DEFINITION
The disease definition according to a specific consensus conference or to The Diseases Database based on the Unified Medical Language System (NLM)
Also the link to the corresponding Mesh term has to be created
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Atrial fibrillation
EPIDEMIOLOGY
age, sex, seasonality, etc
SYMPTOMS
DIAGNOSIS
histopathology
radiology
NMR
laboratory tests
PATHOGENESIS
PATIENT RISK FACTORS
Vascular
Genetic
Acquired
Hormonal
Genetic
Acquired
Pharmacological
atrial+fibrillation+salbutamol
Atrial fibrillation associated with chocolate intake abuse and chronic salbutamol inhalation abuse. 2010
We present a case of atrial fibrillation associated with chocolate intake abuse in a 19-year-old Italian woman with chronic salbutamol inhalation abuse.
TISSUE SPECIFIC RISK FACTORS
anatomical (due its structure)
vascular (due to the local circulation)
physiopathological (due to tissue function and activity)
glutathione+and+atrial+fibrillation
COMPLICATIONS
THERAPY
ace2+and+atrial+fibrillation
[Effects of angiotensin converting enzyme inhibitor on the expression of angiotensin converting enzyme 2 in atrium of patients with atrial fibrillation]. 2007
RESULTS The expression of ACE2 was significantly decreased (P < 0.05), the expression of ACE and pERK1/2 were significantly increased (P < 0.05), and the level of atrial tissue Ang II was significantly increased in patients with chronic atrial fibrillation group (CAF) compared with sinus rhythm group (SR) (P < 0.05).
Angiotensin II and angiotensin 1-7: which is their role in atrial fibrillation? 2020
- Abstract
Atrial fibrillation (AF) is a significant cause of morbidity and mortality as well as a public health burden considering the high costs of AF-related hospitalizations. Pre-clinical and clinical evidence showed a potential role of the renin angiotensin system (RAS) in the etiopathogenesis of AF. Among RAS mediators, angiotensin II (AII) and angiotensin 1-7 (A1-7) have been mostly investigated in AF. Specifically, the stimulation of the pathway mediated by AII or the inhibition of the pathway mediated by A1-7 may participate in inducing and sustaining AF. In this review, we summarize the evidence showing that both RAS pathways may balance the onset of AF through different biological mechanisms involving inflammation, epicardial adipose tissue (EAT) accumulation, and electrical cardiac remodeling. EAT is a predictor for AF as it may induce its onset through direct (infiltration of epicardial adipocytes into the underlying atrial myocardium) and indirect (release of inflammatory adipokines, the stimulation of oxidative stress, macrophage phenotype switching, and AF triggers) mechanisms. Classic RAS blockers such as angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARB) may prevent AF by affecting the accumulation of the EAT, representing a useful therapeutic strategy for preventing AF especially in patients with heart failure and known left ventricular dysfunction. Further studies are necessary to prove this benefit in patients with other cardiovascular diseases. Finally, the possibility of using the A1-7 or ACE2 analogues, to enlarge current therapeutic options for AF, may represent an important field of research.
steroid 11beta-monooxygenase activation
Transforming growth factor beta1 inhibits aldosterone and cortisol production in the human adrenocortical cell line NCI-H295R through inhibition of CYP11B1 and CYP11B2 expression. 2003
We observed that TGFbeta1 strongly inhibits forskolin-induced steroid 11beta-hydroxylase activity and CYP11B1 mRNA levels, as well as angiotensin II-induced aldosterone synthase activity and CYP11B2 mRNA levels.
Progesterone
Hypothermia with Extreme Bradycardia following Spinal Cord Infarction of Septic Origin, 2017
Abstract
Among other autonomic dysfunctions complicating acute spinal cord injury, deep hypothermia is rare but may induce serious cardiovascular complications. There are few pharmacological options to influence hypothermia. A 66-year-old woman was transferred to the intensive care unit (ICU) for serious cardiac arrhythmias (atrial fibrillation and asystole) in the context of a deep hypothermia (axillary temperature below 32°C). She had been admitted to the hospital two months before for an acute L4-L5 infectious spondylodiscitis without any initial neurological deficit. After surgery for epidural abscess drainage, she became paraplegic due to spinal cord infarction (from C7 to T6 levels) in the upper territory of the anterior spinal artery. In the ICU, the patient experienced several episodes of asystole and hypotension associated with a core body temperature below 35°C. Common causes of hypothermia (drugs, hypothyroidism, etc.) were excluded. A definitive pacemaker had to be inserted, but hypotension persisted. The prescription of oral progesterone (200 mg·d-1) helped to maintain a core temperature higher than 35°C, with a withdrawal of vasopressors. This case report illustrates that patients with incomplete spinal cord injury may present with delayed and deep hypothermia leading to serious cardiovascular complications. Progesterone could be able to influence positively central and peripheral thermal regulation.
Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes? 2020
Using a model of high fat diet (HFD) and low-dose streptozotocin (STZ) injection, Shao et al. provide data that demonstrate a direct association between mitochondrial dysfunction and the susceptibility to develop AF.
insulin+resistance+and+atrial+fibrillation
anp+and+atrial+fibrillation
anp+and+adiuretin
arginine+and+atrial+fibrillation
Elimination of cardiac arrhythmias using oral taurine with l-arginine with case histories: Hypothesis for nitric oxide stabilization of the sinus node. 2006
We searched for nutrient deficiencies that could cause cardiac arrhythmias [premature atrial contractions (PACs), premature ventricular contractions (PVCs), atrial fibrillation, and related sinus pauses], and found literature support for deficiencies of taurine and l-arginine.
Recoupling the cardiac nitric oxide synthases: tetrahydrobiopterin synthesis and recycling. 2012
Abstract: Nitric oxide (NO), a key regulator of cardiovascular function, is synthesized from L-arginine and oxygen by the enzyme nitric oxide synthase (NOS). This reaction requires tetrahydrobiopterin (BH4) as a cofactor. BH4 is synthesized from guanosine triphosphate (GTP) by GTP cyclohydrolase I (GTPCH) and recycled from 7,8-dihydrobiopterin (BH2) by dihydrofolate reductase. Under conditions of low BH4 bioavailability relative to NOS or BH2, oxygen activation is “uncoupled” from L-arginine oxidation, and NOS produces superoxide (O2−) instead of NO. NOS-derived superoxide reacts with NO to produce peroxynitrite (ONOO−), a highly reactive anion that rapidly oxidizes BH4 and propagates NOS uncoupling. BH4 depletion and NOS uncoupling contribute to overload-induced heart failure, hypertension, ischemia/reperfusion injury, and atrial fibrillation. L-arginine depletion, methylarginine accumulation, and S-glutathionylation of NOS also promote uncoupling. Recoupling NOS is a promising approach to treating myocardial and vascular dysfunction associated with heart failure.
BH4+and+atrial+fibrillation
Modulating ALDH2 reveals a differential dependence on ROS for hypertrophy and SR Ca2+ release in aldosterone-treated cardiac myocytes. 2020
Elsevier
These changes in reactive species generation were blunted by tetrahydrobiopterin (BH4, a NOS cofactor), suggesting the involvement of an uncoupled NOS. An activator (Alda-1) and an inhibitor (daidzin) of ALDH2 were used, to determine if this enzyme activity is related to aldosterone effects, through possible modulation of ROS.
BH4+synthesis+and+regulation+of+transcription
Modulating ALDH2 reveals a differential dependence on ROS for hypertrophy and SR Ca 2+ release in aldosterone-treated cardiac myocytes, 2021
Aldosterone inhibitors
eplerenone%20and%20atrial%20fibrillation
