Association of lipid composition and unsaturated fatty acids of VLDL with atrial remodeling in metabolic syndrome

Abstract

Subjects with metabolic syndrome (MetS) commonly have atrial remodeling, which indicates a risk for atrial fibrillation. This study determined MetS-related changes in lipid components in very-low-density lipoprotein (VLDL), which has been shown to cause atrial remodeling, the effect of statins on these changes, and the correlation between atrial remodeling and VLDL lipid compositions. Blood samples were collected from 12 non-MetS and 27 sex- and age-matched MetS subjects. Fourteen patients with MetS (MetS-off statin) discontinued statin therapy 14 days before the study, while the remaining 13 remained on it (MetS-on statin). The VLDLs were isolated and processed for mass-based lipid profiling. Lipidomic analyses were performed and associated with atrial remodeling markers measured using standard echocardiography and electrocardiography. Compared with the VLDL components of the non-MetS group, glucosyl/galactosyl ceramide, lyso-phosphatidylcholine, lyso-phosphatidylethanolamine, and triglycerides were enriched in the MetS-off statin group. Statin therapy attenuated all abnormally abundant lipid classes in MetS, except for triglycerides. In addition, lyso-phosphatidylcholine, lyso-phosphatidylethanolamine, and triglycerides were significantly correlated with atrial dilatation, and the latter two were also correlated with the PR interval. Enrichment of double bonds, which indicate unsaturated fatty acids, was also significantly correlated with atrial remodeling and P-wave duration. This study suggests that the pathological lipid payload of MetS-VLDL may contribute to atrial remodeling in patients.

Plasma triglyceride is associated with the recurrence of atrial fibrillation after radiofrequency catheter ablation: A retrospective study

“…23,24 In addition, a study suggests that the amount of unsaturated fatty acids in TGs is positively correlated with the expression of cardiac remodeling markers, including left atrial diameter, maximum volume, emptying volume, left ventricular ejection fraction, and LA contractile force. 25 These studies suggest that lipid metabolism may be involved in the occurrence of AF by altering the structure of the heart. Since the recurrence rate of AF remains high within 12 months of catheter ablation, 28,29 continued treatment and regular follow-up after surgery are required.…”

Metabolic Syndrome and Atrial Fibrillation: Different Entities or Combined Disorders

“…In MetS patients, the left atrium diameter and volume were larger compared to non-MetS individuals (LA diameter: non-MetS 3.2 ± 0.3 cm vs. MetS-off statin 4.4 ± 0.4 cm vs. MetS-on statin 4.3 ± 0.3 cm, p < 0.0001; LA maximum volume: non-MetS 45.2 ± 9.5 mL vs. MetS-off statin 81.9 ± 13.9 mL vs. MetS-on statin 77.5 ± 18.9 mL, p < 0.0001; LA minimum volume: non-MetS 28.1 ± 7.5 mL vs. MetS-off statin 39.3 ± 10.8 mL vs. MetS-on statin 42.0 ± 11.3 mL, p = 0.0065). Additionally, atrioventricular conduction, as measured by PR interval, was prolonged in MetS patients (176.1 ± 19.0 ms vs. 156.2 ± 15.4 ms, p = 0.0014) [ 68 ]. Therefore, it is plausible that dyslipidemia contributes to structural and electrical changes in the cardiac chambers, yet further research is warranted in this area.…”

“…This lends credence to the idea that MetS, as an integrated entity, can indeed instigate AF. Additionally, evidence suggests that MetS patients experience both structural alterations—such as left ventricular and left atrial remodeling—and electrical changes (PR interval in MetS group vs. non-MetS: 167.6 ± 20.0 msec vs. 156.2 ± 24.9 msec, p = 0.0064) [ 67 , 68 ]. Furthermore, both MetS and AF are characterized by inflammation, and their coexistence has been associated with even greater levels of inflammation, potentially introducing another mechanism that leads to fibrosis and AF development [ 70 ].…”