fibrillation (AF) in Chinese population. METHODS: A total of 250 patients with AF and 250 control subjects were selected. Polymerase chain reaction-restricted fragments length polymorphism (PCR-RFLP) was used to determine the ABCA1 genotype, and the serum concentration of C-reactive protein (CRP) and high-density lipoprotein cholesterol (HDL-C) were measured in all the subjects. RESULTS: The frequency of the RR , RK , KK , allele R , allele K genotype of ABCA1 in AF group and control group was 42.0%, 42.8%, 15.2%, 34.0%, 43.2% and 22.8%, 63.4%, 36.6%, 55.6%, 44.4%, respectively. The frequency of the KK genotype was significantly higher in the control group than in the case group (P=0.03), and the frequency of the allele K genotype was significantly different between the two groups (P=0.012). The serum CRP concentrations was significantly higher in AF group than in the control group (P=0.004), but serum HDL-C level showed no difference between the two groups. The serum CRP concentrations were significantly higher in patients with RR genotype than in those with KK genotype (P=0.013), and patients with RR genotype had significantly lower HDL-C level than those with RK and KK genotypes (P=0.009 and 0.027, respectively). CONCLUSION: Patients with AF have elevated serum CRP level in comparison with healthy individuals, and the K allele of R219K polymorphism is an independent protective factor against AF.
