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Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Coronary Sinus Metabolite 12,13-diHOME Is a Novel Biomarker for Left Atrial Remodeling in Patients With Atrial
Xixiang Tang1, Jiafu Wang2, Xiaolan Ouyang2
1VIP Medical Service Center (X.T.), the Third Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Insights
12,13-dihydroxy-9Z-octadecenoic acid (12,13-diHOME) is lower in atrial fibrillation (AF) patients and may predict AF recurrence. This metabolite shows potential in protecting heart cells from damage.
Area of Science:
- Cardiovascular Research
- Metabolomics
- Biomarker Discovery
Background:
- 12,13-dihydroxy-9Z-octadecenoic acid (12,13-diHOME) is known for cardioprotective effects.
- The association between 12,13-diHOME and atrial fibrillation (AF) has not been previously established.
Purpose of the Study:
- To investigate the relationship between 12,13-diHOME levels and atrial fibrillation (AF).
- To evaluate 12,13-diHOME as a potential biomarker for left atrium remodeling and AF recurrence.
Main Methods:
- Untargeted metabolomic profiling of coronary sinus (CS) and femoral vein blood in AF and non-AF subjects.
- Validation of 12,13-diHOME levels in a larger cohort, correlating with left atrium remodeling and AF recurrence.
- In vitro validation of 12,13-diHOME's biological functions in HL-1 cardiomyocytes.
Main Results:
- CS 12,13-diHOME was significantly lower in AF patients compared to controls.
- Decreased CS 12,13-diHOME levels correlated with left atrium remodeling and predicted 1-year postablation AF recurrence.
- 12,13-diHOME treatment protected cardiomyocytes, improved cardiac protein expression, and reduced mitochondrial damage.
Conclusions:
- Coronary sinus 12,13-diHOME is decreased in patients with atrial fibrillation.
- 12,13-diHOME may serve as a novel biomarker for left atrium remodeling in AF patients.
Background:
12,13-dihydroxy-9Z-octadecenoic acid (12,13-diHOME) has shown potential in protecting against heart disease, but its relationship with atrial fibrillation (AF) remains unknown.
Methods:
Coronary sinus (CS) and femoral vein blood samplings were synchronously collected from AF and non-AF subjects (paroxysmal supraventricular tachycardia or idiopathic premature ventricular complexes) who underwent catheter ablation. First, untargeted metabolomic profiling was performed in a discovery cohort (including 12 AF and 12 non-AF subjects) to identify the most promising CS or femoral vein metabolite. Then, the selected metabolite was further measured in a validation cohort (including 119 AF and 103 non-AF subjects) to confirm its relationship with left atrium remodeling and 1-year postablation recurrence of AF. Finally, the biological function of the selected metabolite was validated in a rapid-paced cultured HL-1 atrial cardiomyocytes model.
Results:
Metabolomic analysis identified CS 12,13-diHOME as the most pronounced change metabolite correlated with left atrium remodeling in the discovery cohort. In the validation cohort, CS 12,13-diHOME was significantly lower in patients with AF than non-AF controls (84.32±20.13 versus 96.24±23.56 pg/mL; P<0.01), and associated with worse structural, functional, and electrical remodeling of left atrium. Multivariable regression analyses further demonstrated that decreased CS 12,13-diHOME was an independent predictor of 1-year postablation recurrence of AF (odds ratio, 0.754 [95% CI, 0.648-0.920]; P=0.005). Biological function validations showed that 12,13-diHOME treatment significantly protect the cell viability, improved the expression of MHC (myosin heavy chain) and Cav1.2 (L-type calcium channel α1c), and attenuated mitochondrial damage in the rapid-paced cultured HL-1 cardiomyocytes model.
Conclusions:
CS metabolite 12,13-diHOME is decreased in patients with AF and can serve as a novel biomarker for left atrium remodeling.
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