Drug-induced atrial fibrillation

Hooft, C; Heeringa, Jan; Herpen, Gerard van; Kors, Jan A.; Kingma, J. Herre; Stricker, Bruno H. Ch.

doi:10.1016/j.jacc.2004.08.053

Cited by 118 publications

(69 citation statements)

References 78 publications

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“…Second, several classes of drugs have been reported to induce AF in patients. 21 The mechanisms considered responsible include adrenergic stimulation and cardiotoxicity.…”

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confidence: 99%

Reduced Phosphoinositide 3-Kinase (p110α) Activation Increases the Susceptibility to Atrial Fibrillation

Pretorius

Woodcock

et al. 2009

The American Journal of Pathology

152

133

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Atrial fibrillation (AF) is the most common sustained arrhythmia presenting at cardiology departments. A limited understanding of the molecular mechanisms responsible for the development of AF has hindered treatment strategies. The purpose of this study was to assess whether reduced activation of phosphoinositide 3-kinase (PI3K, p110␣) makes the compromised heart susceptible to AF. Risk factors for AF, including aging, obesity, and diabetes, have been associated with insulin resistance that leads to depressed/defective PI3K signaling. However, to date, there has been no link between PI3K(p110␣) and AF. To address this question, we crossed a cardiac-specific transgenic mouse model of dilated cardiomyopathy (DCM) with a cardiac-specific transgenic mouse expressing a dominant negative mutant of PI3K (dnPI3K; reduces PI3K activity). Adult (ϳ4.5 months) double-transgenic (dnPI3K-DCM), single-transgenic (DCM-Tg, dnPI3K-Tg), and nontransgenic mice were subjected to morphological, functional/ECG, microarray, and biochemical analyses. dnPI3K-DCM mice developed AF and had depressed cardiac function as well as greater atrial enlargement and fibrosis than DCM-Tg mice. AF was not detected in other groups. Aged DCM-Tg mice (ϳ15 months) with a similar phenotype to dnPI3K-DCM mice (4.5 months) did not develop AF , suggesting loss of PI3K activity directly contributed to the AF phenotype. Furthermore, increasing PI3K activity reduced atrial fibrosis and improved cardiac conduction in DCM-Tg mice. Finally, in atrial appendages from patients with AF, PI3K activation was lower compared with tissue from patients in sinus rhythm. These results suggest a link between PI3K(p110␣) and AF. (Am J Pathol

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“…Second, several classes of drugs have been reported to induce AF in patients. 21 The mechanisms considered responsible include adrenergic stimulation and cardiotoxicity.…”

mentioning

confidence: 99%

Reduced Phosphoinositide 3-Kinase (p110α) Activation Increases the Susceptibility to Atrial Fibrillation

Pretorius

Woodcock

et al. 2009

The American Journal of Pathology

152

133

View full text Add to dashboard Cite

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“…Acute temporary causes of AF include alcohol abuse, excessive coffee intake, surgery, pericarditis, myocarditis, and pulmonary embolism. Medications also have been associated with the induction of AF both in case reports and clinical trials (5). This is one report of a first-detected, symptomatic AF probably due to cardiac toxicity of azathioprine.…”

Section: Discussionmentioning

confidence: 92%

Azathioprine-induced atrial fibrillation

Doğan

Grbovic

İnci

et al. 2015

IRDR

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“…In this study, it was revealed that administration of EHE to mice causes atrial fibrillation, one type of cardiac arrhythmia. Atrial fibrillation had been reported to be induced by β 1 adrenergic receptor agonists such as dobutamine and arbutamine, 29) or hypokalemia. 30) Hypokalemia was reported to be induced by ephedrine administration, 31) so we measured serum potassium levels.…”

Section: Discussionmentioning

confidence: 99%

Ephedrine Alkaloids-Free Ephedra Herb Extract, EFE, Has No Adverse Effects Such as Excitation, Insomnia, and Arrhythmias

Takemoto

Takahashi

Hyuga

et al. 2018

Biological & Pharmaceutical Bulletin

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Ephedrine alkaloids-free Ephedra Herb extract (EFE) has been developed to eliminate the adverse effects caused by ephedrine alkaloid-induced sympathetic hyperactivation. Previously, we reported that EFE possesses analgesic, anti-influenza, and cancer metastatic inhibitory effects at comparable levels to that of Ephedra Herb extract (EHE). However, it has not yet been demonstrated that EFE is free from the known side effects of EHE, such as excitation, insomnia, and arrhythmias. In this study, the incidence of these adverse effects was compared between mice administered EHE and those administered EFE. Increased locomotor activity in an open-field test, reduced immobility times in a forced swim test, and reduced sleep times in a pentobarbital-induced sleep test were observed in EHE-treated mice, when compared to the corresponding values in vehicle-treated mice. In contrast, EFE had no obvious effects in these tests. In electrocardiograms, atrial fibrillation (i.e., irregular heart rhythm, absence of P waves, and appearance of f waves) was observed in the EHE-treated mice. It was suggested that this atrial fibrillation was induced by stimulation of adrenaline β 1 receptors, but not by hypokalemia. However, EFE did not affect cardiac electrophysiology. These results suggest that the abovementioned side effects are caused by ephedrine alkaloids in EHE, and that EFE is free from these adverse effects, such as excitation, insomnia, and arrhythmias. Thus, EFE is a promising new botanical drug with few adverse effects.

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Drug-induced atrial fibrillation

Cited by 118 publications

References 78 publications

Reduced Phosphoinositide 3-Kinase (p110α) Activation Increases the Susceptibility to Atrial Fibrillation

Reduced Phosphoinositide 3-Kinase (p110α) Activation Increases the Susceptibility to Atrial Fibrillation

Azathioprine-induced atrial fibrillation

Ephedrine Alkaloids-Free Ephedra Herb Extract, EFE, Has No Adverse Effects Such as Excitation, Insomnia, and Arrhythmias

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