QTc Interval is Associated with Atrial Fibrillation in Individuals with Metabolic Syndrome Phenotype

Abstract

Purpose Manifestations of metabolic syndrome (MetS) carry risks for atrial fibrillation (AF). The study determined whether any electrocardiographic parameter can reflect increased AF risk in individuals with MetS. Patients and Methods From our University Hospital database, we examined the presence of AF and its correlation with MetS manifestations, renal function, lipid profiles, and electrocardiographic parameters (P wave duration, PR interval, QRS width, and QTc intervals). Between January 2008 and December 2015, data from 4479 adults (women 41.6% vs men 58.4%) were identified. Results The overall prevalence of AF was 12.4%, without sex differences (women, 12.8% vs men, 12.1%). Patients with AF were older (age 73.9 ± 11.8 vs non-AF 67 ± 13.5 years), with lower lipid levels (TG, total cholesterol, and LDL-cholesterol, all p < 0.0001), and at lower eGFR level (64.1 ± 30.9 vs non-AF 68.8 ± 41.4 mL/min/1.73m2, p < 0.0001). Besides, sex differences were present in all electrocardiographic parameters (all p < 0.05). Hypertension had the highest odds ratio (1.33; p = 0.026) for AF. Comparing AF to non-AF, the QTc of quartiles was significantly different (p < 0.0089). The shortest and longest QTc quartiles had an increased incidence of AF. Conclusion AF risk in patients with MetS phenotypes can be reflected by QTc quartiles.

An increase in intercellular crosstalk and electrotonic coupling between cardiomyocytes and nonmyocytes reshapes the electrical conduction in the metabolic heart characterized by short QT intervals in ECGs

“…An intriguing finding was observed in MetS rats when they were fed for a relatively brief period (15−16 weeks), displaying a significant shortening in QT‐interval, and decreased contractile activity 19,20 . Clinically, the most of clinical investigations showed the role of QT‐interval and abnormal ventricular arrhythmias in MetS patients while both LQT and SQT through associated with abnormal time course of APs of ventricular myocytes, further leading to sudden cardiac arrest 21 . Here, we aimed to explore potential factors that might lead to the development of SQT.…”

“…19,20 Clinically, the most of clinical investigations showed the role of QT-interval and abnormal ventricular arrhythmias in MetS patients while both LQT and SQT through associated with abnormal time course of APs of ventricular myocytes, further leading to sudden cardiac arrest. 21 Here, we aimed to explore potential factors that might lead to the development of SQT. This included examining alterations in the positioning and phosphorylation of Cx43, as well as the connection between passive electrical conduction by nonmyocytes and the electrical behaviors (i.e., APs) of cardiomyocytes.…”

Electrical interaction between cardiomyocytes and non-myocytes in the metabolic heart contributes to the induction of short QT interval

“…Correspondingly, several investigations presented that congenital or familial SQT syndrome is a genetically heterogeneous cardiac channelopathy without structural heart disease further leading to cardiac arrest [16]. In this regard, there are published data on the role of QT-interval and abnormal ventricular arrhythmias in MetS patients while both prolongation and shortening in the QT-interval are associated with abnormal time course of action potentials (APs) of ventricular myocytes, which may lead to sudden cardiac arrest [17]. Associated with this topic, we previously showed a signi cant prolonged QT-interval (LQT) in ECGs from chronically induced MetS in rats (≥ 24-28 weeks), which is characterized by a low heart rate and depressed contractile activity [18,19].…”