scholarly journals Upstream Therapy for Atrial Fibrillation Prevention: The Role of Sacubitril/Valsartan

2020 ◽  
Vol 11 (4) ◽  
pp. 213-218
Author(s):  
Renato De Vecchis ◽  
Andrea Paccone ◽  
Marco Di Maio
Keyword(s):  
Atrial Fibrillation ◽  
Upstream Therapy

Abstract 286: Role of ATP-sensitive Potassium Channel Openers in Prevention of Atrial Fibrillation

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Cevher Ozcan ◽  
Zhenping Li
Keyword(s):  
Atrial Fibrillation ◽  
Primary Prevention ◽  
Risk Reduction ◽  
Metabolic Regulation ◽  
Control Group ◽  
Male Mice ◽  
Channel Opening ◽  
Metabolic States ◽  
Upstream Therapy

Introduction: The ATP-sensitive potassium (K ATP ) channel dysfunction causes susceptibility to adrenergic atrial fibrillation (AF). However, the therapeutic efficacy of K ATP activation in primary prevention of AF is not known. We hypothesized that K ATP channel opening drugs prevent AF with effective metabolic and mechanosensitive gating of K ATP channels and preserving electro-anatomical stability in atria by regulating oxidative and metabolic states. Methods: This hypothesis was tested in a novel mouse model of AF, cardiac specific LKB1 knockout (KO) mice. Male and female LKB1 KO mice were treated with K ATP channel openers, nicorandil (15 mg/kg/day) and diazoxide (10 mg/kg/day). Control group included untreated littermates of the study group. Incidence of AF, structural and electrophysiological property of atria and sex-based differences were analyzed at the 3 months of age in all groups. Results: The incidence of spontaneous AF was significant reduced in LKB1 KO male mice with nicorandil (0%, n=5) and diazoxide (33%, n=6) treatment compare to untreated mice (84.6%, n=13) (p<0.05). The treatment was also effective in female LKB1 KO mice as AF occurred in 37.5% of nicorandil (n=8) and 40% of diazoxide (n=5) (p<0.05) treated mice as oppose to 71% of untreated mice (n=24). The K ATP openers, particularly nicorandil, were more effective in male mice preventing AF. There was 100% risk reduction with nicorandil in male mice compare to 39% with diazoxide. Nicorandil demonstrated 52% risk reduction in female mice while it was 56% with diazoxide treatment. Prevention of AF was associated with preservation of atrial structural and electrical property including size, heart rate and conduction intervals. Biatrial enlargement was significantly prevented by K ATP openers compare to untreated mice. Incidence of AF was significantly higher in male mice than female with or without treatment. Conclusions: Activation of sarcolemmal and mitochondrial K ATP channels prevents AF by preserving electro-anatomical property of atria and decreasing susceptibility to AF. Metabolic regulation of K ATP is essential in AF. Thus, the K ATP openers are novel upstream therapy for primary prevention of AF in vulnerable population.

The role of angiotensin in electrophysiological gap junction remodeling in human atrial fibrillation

2004 ◽  
Vol 52 (S 1) ◽  
Author(s):  
S Dhein ◽  
A Boldt ◽  
J Garbade ◽  
L Polontchouk ◽  
U Wetzel ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Gap Junction ◽  
Human Atrial Fibrillation

The Role of HbA1c on Mortality in Patients with Medical History of Ischemic Stroke and Paroxysmal Atrial Fibrillation

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2406-PUB
Author(s):  
KONSTANTINA KANELLOPOULOU ◽  
IOANNIS L. MATSOUKIS ◽  
ASIMINA GANOTOPOULOU ◽  
THEODORA ATHANASOPOULOU ◽  
CHRYSOULA TRIANTAFILLOPOULOU ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Ischemic Stroke ◽  
Medical History ◽  
Paroxysmal Atrial Fibrillation ◽  
History Of

Inflammatory Biomarkers in Atrial Fibrillation

2019 ◽  
Vol 26 (5) ◽  
pp. 837-854 ◽  
Author(s):  
Effimia Zacharia ◽  
Nikolaos Papageorgiou ◽  
Adam Ioannou ◽  
Gerasimos Siasos ◽  
Spyridon Papaioannou ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Plasma Levels ◽  
Large Scale ◽  
Inflammatory Biomarkers ◽  
Inflammatory Pathways ◽  
Inflammatory State ◽  
Anti Inflammatory ◽  
Underlying Mechanisms

During the last few years, a significant number of studies have attempted to clarify the underlying mechanisms that lead to the presentation of atrial fibrillation (AF). Inflammation is a key component of the pathophysiological processes that lead to the development of AF; the amplification of inflammatory pathways triggers AF, and, in tandem, AF increases the inflammatory state. Indeed, the plasma levels of several inflammatory biomarkers are elevated in patients with AF. In addition, the levels of specific inflammatory biomarkers may provide information regarding to the AF duration. Several small studies have assessed the role of anti-inflammatory treatment in atrial fibrillation but the results have been contradictory. Large-scale studies are needed to evaluate the role of inflammation in AF and whether anti-inflammatory medications should be routinely administered to patients with AF.

Redox State in Atrial Fibrillation Pathogenesis and Relevant Therapeutic Approaches

2019 ◽  
Vol 26 (5) ◽  
pp. 765-779 ◽  
Author(s):  
Alexios S. Antonopoulos ◽  
Athina Goliopoulou ◽  
Evangelos Oikonomou ◽  
Sotiris Tsalamandris ◽  
Georgios-Angelos Papamikroulis ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Clinical Studies ◽  
Redox State ◽  
Redox Balance ◽  
Therapeutic Approaches ◽  
Critical Determinant ◽  
Electrophysiological Properties ◽  
Antioxidant Agents ◽  
Clinical Benefits

Background: Myocardial redox state is a critical determinant of atrial biology, regulating cardiomyocyte apoptosis, ion channel function, and cardiac hypertrophy/fibrosis and function. Nevertheless, it remains unclear whether the targeting of atrial redox state is a rational therapeutic strategy for atrial fibrillation prevention. Objective: To review the role of atrial redox state and anti-oxidant therapies in atrial fibrillation. Method: Published literature in Medline was searched for experimental and clinical evidence linking myocardial redox state with atrial fibrillation pathogenesis as well as studies looking into the role of redoxtargeting therapies in the prevention of atrial fibrillation. Results: Data from animal models have shown that altered myocardial nitroso-redox balance and NADPH oxidases activity are causally involved in the pathogenesis of atrial fibrillation. Similarly experimental animal data supports that increased reactive oxygen / nitrogen species formation in the atrial tissue is associated with altered electrophysiological properties of atrial myocytes and electrical remodeling, favoring atrial fibrillation development. In humans, randomized clinical studies using redox-related therapeutic approaches (e.g. statins or antioxidant agents) have not documented any benefits in the prevention of atrial fibrillation development (mainly post-operative atrial fibrillation risk). Conclusion: Despite strong experimental and translational data supporting the role of atrial redox state in atrial fibrillation pathogenesis, such mechanistic evidence has not been translated to clinical benefits in atrial fibrillation risk in randomized clinical studies using redox-related therapies.

The Role of Atrial Fibrosis Detected by Delayed - Enhancement MRI in Atrial Fibrillation Ablation

2020 ◽  
Vol 16 (2) ◽  
pp. 135-144 ◽  
Author(s):  
Zsuzsanna Kis ◽  
Astrid Amanda Hendriks ◽  
Taulant Muka ◽  
Wichor M. Bramer ◽  
Istvan Kovacs ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Imaging Modality ◽  
Final Analysis ◽  
Atrial Fibrosis ◽  
Atrial Wall ◽  
Af Ablation ◽  
Left Atrial Wall ◽  
Cmr Imaging

Introduction: Atrial Fibrillation (AF) is associated with remodeling of the atrial tissue, which leads to fibrosis that can contribute to the initiation and maintenance of AF. Delayed- Enhanced Cardiac Magnetic Resonance (DE-CMR) imaging for atrial wall fibrosis detection was used in several studies to guide AF ablation. The aim of present study was to systematically review the literature on the role of atrial fibrosis detected by DE-CMR imaging on AF ablation outcome. Methods: Eight bibliographic electronic databases were searched to identify all published relevant studies until 21st of March, 2016. Search of the scientific literature was performed for studies describing DE-CMR imaging on atrial fibrosis in AF patients underwent Pulmonary Vein Isolation (PVI). Results: Of the 763 citations reviewed for eligibility, 5 articles (enrolling a total of 1040 patients) were included into the final analysis. The overall recurrence of AF ranged from 24.4 - 40.9% with median follow-up of 324 to 540 days after PVI. With less than 5-10% fibrosis in the atrial wall there was a maximum of 10% recurrence of AF after ablation. With more than 35% fibrosis in the atrial wall there was 86% recurrence of AF after ablation. Conclusion: Our analysis suggests that more extensive left atrial wall fibrosis prior ablation predicts the higher arrhythmia recurrence rate after PVI. The DE-CMR imaging modality seems to be a useful method for identifying the ideal candidate for catheter ablation. Our findings encourage wider usage of DE-CMR in distinct AF patients in a pre-ablation setting.

Sign in / Sign up

Export Citation Format

Share Document