Antithrombin III deficiency concomitant with atrial fibrillation causes thrombi in all chambers: 2D and 3D echocardiographic evaluation.
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ABSTRACT:
SUBMITTER: Hayıroglu MI
PROVIDER: S-EPMC5324928 | biostudies-literature | 2016 Dec
REPOSITORIES: biostudies-literature
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Antithrombin III deficiency concomitant with atrial fibrillation causes thrombi in all chambers: 2D and 3D echocardiographic evaluation.
Hayıroğlu Mert İlker Mİ Keskin Muhammed M Dönmez Cevdet C Günay Muhammed Burak MB Ünal Dayı Şennur Ş
Anatolian journal of cardiology 20161201 12
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Project description:Obesity is linked to an increased risk of atrial fibrillation (AF) via increased oxidative stress. While NADPH oxidase II (NOX2), a major source of oxidative stress and reactive oxygen species (ROS) in the heart predisposes to AF, the underlying mechanisms remain unclear. Here, we studied NOX2-mediated ROS production in obesity-mediated AF using Nox2-knock-out (KO) mice and mature human induced pluripotent stem cell-derived atrial cardiomyocytes (hiPSC-aCMs). Diet-induced obesity (DIO) mice and hiPSC-aCMs treated with palmitic acid (PA) were infused with a NOX blocker (apocynin) and a NOX2-specific inhibitor, respectively. We showed that NOX2 inhibition normalized atrial action potential duration and abrogated obesity-mediated ion channel remodeling with reduced AF burden. Unbiased transcriptomics analysis revealed that NOX2 mediates atrial remodeling in obesity-mediated AF in DIO mice, PA-treated hiPSC-aCMs, and human atrial tissue from obese individuals by upregulation of paired-like homeodomain transcription factor 2 (PITX2). Furthermore, hiPSC-aCMs treated with hydrogen peroxide, a NOX2 surrogate, displayed increased PITX2 expression, establishing a mechanistic link between increased NOX2-mediated ROS production and modulation of PITX2. Our findings offer insights into possible mechanisms through which obesity triggers AF and support NOX2 inhibition as a potential novel prophylactic or adjunctive therapy for patients with obesity-mediated AF.
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Project description:Cases with thrombi in multiple cardiac chambers are rare. We report an extremely rare case in which thrombi were formed in all four cardiac chambers at the same time. A 55-year-old man presented with biventricular failure and liver dysfunction. A 12-lead ECG and an echocardiogram revealed an old anteroseptal myocardial infarction with aneurysm formation and atrial flutter. A transesophageal echocardiogram and a CT of the chest revealed thrombi in the right and left atrial appendage, right ventricular apex and left ventricular aneurysm. Pulmonary emboli were also identified. Stasis of the blood due to ventricular dysfunction and atrial flutter was considered to be responsible. The patient died of multiorgan failure due to circulatory failure.
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Project description:BackgroundThe echocardiographic parameters total atrial conduction time (PA-TDI duration), left atrial (LA) volume index (LAVI), and LA strain reflect adverse atrial remodeling and predict atrial fibrillation (AF).ObjectivesThe aim of this study was to investigate echocardiographic parameters indicating reverse LA remodeling and potential associations with AF recurrence after pulmonary vein isolation (PVI).MethodsThis prospective observational study consecutively enrolled patients scheduled for PVI for symptomatic AF. Electrocardiogram (ECG) test and transthoracic echocardiography were performed the day before and after PVI and again 3 months later. AF recurrence was determined by Holter ECG at 3 months, and telephone follow-up at 12 months, after PVI. The parameters of LA remodeling [PA-TDI, LAVI, and LA strain analysis: reservoir strain (LASr), conduit strain (LAScd), contraction strain (LASct)] were determined by transthoracic echocardiography.ResultsA total of 48 patients were included in the study (mean age: 61.4 ± 12.2 years). PA-TDI significantly decreased the day after PVI compared with the baseline (septal PA-TDI 103 ± 13 vs. 82 ± 14.9 ms, p ≤ 0.001; lateral PA-TDI 122.4 ± 14.8 vs. 106.9 ± 14.4 ms, p ≤ 0.001) and at the 3-month follow-up (septal PA-TDI: 77.8 ± 14.5, p ≤ 0.001; lateral PA-TDI 105.2 ± 16.1, p ≤ 0.001). LAVI showed a significant reduction at the 3-month follow-up compared with the baseline (47.7 ± 14.4 vs. 40.5 ± 9.7, p < 0.05). LASr, LAScd, and LASct did not change after PVI compared with the baseline. AF recurred in 10 patients after PVI (21%). Septal PA-TDI, septal a', and LAVI/a' determined the day after PVI were associated with AF recurrence.ConclusionChanges in echocardiographic parameters of LA remodeling and function indicate that functional electromechanical recovery preceded morphological reverse remodeling of the left atrium after PVI. Furthermore, these changes in echocardiographic parameters indicating LA reverse remodeling after PVI may identify patients at high risk of AF recurrence.
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Project description:BackgroundAtrial fibrillation (AFib) exists more frequently in patients with aortic stenosis (AS) than in patients without, and AFib may be a sign of progressive deterioration of AS. Echocardiographic assessment of AS in sinus rhythm is well documented, however, little is known about AFib in AS since such patients often are excluded from clinical echocardiographic trials.AimThe purpose of this study was to assess the prognostic importance of AFib in AS.MethodsThe study was designed as a single-center case-control study. Patients with AS and AFib were enrolled as cases (n = 103) and subsequently matched to controls (103 patients with AS but sinus rhythm). Cases and controls were matched according to age, gender and severity of AS. Primary outcome was all cause mortality and follow-up was 100% complete.ResultsCompared to controls the group with AFib had lower mean ejection fraction (42% vs. 49%; p < 0.001) and stroke volume (47 mL vs. 55 mL; p = 0.004), but higher heart rate (81 bpm vs. 68 bpm; p < 0.001) and no significant difference with regard to cardiac output (3.8 L vs. 4.0 L; p = 0.29). Accordingly, aortic jet velocity and gradients were significantly lower in AFib compared to controls but there were no differences (p = 0.38) in aortic valve area calculated by the continuity equation. During a median follow-up of 2.3 years (IQR: 1.2-3.6), 70 (34%) patients with AS died: 42 patients with AFib and 28 patients with sinus rhythm (p < 0.02). After adjusting for echocardiographic significant differences, AFib remained an independent predictor of mortality (HR 2.72 (95% CI: 1.12-6.61), p < 0.03). There was no significant interaction (p = 0.62) between AFib and AS on the risk of mortality, indicating that AFib predicted bad outcome regardless of the severity of AS.ConclusionsAFib is an independent risk factor in patients with AS and the prognostic impact of AFib seems to be the same despite the severity of AS.
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Project description:BackgroundThere was limited evidence on the clinical benefits of the concomitant Cox-Maze procedure with aortic valve replacement (AVR) in patients with atrial fibrillation. This study aimed to evaluate the early and long-term results of the concomitant Cox-Maze procedure in patients undergoing AVR for aortic valve disease.MethodsWe enrolled 101 patients who underwent AVR and had preoperative atrial fibrillation between January 1994 and December 2020. The early- and long-term clinical outcomes were compared between patients who underwent the concomitant Cox-Maze III procedures and those who did not undergo surgical ablation. Inverse probability of treatment weighting (IPTW) was used to adjust for differences in preoperative characteristics.ResultsForty-seven patients underwent the concomitant Cox-Maze III procedure (CM group), and 54 patients did not undergo surgical ablation for atrial fibrillation (non-CM group). There were no significant differences in early surgical outcomes between the two groups, except for a higher occurrence of acute kidney injury (AKI) in the CM group (P<0.001). The median follow-up duration was 70.7 months (interquartile range 36.2-118.8 months), and there were no significant differences in overall survival, thromboembolic complications, and anticoagulation-related bleeding between the two groups. Atrial fibrillation occurrence was significantly lower (P<0.001) in the CM group, and a greater number of patients discontinued anticoagulation in the CM group compared to the non-CM group (P=0.001).ConclusionsThe concomitant Cox-Maze procedure in patients with atrial fibrillation undergoing AVR did not increase early mortality or morbidity, except for AKI, and showed favorable long-term results in terms of rhythm outcome and anticoagulation discontinuation.
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Project description:Rare and common genetic variants contribute to the risk of atrial fibrillation (AF). Although ion channels were among the first AF candidate genes identified, rare loss-of-function variants in structural genes such as TTN have also been implicated in AF pathogenesis partly by the development of an atrial myopathy, but the underlying mechanisms are poorly understood. While TTN truncating variants (TTNtvs) have been causally linked to arrhythmia and cardiomyopathy syndromes, the role of missense variants (mvs) remains unclear. We report that rare TTNmvs are associated with adverse clinical outcomes in AF patients and we have identified a mechanism by which a TTNmv (T32756I) causes AF. Modeling the TTN-T32756I variant using human induced pluripotent stem cell-derived atrial cardiomyocytes (iPSC-aCMs) revealed that the mutant cells display aberrant contractility, increased activity of a cardiac potassium channel (KCNQ1, Kv7.1), and dysregulated calcium homeostasis without compromising the sarcomeric integrity of the atrial cardiomyocytes. We also show that a titin-binding protein, the Four-and-a-Half Lim domains 2 (FHL2), has increased binding with KCNQ1 and its modulatory subunit KCNE1 in the TTN-T32756I-iPSC-aCMs, enhancing the slow delayed rectifier potassium current (I ks). Suppression of FHL2 in mutant iPSC-aCMs normalized the I ks, supporting FHL2 as an I ks modulator. Our findings demonstrate that a single amino acid change in titin not only affects function but also causes ion channel remodeling and AF. These findings emphasize the need for high-throughput screening to evaluate the pathogenicity of TTNmvs and establish a mechanistic link between titin, potassium ion channels, and sarcomeric proteins that may represent a novel therapeutic target.
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Project description:BackgroundThe purpose of this study was to investigate the risk factors of left atrial (LA) or left atrial appendage (LAA) thrombi in patients with nonvalvular atrial fibrillation (NVAF) and to establish and validate relevant predictive models. It might improve thromboembolic risk stratification in patients with NVAF.MethodsThis study retrospectively included 1210 consecutive patients with NVAF undergoing transesophageal echocardiography (TEE), of whom 139 patients had thrombi in LA or in LAA. Through literature review and the ten events per variable (10EPV) principle, 13 variables were finally identified for inclusion in multivariate analysis. Models were constructed by multivariate logistic stepwise regression and least absolute shrinkage and selection operator (lasso) regression.ResultsAfter logistic regression, five variables (AF type, age, B-type natriuretic peptide, E/e' ratio, and left atrial diameter) were finally screened out as model 1. After Lasso regression, AF type, age, gender, B-type natriuretic peptide, E/e' ratio, left atrial diameter, and left ventricular ejection fraction were finally screened as model 2. After comparing the two models, the simpler model 1 was finally selected. The area under the ROC curve (AUC) of the model 1 was 0.865 (95% CI: 0.838-0.892), the Hosmer-Lemeshow test = 0.898, and the AUC = 0.861 after internal validation. The clinical decision curve showed that the new clinical prediction model could achieve a net clinical benefit when the expected threshold was between 0 and 0.6.ConclusionThis study constructed a new clinical prediction model of LA or LAA thrombi, with a higher discriminative degree than the CHADS2 and CHA2DS2-VASc scoring systems (AUC: 0.865 vs. 0.643; AUC: 0.865 vs 0.652).
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