Is atrial fibrillation in HFpEF a distinct phenotype? Insights from multiparametric MRI and circulating biomarkers
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ABSTRACT:
SUBMITTER: Dattani A
PROVIDER: S-EPMC10848361 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:AimsTo test the ability of four circulating biomarkers of fibrosis, and of low left atrial voltage, to predict recurrence of atrial fibrillation after catheter ablation.BackgroundCirculating biomarkers potentially may be used to improve patient selection for atrial fibrillation ablation. Low voltage areas in the left atrium predict arrhythmia recurrence when mapped in sinus rhythm. This study tested type III procollagen N terminal peptide (PIIINP), galectin-3 (gal-3), fibroblast growth factor 23 (FGF-23), and type I collagen C terminal telopeptide (ICTP), and whether low voltage areas in the left atrium predicted atrial fibrillation recurrence, irrespective of the rhythm during mapping.Methods92 atrial fibrillation ablation patients were studied. Biomarker levels in peripheral and intra-cardiac blood were measured with enzyme-linked immunosorbent assay. Low voltage (<0.5mV) was expressed as a proportion of the mapped left atrial surface area. Follow-up was one year. The primary endpoint was recurrence of arrhythmia. The secondary endpoint was a composite of recurrence despite two procedures, or after one procedure if no second procedure was undertaken.ResultsThe biomarkers were not predictive of either endpoint. After multivariate Cox regression analysis, high proportion of low voltage area in the left atrium was found to predict the primary endpoint in sinus rhythm mapping (hazard ratio 4.323, 95% confidence interval 1.337-13.982, p = 0.014) and atrial fibrillation mapping (hazard ratio 5.195, 95% confidence interval 1.032-26.141, p = 0.046). This effect was also apparent for the secondary endpoint.ConclusionThe studied biomarkers do not predict arrhythmia recurrence after catheter ablation. Left atrial voltage is an independent predictor of recurrence, whether the left atrium is mapped in atrial fibrillation or sinus rhythm.
| S-EPMC5749720 | biostudies-literature
Project description:BackgroundCardiac fibrosis is thought to play a central role in the pathogenesis of atrial fibrillation (AF). Retrospective studies have suggested that circulating fibrosis biomarkers are associated with AF, but prospective studies are limited.MethodsWe measured circulating levels of 2 fibrosis biomarkers, procollagen type III, N-terminal propeptide (PIIINP) and transforming growth factor β1 among participants of the CHS, a population-based study of older Americans. We used Cox proportional hazards and competing risks models to examine adjusted risk of incident AF over a median follow-up of 8.8 years.ResultsLevels of PIIINP were assessed in 2,935 participants, of whom 767 developed AF. Compared with the median PIIINP level (4.45 μg/L), adjusted hazard ratios (95% CIs) were 0.85 (0.72-1.00) at the 10th percentile, 0.93 (0.88-0.99) at the 25th percentile, 1.04 (0.95-1.04) at the 75th percentile, and 1.07 (0.90-1.26) at the 90th. Transforming growth factor β1 levels, assessed in 1,538 participants with 408 cases of incident AF, were not associated with AF risk.ConclusionIn older adults, PIIINP levels were associated with risk of incident AF in a complex manner, with an association that appeared to be positive up to median levels but with little relationship beyond that. Further studies are required to confirm and possibly delineate the mechanism for this relationship.
| S-EPMC4060155 | biostudies-literature
Project description:BackgroundHeart failure with preserved ejection fraction (HFpEF) and atrial fibrillation (AF) commonly coexist with overlapping pathophysiology like left atrial (LA) remodeling, which might differ given different underlying mechanisms.ObjectivesWe sought to investigate the different patterns of LA wall remodeling in AF vs. HFpEF.MethodsWe compared LA wall characteristics including wall volume (LAWV), wall thickness (LAWT), and wall thickness heterogeneity (LAWT[SD]) and LA structure, function among the controls (without AF or HFpEF, n = 115), HFpEF alone (n = 59), AF alone (n = 37), and HFpEF+AF (n = 38) groups using multi-detector computed tomography and echocardiography.ResultsLA wall remodeling was most predominant and peak atrial longitudinal strain (PALS) was worst in HFpEF+AF patients as compared to the rest. Despite lower E/e' (9.8 ± 3.8 vs. 13.4 ± 6.4) yet comparable LA volume, LAWT and PALS in AF alone vs. HFpEF alone, LAWV [12.6 (11.6-15.3) vs. 12.0 (10.2-13.7); p = 0.01] and LAWT(SD) [0.68 (0.61-0.71) vs. 0.60 (0.56-0.65); p < 0.001] were significantly greater in AF alone vs. HFpEF alone even after multi-variate adjustment and propensity matching. After excluding the HFpEF+AF group, both LAWV and LAWT [SD] provided incremental values when added to PALS or LAVi (all p for net reclassification improvement <0.05) in discriminating AF alone, with LAWT[SD] yielding the largest C-statistic (0.78, 95% CI: 0.70-0.86) among all LA wall indices.ConclusionsDespite a similar extent of LA enlargement and dysfunction in HFpEF vs. AF alone, larger LAWV and LAWT [SD] can distinguish AF from HFpEF alone, suggesting the distinct underlying pathophysiological mechanism of LA remodeling in AF vs. HFpEF.
| S-EPMC9086706 | biostudies-literature
Project description:BackgroundAtrial fibrillation (AF) is the most common sustained arrhythmia, and it causes a high rate of complications such as stroke. It is known that AF begins as paroxysmal form and gradually progresses to persistent form, and sometimes it is difficult to identify paroxysmal AF (PAF) before having stroke. The aim of this study is to evaluate the risk of PAF and stroke using genetic analysis and circulating biomarkers.Materials and methodsA total of 600 adult subjects were enrolled (300 from PAF and control groups). Peripheral blood was drawn to identify the genetic variation and biomarkers. Ten single nucleotide polymorphisms (SNPs) were analyzed, and circulating cell-free DNA (cfDNA) was measured from plasma. Four microRNAs (miR-99a-5p, miR-192-5p, miR-214-3p, and miR-342-5p) were quantified in serum using quantitative RT-PCR.ResultsGenotyping identified 4 single nucleotide polymorphisms (SNPs) that were significantly associated with AF (rs6817105, rs3807989, rs10824026, and rs2106261), and the genetic risk score using 4 SNPs showed the area under the curve (AUC) of 0.631. Circulating miRNAs and cfDNA did not show significant differences between PAF and control groups. The concentration of cfDNA was significantly higher in patients with a history of stroke, and the AUC was 0.950 to estimate the association with stroke.ConclusionThe risk of AF could be assessed by genetic risk score. Furthermore, the risk of stroke might be evaluated by plasma cfDNA level.
| S-EPMC10569505 | biostudies-literature
Project description:AF is the most common arrhythmia in clinical practice. In addition to the severe effect on quality of life, patients with AF are at higher risk of stroke and mortality. Recent studies have suggested that atrial and ventricular substrate play a major role in the development and maintenance of AF. Cardiac MRI has emerged as a viable tool for interrogating the underlying substrate in AF patients. Its advantage includes localisation and quantification of structural remodelling. Cardiac MRI of the atrial substrate is not only a tool for management and treatment of arrhythmia, but also to individualise the prevention of stroke and major cardiovascular events. This article provides an overview of atrial imaging using cardiac MRI and its clinical implications in the AF population.
| S-EPMC7788396 | biostudies-literature
Project description:Understanding the microstructural changes related to physiological aging of the cerebral cortex is pivotal to differentiate healthy aging from neurodegenerative processes. The aim of this study was to investigate the age-related global changes of cortical microstructure and regional patterns using multiparametric quantitative MRI (qMRI) in healthy subjects with a wide age range. 40 healthy participants (age range: 2nd to 8th decade) underwent high-resolution qMRI including T1, PD as well as T2, T2* and T2' mapping at 3 Tesla. Cortical reconstruction was performed with the FreeSurfer toolbox, followed by tests for correlations between qMRI parameters and age. Cortical T1 values were negatively correlated with age (p=0.007) and there was a widespread age-related decrease of cortical T1 involving the frontal and the parietotemporal cortex, while T2 was correlated positively with age, both in frontoparietal areas and globally (p=0.004). Cortical T2' values showed the most widespread associations across the cortex and strongest correlation with age (r= -0.724, p=0.0001). PD and T2* did not correlate with age. Multiparametric qMRI allows to characterize cortical aging, unveiling parameter-specific patterns. Quantitative T2' mapping seems to be a promising imaging biomarker of cortical age-related changes, suggesting that global cortical iron deposition is a prominent process in healthy aging.
| S-EPMC7485732 | biostudies-literature
Project description:BackgroundAtrial fibrillation (AF) is common in heart failure with preserved ejection fraction (HFpEF).ObjectivesThis study aimed to investigate the prognostic value of echocardiographic markers of congestion that can be applied to both AF and patients without AF with HFpEF.MethodsWe conducted a multicenter study of 505 patients with HFpEF admitted to hospitals for acute decompensated heart failure. The ratio of early diastolic transmitral flow velocity to mitral annulus velocity (E/e'), the tricuspid regurgitation peak velocity, and the collapsibility of the inferior vena cava were obtained at discharge. Congestion was determined by echocardiography if any one of E/e' ≥14 (E/e' ≥11 for AF), tricuspid regurgitation peak velocity ≥2.8 m/s, or inferior vena cava collapsibility <50% was positive. We classified patients into grade A, grade B, and grade C according to the number of positive congestion indices. The primary endpoint was the composite of cardiovascular death and heart failure hospitalization.ResultsDuring the follow-up period (median: 373 days), 162 (32%) patients experienced the primary endpoint. Grade C patients had a higher risk for the primary endpoint than grade A (HR: 2.98; 95% CI: 1.97-4.52) and grade B patients (HR: 1.92; 95% CI: 1.29-2.86) (log-rank P < 0.0001). Echocardiographic congestion grade improved the predictive value when added to the age, sex, New York Heart Association functional class, and N-terminal pro-B-type natriuretic peptide, not only in sinus rhythm (Uno C-statistic: 0.670 vs 0.655) but in AF (Uno C-statistic: 0.667 vs 0.639).ConclusionsEchocardiographic congestion grade has prognostic value in patients with HFpEF with and without AF.
| S-EPMC9627800 | biostudies-literature
Project description:Background: Overweight and mildly obese individuals have a lower risk of death than their normal-weight counterparts; this phenomenon is termed "obesity paradox." Whether this "obesity paradox" exists in patients with heart failure (HF) or can be modified by comorbidities is still controversial. Our current study aimed to determine the association of body mass index (BMI) with outcomes with patients with HF with preserved ejection fraction (HFpEF) with or without coexisting atrial fibrillation (AF). Methods: Patients with HFpEF from the Americas in the TOPCAT trial were categorized into the 3 groups: normal weight (18.5-24.9 kg/m2), overweight (25.0-29.9 kg/m2), and obesity (≥30 kg/m2). The Cox proportional-hazards models were used to calculate the adjusted hazard ratios (HRs) and CIs. Results: We identified 1,749 patients with HFpEF, 42.1% of which had baseline AF. In the total population of HFpEF, both overweight (HR = 0.59, 95% CI: 0.42-0.83) and obesity (HR = 0.49, 95% CI: 0.35-0.69) were associated with a reduced risk of all-cause death. Among patients with HFpEF without AF, overweight (HR = 0.51, 95% CI: 0.27-0.95) and obesity (HR = 0.64, 95% CI: 0.43-0.98) were associated with a lower risk of all-cause death. In those with AF, obesity (HR = 0.62, 95% CI: 0.40-0.95) but not overweight (HR = 0.81, 95% CI: 0.54-1.21) was associated with a decreased risk of all-cause death. Conclusions: The "obesity paradox" assessed by BMI exists in patients with HFpEF regardless of comorbid AF. Clinical Trial Registration: https://clinicaltrials.gov, identifier: NCT00094302.
| S-EPMC8787078 | biostudies-literature
Project description:BACKGROUND:Nonvalvular atrial fibrillation (AF) is the most common cardiac arrhythmia, and it is associated with the prothrombotic state. Circulating microparticles (cMPs) are membrane vesicles that are shed from many cell types in response to cell activation and cell apoptosis. Several studies reported that cMPs may play a role in the hypercoagulable state that can be observed in patients with AF. The aim of this study was to determine the levels of total cMPs and characterize their cellular origins in AF patients. METHODS:Atotal of 66 AF patients and 33 healthy controls were enrolled. This study investigated total cMP levels and their cellular origin in AF patients using polychromatic flow cytometry. RESULTS:AF patients had significantly higher levels of total cMPs (median 36.38, interquartile range [IQR] 21.16-68.50 × 105 counts/mL vs median 15.21, IQR 9.91-30.86 × 105 counts/mL; P = 0.004), platelet-derived MPs (PMPs) (median 10.61, IQR 6.55-18.04 × 105 counts/mL vs median 7.83, IQR 4.44-10.26 × 10/mL; P = 0.009), and endothelial-derived MPs (EMPs CD31+ CD41-) (median 2.94, IQR 1.78-0.60 × 105 counts/mL vs median 1.16, IQR 0.71-2.30 × 105 counts/mL; P = 0.001) than healthy controls after adjusting for potential confounders. Phosphatidylserine positive MP (PS + MP) levels were similar compared between AF patients and healthy controls. CONCLUSION:The results of this study revealed a marked increase in total cMP levels, and evidence of elevated endothelial damage and platelet activation, as demonstrated by increased PMP and EMP levels, in AF patients. Additional study is needed to further elucidate the role of cMPs (PMPs and EMPs) in the pathophysiology of and the complications associated with AF.
| S-EPMC6712324 | biostudies-other
Project description:BackgroundBiomarkers of multiple pathophysiological pathways have been related to incident atrial fibrillation (AF), but their predictive ability remains controversial.Methods and resultsIn 3120 Framingham cohort participants (mean age 58.4+/-9.7 years, 54% women), we related 10 biomarkers that represented inflammation (C-reactive protein and fibrinogen), neurohormonal activation (B-type natriuretic peptide [BNP] and N-terminal proatrial natriuretic peptide), oxidative stress (homocysteine), the renin-angiotensin-aldosterone system (renin and aldosterone), thrombosis and endothelial function (D-dimer and plasminogen activator inhibitor type 1), and microvascular damage (urinary albumin excretion; n=2673) to incident AF (n=209, 40% women) over a median follow-up of 9.7 years (range 0.05 to 12.8 years). In multivariable-adjusted analyses, the biomarker panel was associated with incident AF (P<0.0001). In stepwise-selection models (P<0.01 for entry and retention), log-transformed BNP (hazard ratio per SD 1.62, 95% confidence interval 1.41 to 1.85, P<0.0001) and C-reactive protein (hazard ratio 1.25, 95% confidence interval 1.07 to 1.45, P=0.004) were chosen. The addition of BNP to variables recently combined in a risk score for AF increased the C-statistic from 0.78 (95% confidence interval 0.75 to 0.81) to 0.80 (95% confidence interval 0.78 to 0.83) and showed an integrated discrimination improvement of 0.03 (95% confidence interval 0.02 to 0.04, P<0.0001), with 34.9% relative improvement in reclassification analysis. The combined analysis of BNP and C-reactive protein did not appreciably improve risk prediction over the model that incorporated BNP in addition to the risk factors.ConclusionsBNP is a predictor of incident AF and improves risk stratification based on well-established clinical risk factors. Whether knowledge of BNP concentrations may be used to target individuals at risk of AF for more intensive monitoring or primary prevention requires further investigation.
| S-EPMC3224826 | biostudies-literature