An Unusual Etiology for a 37-Year-Old Man With Paroxysmal Atrial Fibrillation and Termination Pause.
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ABSTRACT:
SUBMITTER: Yang HC
PROVIDER: S-EPMC8305670 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:ObjectiveAtrial fibrillation (AF) often progresses from paroxysmal AF (PAF) to more permanent forms. To improve personalised medicine, we aim to develop a new AF progression risk prediction model in patients with PAF.MethodsIn this interim-analysis of the Reappraisal of AF: Interaction Between HyperCoagulability, Electrical Remodelling, and Vascular Destabilisation in the Progression of AF study, patients with PAF undergoing extensive phenotyping at baseline and continuous rhythm monitoring during follow-up of ≥1 year were analysed. AF progression was defined as (1) progression to persistent or permanent AF or (2) progression of PAF with >3% burden increase. Multivariable analysis was done to identify predictors of AF progression.ResultsMean age was 65 (58-71) years, 179 (43%) were female. Follow-up was 2.2 (1.6-2.8) years, 51 of 417 patients (5.5%/year) showed AF progression. Multivariable analysis identified, PR interval, impaired left atrial function, mitral valve regurgitation and waist circumference to be associated with AF progression. Adding blood biomarkers improved the model (C-statistic from 0.709 to 0.830) and showed male sex, lower levels of factor XIIa:C1-esterase inhibitor and tissue factor pathway inhibitor, and higher levels of N-terminal pro-brain natriuretic peptide, proprotein convertase subtilisin/kexin type 9 and peptidoglycan recognition protein 1 were associated with AF progression.ConclusionIn patients with PAF, AF progression occurred in 5.5%/year. Predictors for progression included markers for atrial remodelling, sex, mitral valve regurgitation, waist circumference and biomarkers associated with coagulation, inflammation, cardiomyocyte stretch and atherosclerosis. These prediction models may help to determine risk of AF progression and treatment targets, but validation is needed.Trial registration numberNCT02726698.
| S-EPMC9872250 | biostudies-literature
Project description: Not available
| S-EPMC11022747 | biostudies-literature
Project description:BackgroundInflammation is closely related to atrial fibrillation (AF) pathogenesis, and interleukin-37 (IL-37) represents a new member of the anti-inflammatory cytokines.HypothesisIL-37 might play an important role in AF development and act as a potential risk factor for AF diagnosis.MethodsThe mRNA level of IL-37 in peripheral blood mononuclear cells (PBMCs) and serum IL-37 levels in AF patients and healthy controls were measured by real-time polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). PBMCs from AF patients were stimulated with recombinant IL-37. Levels of pro-inflammatory cytokines IL-6 and C-reactive protein were determined by RT-PCR and ELISA.ResultsIL-37 mRNAs and serum protein levels were higher in patients with AF or lone AF compared with healthy controls. Patients with paroxysmal AF or persistent AF showed higher IL-37 mRNAs and serum protein levels compared with those with permanent AF as well as healthy controls. In vitro, IL-37 inhibited the production of IL-6 and C-reactive protein in PBMCs of patients with AF.ConclusionsIL-37 is elevated in AF patients and its expression is closely associated with AF subgroups. Thus, IL-37 may provide a novel research target for the pathogenesis and therapy of AF. This study is the first to document elevated IL-37 in AF patients.
| S-EPMC6490375 | biostudies-literature
Project description:AimsTo assess left atrial (LA) function in sinus rhythm in veteran athletes with a history of paroxysmal atrial fibrillation (AF) exposed to prolonged endurance exercise compared with veteran athletes without AF and controls with and without paroxysmal AF from a non-athletic population.Methods and resultsThree hundred and two male participants from four groups, veteran recreational skiers with paroxysmal AF (n = 62), veteran skiers without AF (n = 89), and controls from a non-athletic population with (n = 62) and without paroxysmal AF (n = 89) underwent an echocardiographic examination in sinus rhythm to evaluate LA anatomy and function. The skiers (mean age 70.8±6.7 years) reported an average exposure to regular endurance exercise for 40-50 years. LA maximum and minimum volumes were larger in skiers (P < 0.001). LA volumes differed within the athletic and non-athletic groups with larger volumes in the AF groups ( P < 0.001). We observed a considerable overlap in LA volumes among non-athletes with AF and athletes without AF. LA reservoir strain (33.6% ± 4.8% vs. 28.3% ± 6.7% P < 0.001) and contractile strain (18.3% ± 4.0% vs. 15.0% ± 5.2% P < 0.001) were lower in both AF groups regardless of athletic status. LA reservoir strain was superior to volumetric measurements at identifying participants with AF (area under the curve 0.740 ±0.041).ConclusionMale veteran athletes had significantly larger LA volumes than non-athletes. In contrast, LA strain values were similar in athletes and non-athletes with paroxysmal AF, and significantly lower than in subjects without AF.
| S-EPMC8685599 | biostudies-literature
Project description:The molecular mechanisms underlying the early development of atrial fibrillation (AF) remain poorly understood. Emerging evidence suggests that abnormal epigenetic modulation via microRNAs (miRNAs) might be involved in the pathogenesis of paroxysmal AF (pAF).To identify key molecular changes associated with pAF, we conducted state-of-the-art transcriptomic studies to identify the abnormal miRNA-mRNA interactions potentially driving AF development.High-quality total RNA including miRNA was isolated from atrial biopsies of age-matched and sex-matched pAF patients and control patients in sinus rhythm (SR; n=4 per group) and used for RNA-sequencing and miRNA microarray. Results were analyzed bioinformatically and validated using quantitative real-time (qRT)-PCR and 3'UTR luciferase reporter assays.113 genes and 49 miRNAs were differentially expressed (DE) in pAF versus SR patients. Gene ontology analysis revealed that most of the DE genes were involved in the "gonadotropin releasing hormone receptor pathway" and "p53 pathway". Of these DE genes, bioinformatic analyses identified 23 pairs of putative miRNA-mRNA interactions that were altered in pAF (involving 15 miRNAs and 17 mRNAs). Using qRT-PCR and 3'UTR luciferase reporter assays, the interaction between upregulation of miR-199a-5p and downregulation of FKBP5 was confirmed in samples from pAF patients.Our combined transcriptomic analysis and miRNA microarray study of atrial samples from pAF patients revealed novel pathways and miRNA-mRNA regulations that may be relevant in the development of pAF. Future studies are required to investigate the potential involvement of the gonadotropin releasing hormone receptor and p53 pathways in AF pathogenesis.
| S-EPMC4417399 | biostudies-literature
Project description:Background and purposeOral anticoagulants are highly efficacious for the prevention of stroke in atrial fibrillation, and are the preferred treatment by current guidelines. The purpose of our study was to assess the utilization of antithrombotic drugs in atrial fibrillation patients at the time of ischemic stroke and the factors associated with their use.MethodsWe enrolled 759 consecutive patients admitted with ischemic stroke at Boston Medical Center, Geisinger Health System, and the University of Alabama. To be eligible, patients had to have electrocardiographically-confirmed atrial fibrillation at the time of admission or within 6 months of the index stroke. All stroke events and electrocardiograms were validated by study physicians. Patients with newly diagnosed atrial fibrillation were not eligible.ResultsThe mean age was 78 years, 43% were male, 19% black, and the mean CHADS2 score is 3.0. Atrial fibrillation was paroxysmal in 31%. At presentation, 181 (24%) patients were taking warfarin only, 96 (13%) both warfarin and aspirin, 294 (39%) aspirin alone, and 189 (25%) no antithrombotic therapy. The mean international normalized ratio was 1.6. Among patients with paroxysmal atrial fibrillation, one in five was taking warfarin. Although increasing stroke risk was associated with a greater likelihood of warfarin use, only 39% of highest risk CHADS2 3-6 were taking warfarin at the time of stroke.ConclusionsAmong high-risk individuals with atrial fibrillation, only 37% were taking warfarin at the time of stroke. Paroxysmal atrial fibrillation was associated with the highest risk of not receiving warfarin.
| S-EPMC5527994 | biostudies-literature
Project description:Atrial fibrillation (AF) is the most common cardiac arrhytmia, characterized by the chaotic motion of electrical wavefronts in the atria. In clinical practice, AF is classified under two primary categories: paroxysmal AF, short intermittent episodes separated by periods of normal electrical activity; and persistent AF, longer uninterrupted episodes of chaotic electrical activity. However, the precise reasons why AF in a given patient is paroxysmal or persistent is poorly understood. Recently, we have introduced the percolation-based Christensen-Manani-Peters (CMP) model of AF which naturally exhibits both paroxysmal and persistent AF, but precisely how these differences emerge in the model is unclear. In this paper, we dissect the CMP model to identify the cause of these different AF classifications. Starting from a mean-field model where we describe AF as a simple birth-death process, we add layers of complexity to the model and show that persistent AF arises from reentrant circuits which exhibit an asymmetry in their probability of activation relative to deactivation. As a result, different simulations generated at identical model parameters can exhibit fibrillatory episodes spanning several orders of magnitude from a few seconds to months. These findings demonstrate that diverse, complex fibrillatory dynamics can emerge from very simple dynamics in models of AF.
| S-EPMC7326608 | biostudies-literature
Project description:Background Low-level tragus stimulation (LLTS) has been shown to significantly reduce atrial fibrillation (AF) burden in patients with paroxysmal AF. P-wave alternans (PWA) is believed to be generated by the same substrate responsible for AF. Hence, PWA may serve as a marker in guiding LLTS therapy. We investigated the utility of PWA in guiding LLTS therapy in patients with AF. Methods and Results Twenty-eight patients with AF were randomized to either active LLTS or sham (earlobe stimulation). LLTS was delivered through a transcutaneous electrical nerve stimulation device (pulse width 200 μs, frequency 20 Hz, amplitude 10-50 mA), for 1 hour daily over a 6-month period. AF burden over 2-week periods was assessed by noninvasive continuous ECG monitoring at baseline, 3 months, and 6 months. A 5-minute control ECG for PWA analysis was recorded during all 3 follow-up visits. Following the control ECG, an additional 5-minute ECG was recorded during active LLTS in all patients. At baseline, acute LLTS led to a significant rise in PWA burden. However, active patients receiving chronic LLTS demonstrated a significant reduction in both PWA and AF burden after 6 months (P<0.05). Active patients who demonstrated an increase in PWA burden with acute LLTS showed a significant drop in AF burden after 6 months of chronic LLTS. Conclusions Chronic, intermittent LLTS resulted in lower PWA and AF burden than did sham control stimulation. Our results support the use of PWA as a potential marker for guiding LLTS treatment of paroxysmal AF.
| S-EPMC8477868 | biostudies-literature
Project description:The purpose of the present study was to identify aberrantly expressed lncRNAs in pAF and predict their potential functions. We recruited three pAF patients undergoing radiofrequency catheter ablation into our study. Peripheral blood leukocytes (PBL) and coronary sinus blood leukocytes (CSBL) were harvested from pAF patients at the same time during the operation. LncRNAs and mRNAs profiles in leukocytes were detected by microarray between pAF patients and controls. We identified 2095 lncRNAs and 1584 mRNAs differentially expressed between pAF patients and controls. Furthermore, expressions of lncRNAs and mRNAs in leukocytes were also measured between peripheral blood (PB) and coronary sinus blood (CSB). The 866 lncRNAs and 528 mRNAs were shown to be aberrantly expressed between CSBL and PBL in all three pAF patients. Bioinformatic analyses (lncRNA classification and subgroup, gene ontology analysis, pathway analysis and gene co-expression network construction) were performed for differentially expressed lncRNAs and mRNAs. Lastly, we confirmed seven aberrant lncRNAs and five dysregulated mRNAs by qRT-PCR. Our results demonstrated the aberrantly expressed lncRNAs and mRNAs in pAF and these lncRNAs/mRNAs may exert a vital role in pAF biology.
2017-07-31 | GSE75092 | GEO
Project description:Electrical, structural, and Ca2+ -handling remodeling contribute to the perpetuation/progression of atrial fibrillation (AF). Recent evidence has suggested a role for spontaneous sarcoplasmic reticulum Ca2+ -release events in long-standing persistent AF, but the occurrence and mechanisms of sarcoplasmic reticulum Ca2+ -release events in paroxysmal AF (pAF) are unknown.Right-atrial appendages from control sinus rhythm patients or patients with pAF (last episode a median of 10-20 days preoperatively) were analyzed with simultaneous measurements of [Ca2+]i (fluo-3-acetoxymethyl ester) and membrane currents/action potentials (patch-clamp) in isolated atrial cardiomyocytes, and Western blot. Action potential duration, L-type Ca2+ current, and Na+ /Ca2+ -exchange current were unaltered in pAF, indicating the absence of AF-induced electrical remodeling. In contrast, there were increases in SR Ca2+ leak and incidence of delayed after-depolarizations in pAF. Ca2+ -transient amplitude and sarcoplasmic reticulum Ca2+ load (caffeine-induced Ca2+ -transient amplitude, integrated Na+/Ca2+ -exchange current) were larger in pAF. Ca2+ -transient decay was faster in pAF, but the decay of caffeine-induced Ca2+ transients was unaltered, suggesting increased SERCA2a function. In agreement, phosphorylation (inactivation) of the SERCA2a-inhibitor protein phospholamban was increased in pAF. Ryanodine receptor fractional phosphorylation was unaltered in pAF, whereas ryanodine receptor expression and single-channel open probability were increased. A novel computational model of the human atrial cardiomyocyte indicated that both ryanodine receptor dysregulation and enhanced SERCA2a activity promote increased sarcoplasmic reticulum Ca2+ leak and sarcoplasmic reticulum Ca2+ -release events, causing delayed after-depolarizations/triggered activity in pAF.Increased diastolic sarcoplasmic reticulum Ca2+ leak and related delayed after-depolarizations/triggered activity promote cellular arrhythmogenesis in pAF patients. Biochemical, functional, and modeling studies point to a combination of increased sarcoplasmic reticulum Ca2+ load related to phospholamban hyperphosphorylation and ryanodine receptor dysregulation as underlying mechanisms.
| S-EPMC4342412 | biostudies-literature