Atrial Fibrillation
Diseases

Author: Gianpiero Pescarmona
Date: 16/06/2013

Description

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

DatabaseLink
WikipediaFabry
The Diseases DatabaseURL
MedlinePlus"URL":
OMIM single geneFabry
WikigenesAGAL
GeneCards"AGAL":
Kegg PathwayAGAL

Se ci sono piĆ¹ voci su OMIM usare questo formato di ricerca:

Autism

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.
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