Az interatrialis blokk és klinikai jelentősége. Egy EKG-entitás reneszánsza

2018 ◽  
Vol 159 (3) ◽  
pp. 91-95
Author(s):  
János Tomcsányi

Abstract: Interatrial block involves conduction delay between the right and left atria during sinus rhythm. The review describes the classification, pathomechanism and clinical significance of this under-recognised ECG sign, nominated Bayés syndrome. The presented ECGs help to recognise the differentypes of interatrial blocks. Orv Hetil. 2018; 159(3): 91–95.

2020 ◽  
Vol 9 (2) ◽  
pp. 558
Author(s):  
Lisette J.M.E. van der Does ◽  
Rohit K. Kharbanda ◽  
Christophe P. Teuwen ◽  
Paul Knops ◽  
Charles Kik ◽  
...  

The predisposition of atrial extrasystoles (AES) to trigger cardiac tachyarrhythmia may arise from intramural conduction disorders causing endo-epicardial asynchrony (EEA). This study aimed to determine whether spontaneous AES disturb endo-epicardial conduction. Simultaneous endo-epicardial mapping of the right atrium was performed in patients during cardiac surgery with two 128-electrode arrays. Sixty spontaneous AES were observed in 23 patients and were analyzed for incidence of conduction delay, conduction block and amount of EEA compared to the previous sinus rhythm beat. Both conduction delay and block occurred more often in AES compared to sinus rhythm. The difference in lines of conduction block between the epicardium and endocardium increased in AES causing a greater imbalance of conduction disorders between the layers. The incidence of EEA with differences ≥10 ms increased significantly in AES. AES caused delays between the epicardium and endocardium up to 130 ms and EEA to increase for up to half (47%) of the mapping area. Conduction disturbances between the epicardial and endocardial layer giving rise to EEA increase during AES. Asynchronous activation of the atrial layers increases during AES which may be a mechanism for triggering cardiac tachyarrhythmia under the right conditions but EEA cannot be recognized by current mapping tools.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Martinez-Selles ◽  
R Elosua ◽  
M Ibarrola ◽  
M De Andres ◽  
P Diez-Villanueva ◽  
...  

Abstract Background Advanced interatrial block (IAB), prolonged and bimodal P waves in surface ECG inferior leads, is an unrecognized surrogate of atrial dysfunction and a trigger of atrial dysrhythmias, mainly atrial fibrillation (AF). Our aim was to prospectively assess whether advanced IAB in sinus rhythm precedes AF and stroke in elderly outpatients with structural heart disease, a group not previously studied. Methods Prospective observational registry that included outpatients aged ≥70 years with structural heart disease and no previous diagnosis of AF. Patients were divided into three groups according to P-wave characteristics. Results Among 556 individuals, 223 had normal P-wave (40.1%), 196 partial IAB (35.3%), and 137 advanced IAB (24.6%). After a median follow-up of 694 days; 93 patients (16.7%) developed AF, 30 stroke (5.4%), and 34 died (6.1%). Advanced IAB was independently associated with AF (hazard ratio [HR] 2.9, 95% confidence interval [CI] 1.7–5.1, p<0.001), stroke (HR 3.8, 95% CI 1.4–10.7, p=0.010), and AF/stroke (HR 2.6, 95% CI 1.5–4.4, p=0.001). P-wave duration (ms) was independently associated with AF (HR 1.05, 95% CI 1.03–1.07, p<0.001), AF/stroke (HR 1.04, 95% CI 1.02–1.06, p<0.001), and mortality (HR 1.04, 95% CI 1.00–1.08, p=0.021). Conclusions The presence of advanced IAB in sinus rhythm is a risk factor for AF and stroke in an elderly population with structural heart disease and no previous diagnosis of AF. P-wave duration was also associated with all-cause mortality. Figure. Age- and sex-adjusted linear and non-linear association between P-wave duration (msec) and atrial fibrillation (A), stroke (B), and atrial fibrillation or stroke (C) risk. Results of a generalized additive model with spline smoothing functions and 4 degrees of freedom. Figure 1. Kaplan-Meyer curves of survival free of atrial fibrillation (A), stroke (B) and atrial fibrillation or stroke (C) in patients with normal P-wave, partial interatrial block (IAB) and advanced IAB. Funding Acknowledgement Type of funding source: None


2021 ◽  
Vol 22 (2) ◽  
pp. 484
Author(s):  
Martijn H. van der Ree ◽  
Jeroen Vendrik ◽  
Jan A. Kors ◽  
Ahmad S. Amin ◽  
Arthur A. M. Wilde ◽  
...  

Patients with Brugada syndrome (BrS) can show a leftward deviation of the frontal QRS-axis upon provocation with sodium channel blockers. The cause of this axis change is unclear. In this study, we aimed to determine (1) the prevalence of this left axis deviation and (2) to evaluate its cause, using the insights that could be derived from vectorcardiograms. Hence, from a large cohort of patients who underwent ajmaline provocation testing (n = 1430), we selected patients in whom a type-1 BrS-ECG was evoked (n = 345). Depolarization and repolarization parameters were analyzed for reconstructed vectorcardiograms and were compared between patients with and without a >30° leftward axis shift. We found (1) that the prevalence of a left axis deviation during provocation testing was 18% and (2) that this left axis deviation was not explained by terminal conduction slowing in the right ventricular outflow tract (4th QRS-loop quartile: +17 ± 14 ms versus +13 ± 15 ms, nonsignificant) but was associated with a more proximal conduction slowing (1st QRS-loop quartile: +12[8;18] ms versus +8[4;12] ms, p < 0.001 and 3rd QRS-loop quartile: +12 ± 10 ms versus +5 ± 7 ms, p < 0.001). There was no important heterogeneity of the action potential morphology (no difference in the ventricular gradient), but a left axis deviation did result in a discordant repolarization (spatial QRS-T angle: 122[59;147]° versus 44[25;91]°, p < 0.001). Thus, although the development of the type-1 BrS-ECG is characterized by a terminal conduction delay in the right ventricle, BrS-patients with a left axis deviation upon sodium channel blocker provocation have an additional proximal conduction slowing, which is associated with a subsequent discordant repolarization. Whether this has implications for risk stratification is still undetermined.


2018 ◽  
Vol 4 (11) ◽  
pp. 553-555
Author(s):  
Marina Arai ◽  
Seiji Fukamizu ◽  
Rintaro Hojo ◽  
Masayasu Hiraoka

2021 ◽  
Vol 10 (5) ◽  
pp. 1025
Author(s):  
Nicolò Martini ◽  
Martina Testolina ◽  
Gian Luca Toffanin ◽  
Rocco Arancio ◽  
Luca De Mattia ◽  
...  

The so-called Brugada syndrome (BS), first called precordial early repolarization syndrome (PERS), is characterized by the association of a fascinating electrocardiographic pattern, namely an aspect resembling right bundle branch block with a coved and sometime upsloping ST segment elevation in the precordial leads, and major ventricular arrhythmic events that could rarely lead to sudden death. Its electrogenesis has been related to a conduction delay mostly, but not only, located on the right ventricular outflow tract (RVOT), probably due to a progressive fibrosis of the conduction system. Many tests have been proposed to identify people at risk of sudden death and, among all, ajmaline challenge, thanks to its ability to enhance latent conduction defects, became so popular, even if its role is still controversial as it is neither specific nor sensitive enough to guide further invasive investigations and managements. Interestingly, a type 1 pattern has also been induced in many other cardiac diseases or systemic diseases with a cardiac involvement, such as long QT syndrome (LQTS), arrhythmogenic right ventricular cardiomyopathy (ARVC), hypertrophic cardiomyopathy (HCM) and myotonic dystrophy, without any clear arrhythmic risk profile. Evidence-based studies clearly showed that a positive ajmaline test does not provide any additional information on the risk stratification for major ventricular arrhythmic events on asymptomatic individuals with a non-diagnostic Brugada ECG pattern.


2014 ◽  
Vol 15 (6) ◽  
pp. 717-725 ◽  
Author(s):  
Sibel A Antonson ◽  
Ozlem Tulunoglu ◽  
Ibrahim Fevzi Tulunoglu ◽  
Marc Campillo-Funollet ◽  
Donald Antonson ◽  
...  

ABSTRACT Aim The aim of this in vitro study was to evaluate the effectiveness of a resin infiltrant (ICON) on marginal sealing ability of class II resin restorations with/without-caries. Materials and methods Forty-eight noncarious human premolar teeth were embedded and MO and DO preparations of standard dimensions were prepared. The left side of dentin margins of the cavities were left nonbonded (UB) while the right side were bonded using total etch-bonding agent and all restored with a Nanohybrid composite. The teeth were thermocycled and half of the specimens in the UB and B groups were subjected to an artificial caries process. ICON was applied to caries and noncaries subgroups following the manufacturer's directions. Impressions were made at each step: after the restorations were completed, thermocycling, artificial caries procedures, and infiltrant application and the silicone tag lengths were measured with a stereomicroscope. The specimens were immersed in 0.5% basic fuchsine at 37° C for 24 hours, sectioned and microleakage was evaluated with a stereomicroscope. Selected samples and their replicas were assessed for marginal quality under a stereomicroscope and SEM. Statistical evaluation of the data were made using Kruskal-Wallis, Mann-Whitney U and Wilcoxon Sign Rank tests. Results While bonding application did not create a meaningful difference, the thermocycling and artificial caries significantly increased the gap length and microleakage (p < 0.05). ICON application was decreased the microleakage, created gap-free margins and closed the gaps which were previously occurred at the same cavities (p < 0.05). Conclusion A resin infiltrant (ICON) application decreased the microleakage, created gap-free margins and closed the gaps, which previously occurred at the same cavities. Clinical significance Approximal application of resin infiltrant may increase the success of the class II composite restorations also reduced the risk of needing more complex restoration therapy. How to cite this article Tulunoglu O, Tulunoglu IF, Antonson SA, Campillo-Funollet M, Antonson D, Munoz-Viveros C. Effectiveness of an Infiltrant on Sealing of Composite Restoration Margins with/without Artificial Caries. J Contemp Dent Pract 2014;15(6): 717-725.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
N I Bork ◽  
N G Pavlidou ◽  
B Reiter ◽  
H Reichenspurner ◽  
T Christ ◽  
...  

Abstract Background Atrial fibrillation (AF) is accompanied by a profound remodeling of membrane receptors and alterations in cyclic nucleotides-dependent regulation of Ca2+-handling. Thus, while basal ryanodine receptors activity is upregulated, L-type calcium current (ICa,L) density is diminish in AF, due to local microdomain-specific cAMP dynamics. The same seems true for cGMP regulation in AF. In AF cGMP-mediated increase in ICa,L is blunted but NO-mediated attenuation of β-adrenoceptors stimulation-mediated increase is preserved. However, although the role of cGMP in controling atrial function and pathophysiology is controversial, no study has been ever performed in human myocytes to measure cGMP directly. Methods We isolated myocytes from the right and/or left atrium of 27 patients in sinus rhythm (SR), and with AF. Cells were then transfected with adenovirus to express the cytosolic FRET-based cGMP sensor red-cGES-DE5 and cultured for 48 hours. Förster resonance energy transfer (FRET) was used to measure cGMP in 61 living human atrial myocytes. We stimulated cells with the C-type natriuretic peptide CNP (100 nM and 1 μM), and the non-selective phosphodiesterases (PDEs) inhibitor IBMX (100 μM). Additionally, PDE specific inhibitors for PDE2 (Bay 60–7550, 100 nM) and PDE3 (Cilostamide, 10 μM) as well as inhibitor of the soluble guanylyl cyclase (ODQ, 50 μM) were used. We also measured PDE2 and PDE3 mRNA levels in atrial tissue samples from both groups of patients using RT-qPCR. Results We could show that stimulation with CNP increased cGMP levels in human atrial myocytes. However, in myocytes from patients with AF global cGMP responses to CNP and to IBMX was reduced compared to SR. Additionally, there was a difference in response to CNP and IBMX in patients with AF between the right and the left atria. Whereas in the right atria IBMX could further increase cGMP levels in the cell, in the left atria leaded to a reduction in cGMP levels. RT-qPCR showed a tendency of PDE3 to be reduced in AF. On the other hand, PDE2A gene expression was upregulated in the left atria. Conclusions We have shown that PDEs contributes cGMP signaling in the human atria and that they are involved in atrial pathophysiology. Now our data clearly show differences in cGMP regulation in cardiomyocytes isolated from left and right atrium from patients in atrial fibrillation and sinus rhythm. We observe a major role of PDEs, regulating cGMP pathway promoted by the reduced responses in AF, especially PDE2 in the left atria.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
C C Oliveira ◽  
C Vieira ◽  
I Campos ◽  
C Rodrigues ◽  
P Medeiros ◽  
...  

Abstract We report the case of a 17 years old athlete who resorted to the emergency service for palpitations and dizziness during exercising. He mentioned two episodes of syncope associated with exercise in the last 6 months. He was tachycardic (200 bpm) and hypotensive (85/56 mmHg). The electrocardiogram showed regular wide complex tachycardia with left bundle branch block morphology with superior axis restored to sinus rhythm after electrical cardioversion. In sinus rhythm, it showed T-wave inversion in V1-V5. Patient was admitted for study. Transthoracic echocardiography demonstrated mild enlargement and dysfunction of the right ventricle (RV) with global hypocontractility (FAC of 29%). The cardiac magnetic resonance (CMR revealed a RV end-diastolic volume indexed to surface body area of 180 mL/m2, global hypocinesia and RV dyssynchrony, subepicardial late enhancement in the distal septum and in the middle segment of the infero-septal wall. The patient underwent genetic study which showed a mutation in the gene that encodes the desmocolin-2 protein (DSC-2) involved in the pathogenesis of arrhythmogenic right ventricular cardiomyopathy (ARVC). According to the 2010 modified Task Force criteria for this diagnosis, the patient presented 4 major criteria for ARVC (characteristic ventricular tachycardia, repolarization and morphofunctional changes and the presence of pathogenic mutation) and the diagnosis was made. Thus, given the clinical presentation, it was implanted a subcutaneous cardioverter and patient is currently in follow-up at the Cardiology service. ARVC is present in 1 to 1000-5000 people and is responsible for 20% of all sudden cardiac deaths, especially in athletes. Diagnosis is based on structural, functional, electrophysiological and genetic criteria reflecting underlying histological changes. This case shows and reviews the essential characteristics to the disease recognition and, therefore, to the prevention of its most feared complication: sudden cardiac death.


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