Abstract 1364: Not All Refractory Period Abbreviation Promotes Atrial Fibrillation Equally: A Comparison Between Vagal and Atrial Tachycardia Remodeled Substrates

Background: Vagal (VG) and atrial tachycardia remodeled (ATR) AF substrates share many features: reduced effective refractory period (ERP), increased ERP heterogeneity and some common molecular mechanisms (I KACh enhancement by acetylcholine release in VG, constitutive I KACh enhancement in ATR). This study compared VG and ATR substrates at comparable ERP abbreviation. Methods: In each of 5 VG dogs, bilateral cervical VG stimulation parameters were adjusted (mean±SD: 3.6±1.7 V and 12.2±1.5 Hz; 0.2 ms) to produce the same mean ERP (at 4 RA and 4 LA sites) as a sex and weight matched ATR dog (RA paced 400 bpm × 7 days). Mean duration of burst pacing induced AF (DAF) and local dominant frequencies (DFs, analyzed by FFT at 240 bipolar electrodes, Fig A ) were determined. Results: Mean ERP was 79±13 ms in VG and 78±13 ms in ATR dogs. DAF was greater in VG than ATR dogs (1056±323 vs 289±510 s *P<0.01; both significantly > control, 43±61 s). Despite matched ERPs, there were significant differences in DF distribution (Fig B ): DF was faster (mean DF: 11.8±1.1 Hz VG vs 9.7±1.3 Hz ATR*) and DF variability greater (indicated by SD: 1.8±0.6 Hz VG vs 0.8±0.5 Hz ATR*) in VG dogs. AF drivers reflected by maximum DF zones were adjacent to autonomic ganglia (over RA in 4/5) for VG dogs; in ATR dogs driver zones were less clear and showed variable location. Conclusions: For a comparable atrial ERP, VG AF is faster and more persistent than AF with an ATR substrate. These results are consist with modeling work suggesting that VG-induced hyperpolarization is an important contributor to AF-maintaining rotor stabilization and acceleration, and indicate important differences between these superficially similar AF substrates.

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Angiotensin-(1–7) attenuates atrial tachycardia-induced sympathetic nerve remodeling

Journal of the Renin-Angiotensin-Aldosterone System ◽

10.1177/1470320317729281 ◽

2017 ◽

Vol 18 (3) ◽

pp. 147032031772928 ◽

Cited By ~ 1

Author(s):

Wenfeng Shangguan ◽

Wen Shi ◽

Guangping Li ◽

Yuanyuan Wang ◽

Jian Li ◽

...

Keyword(s):

Atrial Fibrillation ◽

Nerve Growth Factor ◽

Growth Factor ◽

Tyrosine Hydroxylase ◽

Sympathetic Nerve ◽

Refractory Period ◽

Atrial Tachycardia ◽

Effective Refractory Period ◽

Sympathetic Nerve Stimulation ◽

Atrial Effective Refractory Period

Introduction: The effect of Angiotensin-(1–7) (Ang-(1–7)) on atrial autonomic remodeling is still unknown. We hypothesized that Ang-(1–7) could inhibit sympathetic nerve remodeling in a canine model of chronic atrial tachycardia. Materials and methods: Eighteen dogs were randomly assigned to sham group, pacing group and Ang-(1–7) group. Rapid atrial pacing was maintained for 14 days in the pacing and Ang-(1–7) groups. Ang-(1–7) was administered intravenously in the Ang-(1–7) group. The atrial effective refractory period and atrial fibrillation inducibility level were measured at baseline and under sympathetic nerve stimulation after 14 days of measurement. The atrial sympathetic nerves labeled with tyrosine hydroxylase were detected using immunohistochemistry and Western blotting, and tyrosine hydroxylase and nerve growth factor mRNA levels were measured by reverse transcription polymerase chain reaction. Results: Pacing shortened the atrial effective refractory period and increased the atrial fibrillation inducibility level at baseline and under sympathetic nerve stimulation. Ang-(1–7) treatment attenuated the shortening of the atrial effective refractory period and the increase in the atrial fibrillation inducibility level. Immunohistochemistry and Western blotting showed sympathetic nerve hyperinnervation in the pacing group, while Ang-(1–7) attenuated sympathetic nerve proliferation. Ang-(1–7) alleviated the pacing-induced increases in tyrosine hydroxylase and nerve growth factor mRNA expression levels. Conclusion: Ang-(1–7) can attenuate pacing-induced atrial sympathetic hyperinnervation.

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Effects of procainamide on electrical activity in thoracic veins and atria in canine model of sustained atrial fibrillation

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00754.2003 ◽

2004 ◽

Vol 286 (5) ◽

pp. H1936-H1945 ◽

Cited By ~ 26

Author(s):

Chung-Chuan Chou ◽

Shengmei Zhou ◽

Yasushi Miyauchi ◽

Hui-Nam Pak ◽

Yuji Okuyama ◽

...

Keyword(s):

Atrial Fibrillation ◽

High Resolution ◽

Cumulative Dose ◽

Refractory Period ◽

Atrial Tachycardia ◽

Canine Model ◽

Dominant Frequency ◽

Wave Fronts ◽

High Resolution Mapping ◽

Resolution Mapping

Focal discharges (FDs) are present in thoracic veins during atrial fibrillation (AF). We hypothesize that procainamide exerts its anti-AF action by suppressing FDs in the thoracic veins. We studied six mongrel dogs (22–27 kg) with sustained (>6 h) AF induced by 47 ± 20 days of chronic rapid LA appendage (LAA) or pulmonary vein (PV) pacing. Procainamide was infused intravenously until AF was terminated or a cumulative dose of 20 mg/kg was reached. High-resolution mapping during AF showed FDs in the vein of Marshall, PVs, and the LAA. Procainamide significantly ( P < 0.05) reduced the frequency of these FDs and suppressed the interactions of wave fronts between PVs and LA. The cumulative dose of PA needed to terminate AF correlated negatively ( r =–0.9, P < 0.05) with the baseline effective refractory period (ERP) of PV and positively ( r = 0.8, P < 0.05) with the baseline maximum dominant frequency (DF) of AF. In four of five dogs, AF converted to atrial tachycardia originating from the PVs before termination. Attempts to reinduce sustained AF were unsuccessful in these five dogs. AF was resistant to procainamide in the sixth dog. In conclusion, procainamide reduced the rate of FDs in the thoracic veins and the LA and suppressed the interaction between PVs and LA. Second, FDs in the PV are more resistant to procainamide's action than FDs in the atria. Third, inherent PV ERP is important in determining the antifibrillatory efficacy of procainamide.

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Optimising the diagnostics of atrial fibrillation (AF) in implantable devices by checking atrial refractory period and atrial sensitivity

EP Europace ◽

10.1016/s1099-5129(01)80190-2 ◽

2001 ◽

Vol 2 ◽

pp. A41-A41

Keyword(s):

Atrial Fibrillation ◽

Refractory Period ◽

Implantable Devices

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Prevalence of atrial arrhythmia in patients with arrhythmogenic right ventricular cardiomyopathy: a systematic review and meta-analysis

European Heart Journal ◽

10.1093/ehjci/ehaa946.0504 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

P Rujirachun ◽

P Wattanachayakul ◽

N Charoenngam ◽

A Winijkul ◽

P Ungprasert

Keyword(s):

Atrial Fibrillation ◽

Cohort Studies ◽

Right Ventricular ◽

Atrial Tachycardia ◽

Arrhythmogenic Right Ventricular Cardiomyopathy ◽

Meta Analysis ◽

Atrial Arrhythmia ◽

Funding Source ◽

Ventricular Cardiomyopathy ◽

Pooled Prevalence

Abstract Background and objectives Little is known about atrial involvement in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Recent studies have suggested that atrial arrhythmia (AA), including atrial fibrillation (AF), atrial flutter (AFL), and atrial tachycardia (AT), was common among these patients although the reported prevalence varied considerably across the studies. Methods We searched for published articles indexed in MEDLINE and EMBASE databases from inception through Sep 22, 2019 to identify cohort studies of patients with ARVC that described the prevalence of atrial arrhythmia among the participants. The pooled prevalence across studies was calculated. Results A total of 16 cohort studies with 1,986 patients with ARVC were included into this meta-analysis. The pooled prevalence of overall AA among patients with ARVC was 17.9% (95% CI, 13.0%–24.0%; I2 88%), the pooled prevalence of AF of 12.9% (95% CI, 9.6%–17.0%; I2 78%), the pooled prevalence of AFL of 5.9% (95% CI, 3.7%–9.2%; I2 70%), and the pooled prevalence of AT of 7.1% (95% CI, 3.7%–13.0%; I2 49%). Conclusions AA is common among patient with ARVC with the pooled prevalence of approximately 18%, which is substantially higher than the reported prevalence of AA in general population. Funding Acknowledgement Type of funding source: None

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Abolishment of high-risk left lateral accessory pathway by myocardial infarction: a blessing in disguise? A case report

European Heart Journal - Case Reports ◽

10.1093/ehjcr/ytab050 ◽

2021 ◽

Vol 5 (2) ◽

Author(s):

Jim O’Brien ◽

Nikola Kozhuharov ◽

Shui Hao Chin ◽

Mark Hall

Keyword(s):

Atrial Fibrillation ◽

Acute Coronary Syndrome ◽

Case Report ◽

High Risk ◽

Coronary Sinus ◽

Refractory Period ◽

Accessory Pathway ◽

Coronary Syndrome ◽

Electrophysiology Study ◽

Anomalous Coronary

Abstract Background Antegradely conducting left lateral accessory pathways are a risk for supraventricular tachycardias and pre-excited atrial fibrillation. Rarely, an anomalous coronary sinus can cause difficulty in locating the pathway. The left circumflex coronary artery and obtuse marginal branches supply the posterolateral left ventricle. We describe a case report of a high-risk accessory pathway associated with an anomalous coronary sinus which, between successive electrophysiology studies, was obliterated by a felicitous acute coronary syndrome in the left circumflex territory. Case summary A 49-year-old male with palpitations and manifest pre-excitation was referred for electrophysiology study. Initial study revealed a high-risk left lateral accessory pathway with antegrade effective refractory period of 240 ms and rapidly conducting pre-excited atrial fibrillation. The coronary sinus could not be cannulated to localize the pathway. Coronary angiography and cardiac computed tomography showed an anomalous coronary sinus emptying into the right atrial free wall and patent coronaries. While awaiting repeat electrophysiology study, the patient suffered an acute coronary syndrome with immediate loss of previously visible pre-excitation on electrocardiogram, and underwent stenting of an occluded marginal branch of the circumflex. Repeat electrophysiology study demonstrated a now low-risk accessory pathway (effective refractory period 390 ms). Since infarction, the patient’s palpitations have fully settled with all subsequent electrocardiograms devoid of manifest pre-excitation. Discussion Left lateral accessory pathways, which can associate with an anomalous coronary sinus, derive from tissue similar to normal ventricular myocardium and are vulnerable to ischaemic insults in the area subtended by the circumflex artery.

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Atrial Tachycardia Transition During Ablation of Persistent Atrial Fibrillation: What is the Mechanism?

Journal of Cardiovascular Electrophysiology ◽

10.1111/j.1540-8167.2007.00870.x ◽

2007 ◽

Vol 18 (10) ◽

pp. 1109-1111 ◽

Cited By ~ 2

Author(s):

LEONARDO BANDEIRA ARANTES ◽

GEORGE J. KLEIN ◽

PIERRE JAIS ◽

SEIISCHIRO MATSUO ◽

KANG TENG LIM ◽

...

Keyword(s):

Atrial Fibrillation ◽

Atrial Tachycardia ◽

Persistent Atrial Fibrillation

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P1151Structural remodeling and conduction velocity dynamics in the human left atrium: relationship with reentrant mechanisms sustaining atrial tachycardia and atrial fibrillation

EP Europace ◽

10.1093/europace/euy015.637 ◽

2018 ◽

Vol 20 (suppl_1) ◽

pp. i219-i219

Author(s):

S Honarbakhsh ◽

R J Schilling ◽

M Orini ◽

R Providencia ◽

E Keating ◽

...

Keyword(s):

Atrial Fibrillation ◽

Left Atrium ◽

Conduction Velocity ◽

Atrial Tachycardia

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Cellular and mitochondrial mechanisms of atrial fibrillation

Basic Research in Cardiology ◽

10.1007/s00395-020-00827-7 ◽

2020 ◽

Vol 115 (6) ◽

Author(s):

Fleur E. Mason ◽

Julius Ryan D. Pronto ◽

Khaled Alhussini ◽

Christoph Maack ◽

Niels Voigt

Keyword(s):

Atrial Fibrillation ◽

Nicotinamide Adenine Dinucleotide ◽

Molecular Mechanisms ◽

Treatment Options ◽

Specific Treatment ◽

Nicotinamide Adenine Dinucleotide Phosphate ◽

Nicotinamide Adenine ◽

Mitochondrial Activity ◽

Atp Production

AbstractThe molecular mechanisms underlying atrial fibrillation (AF), the most common form of arrhythmia, are poorly understood and therefore target-specific treatment options remain an unmet clinical need. Excitation–contraction coupling in cardiac myocytes requires high amounts of adenosine triphosphate (ATP), which is replenished by oxidative phosphorylation in mitochondria. Calcium (Ca2+) is a key regulator of mitochondrial function by stimulating the Krebs cycle, which produces nicotinamide adenine dinucleotide for ATP production at the electron transport chain and nicotinamide adenine dinucleotide phosphate for the elimination of reactive oxygen species (ROS). While it is now well established that mitochondrial dysfunction plays an important role in the pathophysiology of heart failure, this has been less investigated in atrial myocytes in AF. Considering the high prevalence of AF, investigating the role of mitochondria in this disease may guide the path towards new therapeutic targets. In this review, we discuss the importance of mitochondrial Ca2+ handling in regulating ATP production and mitochondrial ROS emission and how alterations, particularly in these aspects of mitochondrial activity, may play a role in AF. In addition to describing research advances, we highlight areas in which further studies are required to elucidate the role of mitochondria in AF.

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Atrial fibrillation and atrial tachycardia in patients with chronic thromboembolic pulmonary hypertension treated with pulmonary endarterectomy

European Heart Journal Supplements ◽

10.1093/eurheartj/suaa096 ◽

2020 ◽

Vol 22 (Supplement_F) ◽

pp. F30-F37

Author(s):

Stepan Havranek ◽

Zdenka Fingrova ◽

David Ambroz ◽

Pavel Jansa ◽

Jan Kuchar ◽

...

Keyword(s):

Atrial Fibrillation ◽

Pulmonary Hypertension ◽

Atrial Tachycardia ◽

Cox Regression ◽

Systolic Pressure ◽

Chronic Thromboembolic Pulmonary Hypertension ◽

Walking Distance ◽

Pulmonary Artery Systolic Pressure ◽

Pulmonary Endarterectomy ◽

Thromboembolic Pulmonary Hypertension

Abstract Atrial fibrillation (AF) and atrial tachycardia (AT) are frequently observed in patients with chronic thromboembolic pulmonary hypertension (CTEPH) who were treated with pulmonary endarterectomy (PEA). Their prevalence and impact on prognosis of patients are not known. We analysed the prevalence of AF/AT and the clinical outcome in 197 patients with CTEPH treated with PEA (median age 62; interquartile range 53–68 years; 62% males). The prevalence of AF/AT was 29% (57 patients). Compared to patients without arrhythmia, the subjects with AF/AT were older [60 (50–67) vs. 62 (57–70) years], manifested an increased size of the left atrium [39 (35–44) vs. 45 (40–50) mm], had a reduced 6-min walking distance [411 (321–506) vs. 340 (254–460) m], and higher pulmonary artery systolic pressure after PEA [38 (30–47) vs. 45 (38–71) mmHg], all results with P-value <0.05. During the follow-up with a median 4.2 (1.6–6.3) years, 45 (23%) patients died. In a multivariate Cox regression model only the male gender [hazard ratio (HR) 2.27, 95% confidence interval (CI) 1.15–4.50], a reduced 6-min walking distance (HR 3.67, 95% CI 1.74–7.73), and an increased New York Heart Association class (HR 8.56, 95% CI 4.17–17.60) were associated with mortality (P < 0.05). The prevalence of AF/AT in patients with CTEPH treated with PEA is high. Arrhythmias are associated with reduced functional capacity but not with mortality.

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