Atrial fibrillation: Neurogenic or myogenic?

Scridon, Alina; Șerban, Răzvan Constantin; Chevalier, Philippe

doi:10.1016/j.acvd.2017.11.001

Cited by 22 publications

(29 citation statements)

References 94 publications

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“…In atherosclerosis, concepts have moved from a purely lipid-related, to a more complex, lipid-inflammatory pathophysiology [ 45 ]. In atrial fibrillation, concepts have moved from a purely electrical disease to a more tangled combination of electrical, structural, autonomic, and molecular underlying changes [ 46 , 47 , 48 ]. In AMI, for years, biomarkers have been focused on the concept of myocardial necrosis.…”

Section: Newer Biomarkers For Laboratory Diagnosis Of Acute Myocardial Infarctionmentioning

confidence: 99%

“…Myocardial inflammation is a critical process occurring in the setting of AMI that has been related to a variety of deleterious consequences, including electrical instability and increased risk of cardiac arrhythmias, autonomic dysfunction, and fibrosis development [ 48 , 62 , 63 , 64 ]. A wide variety of pro-inflammatory cytokines have been shown to increase in the setting of AMI and to predict prognosis in this population.…”

Section: Newer Biomarkers For Laboratory Diagnosis Of Acute Myocardial Infarctionmentioning

confidence: 99%

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Past, Present, and Future of Blood Biomarkers for the Diagnosis of Acute Myocardial Infarction—Promises and Challenges

Ţilea

Varga

Șerban³

2021

Diagnostics

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Despite important advancements in acute myocardial infarction (AMI) management, it continues to represent a leading cause of mortality worldwide. Fast and reliable AMI diagnosis can significantly reduce mortality in this high-risk population. Diagnosis of AMI has relied on biomarker evaluation for more than 50 years. The upturn of high-sensitivity cardiac troponin testing provided extremely sensitive means to detect cardiac myocyte necrosis, but this increased sensitivity came at the cost of a decrease in diagnostic specificity. In addition, although cardiac troponins increase relatively early after the onset of AMI, they still leave a time gap between the onset of myocardial ischemia and our ability to detect it, thus precluding very early management of AMI. Newer biomarkers detected in processes such as inflammation, neurohormonal activation, or myocardial stress occur much earlier than myocyte necrosis and the diagnostic rise of cardiac troponins, allowing us to expand biomarker research in these areas. Increased understanding of the complex AMI pathophysiology has spurred the search of new biomarkers that could overcome these shortcomings, whereas multi-omic and multi-biomarker approaches promise to be game changers in AMI biomarker assessment. In this review, we discuss the evolution, current application, and emerging blood biomarkers for the diagnosis of AMI; we address their advantages and promises to improve patient care, as well as their challenges, limitations, and technical and diagnostic pitfalls. Questions that remain to be answered and hotspots for future research are also emphasized.

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Section: Newer Biomarkers For Laboratory Diagnosis Of Acute Myocardial Infarctionmentioning

confidence: 99%

Section: Newer Biomarkers For Laboratory Diagnosis Of Acute Myocardial Infarctionmentioning

confidence: 99%

Past, Present, and Future of Blood Biomarkers for the Diagnosis of Acute Myocardial Infarction—Promises and Challenges

Ţilea

Varga

Șerban³

2021

Diagnostics

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“…A few studies have suggested that autonomic imbalance is closely associated with AF, and the autonomic nervous system could be regulated by the renin–angiotensin–aldosterone system (RAAS). 2 , 3 Atrial ionic and structural remodeling is the substrate and mechanism for the process of AF. 4 Therefore, suppression of atrial remodeling may be a novel treatment for AF.…”

Section: Introductionmentioning

confidence: 99%

<p>The Potential Effects of Aliskiren on Atrial Remodeling Induced by Chronic Intermittent Hypoxia in Rats</p>

Song¹,

Yu²,

Li³

et al. 2020

DDDT

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Purpose Atrial remodeling takes part in the pathogenesis of atrial fibrillation (AF). Aliskiren, as a direct renin inhibitor, has been shown to exert protective effects against arrhythmia. The aim of this study was to investigate the potential role of aliskiren in atrial remodeling in a chronic intermittent hypoxia (CIH) rat model. Methods A total of 45 Sprague–Dawley rats were randomly assigned into three groups (n=15 per group): control group; CIH group; and CIH with aliskiren (CIH-A) group. CIH and CIH-A rats were subjected to CIH for 6 h per day for 4 weeks. Atrial fibrosis was evaluated using Masson’s trichrome staining. Electrophysiological tests were conducted in the isolated perfused hearts to assess the atrial effective refractory period and inducibility of AF. Atrial ionic remodeling was measured using the whole-cell patch-clamp technique, and Western blotting and real-time quantitative polymerase chain reactionwere performed to evaluate changes in ion channels. Results CIH induced obvious collagen deposition, and the abnormal fibrosis was significantly attenuated by aliskiren. The inducibility of AF was increased significantly in the CIH group compared with the control and CIH-A groups (23±24.5% vs 2.0±4.2% vs 5.0±7.0%, respectively; P <0.05). Compared with the control group, the densites of the calcium current ( I CaL ) and sodium current ( I Na ) were reduced significantly in the CIH group ( I CaL : −3.16±0.61 pA/pF vs −7.13±1.98 pA/pF; I Na : −50.97±8.71 pA/pF vs −132.58±25.34 pA/pF, respectively; all P <0.05). Following intervention with aliskiren, the reductions in I CaL and I Na were significantly improved, and the ionic modeling changes assessed at the mRNA and protein levels were also significantly improved. Conclusion CIH could alter atrial modeling and subsequently promote the occurrence and development of AF, which could be attenuated by treatment with aliskiren.

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“…suggests that the beneficial effects of ivabradine could extend to other settings associated with increased sympathetic activity, in which the ivabradine-induced increase in vagal modulation could reduce myocardial oxygen demand and ischemia, diminish sympathetic stimulation and adrenoreceptor-mediated cytotoxicity, apoptosis, and hypertrophy, and reduce the likelihood of ventricular tachyarrhythmias and sudden death (Böhm et al, 2015). On the other hand, vagal hyperactivity has been shown to promote ectopic activity, reentry, and atrial fibrillation via multiple mechanisms (Scridon et al, 2018). Given the highly proarrhythmic effects of vagal activation at the atrial level, the increase in vagal modulation induced by ivabradine demonstrated in the present study could provide an explanation for the increased risk of atrial fibrillation associated with ivabradine use in clinical trials (Martin et al, 2014;Cammarano et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Long-Term Effects of Ivabradine on Cardiac Vagal Parasympathetic Function in Normal Rats

et al. 2021

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Background: The complex interactions that exist between the pacemaker current, If, and the parasympathetic nervous system could significantly influence the course of patients undergoing chronic therapy with the If blocker ivabradine. We thus aimed to assess the effects of chronic ivabradine therapy on autonomic modulation and on the cardiovascular response to in situ and in vitro parasympathetic stimulation. The right atrial expression of HCN genes, encoding proteins for If, was also evaluated.Methods: Sympathetic and parasympathetic heart rate variability parameters and right atrial HCN(1-4) RNA levels were analyzed in 6 Control and 10 ivabradine-treated male Wistar rats (IVA; 3 weeks, 10 mg/kg/day). The heart rate (HR) and systolic blood pressure (SBP) responses to in situ electrical stimulation of the vagus nerve (2–20 Hz) were assessed in 6 additional Control and 10 IVA rats. The spontaneous sinus node discharge rate (SNDR) response to in vitro cholinergic receptors stimulation using carbamylcholine (10−9–10−6 mol/L) was also assessed in these later rats.Results: Ivabradine significantly increased vagal modulation and shifted the sympatho-vagal balance toward vagal dominance. In Control, in situ vagus nerve stimulation induced progressive decrease in both the SBP (p = 0.0001) and the HR (p< 0.0001). Meanwhile, in IVA, vagal stimulation had no effect on the HR (p = 0.16) and induced a significantly lower drop in SBP (p< 0.05). IVA also displayed a significantly lower SNDR drop in response to carbamylcholine (p< 0.01) and significantly higher right atrial HCN4 expression (p = 0.02).Conclusion: Chronic ivabradine administration enhanced vagal modulation in healthy rats. In addition, ivabradine reduced the HR response to direct muscarinic receptors stimulation, canceled the cardioinhibitory response and blunted the hemodynamic response to in situ vagal stimulation. These data bring new insights into the mechanisms of ivabradine-related atrial proarrhythmia and suggest that long-term If blockade may protect against excessive bradycardia induced by acute vagal activation.

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Atrial fibrillation: Neurogenic or myogenic?

Cited by 22 publications

References 94 publications

Past, Present, and Future of Blood Biomarkers for the Diagnosis of Acute Myocardial Infarction—Promises and Challenges

Past, Present, and Future of Blood Biomarkers for the Diagnosis of Acute Myocardial Infarction—Promises and Challenges

<p>The Potential Effects of Aliskiren on Atrial Remodeling Induced by Chronic Intermittent Hypoxia in Rats</p>

Long-Term Effects of Ivabradine on Cardiac Vagal Parasympathetic Function in Normal Rats

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