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Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which...
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β-receptor blockers significantly impact the cardiovascular system by counteracting catecholamine-induced sympathetic responses. These medications decrease heart rate, contractility, and cardiac output, potentially leading to cardiac depression, life-threatening bradycardia, and death. Therapeutically, β-blockers function as mild antihypertensives and are utilized in treating angina pectoris and cardiac arrhythmias. However, nonselective β-blockers inhibit β2-receptors in...
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Heart Failure VI: Adjunct Therapies01:22

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Additional therapies for treating patients with heart failure (HF) may include procedural interventions, supplemental oxygen, the management of sleep disorders, and nutritional therapy.Procedural InterventionsImplantable Cardioverter-Defibrillator: For patients at risk of life-threatening arrhythmias due to severe left ventricular dysfunction, an Implantable Cardioverter-Defibrillator (ICD) can detect and terminate these arrhythmias, preventing sudden cardiac death and improving survival rates.
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Dysrhythmias VI: Management of Dysrhythmias01:25

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Dysrhythmia management involves a multifaceted approach, incorporating pharmacological treatments, medical procedures, surgical interventions, lifestyle modifications, and patient education.Pharmacological ManagementAntiarrhythmic Drugs:Class I (Sodium Channel Blockers): This class includes quinidine and procainamide, which reduce the speed of impulse conduction in the heart, stabilize the cardiac membrane, and control arrhythmias. Quinidine and procainamide are Class IA agents that prolong the...
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Updated: Sep 13, 2025

Establishment of Rat Models Mimicking Gender-affirming Hormone Therapies
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Transgender-Affirming Hormone Therapies, QT Prolongation, and Cardiac Repolarization.

Virginie Grouthier1,2, Marie Matamala1, Antoine Tabarin1

  • 1Department of Endocrinology, Diabetes and Nutrition, Centre Hospitalier Universitaire de Bordeaux, Haut-Leveque Hospital, F-33604 Pessac, France.

JAMA Network Open
|July 30, 2025
PubMed
Summary

Gender-affirming hormone therapies (GAHTs) impact cardiac repolarization differently in transgender men and women. Testosterone shortened QTc in transgender men, while antiandrogen therapy prolonged it in transgender women, mirroring cisgender sexual dimorphism.

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Area of Science:

  • Cardiology
  • Endocrinology
  • Transgender Health

Background:

  • Gender-affirming hormone therapies (GAHTs) involve androgens for transgender men and antiandrogens with estrogens for transgender women.
  • Cardiovascular outcomes of GAHTs are not well-studied, particularly effects on cardiac repolarization.

Purpose of the Study:

  • To investigate the association between GAHT and cardiac repolarization alterations in transgender individuals.
  • To analyze electrocardiographic changes in relation to hormone levels during GAHT.

Main Methods:

  • A prospective cohort study of 120 transgender individuals (64 men, 56 women) in France from 2021-2023.
  • Electrocardiographic parameters (QTc, TAmp, QTp) and circulating sex hormones were assessed.
  • Nonlinear mixed models were used to analyze associations, controlling for confounding factors.

Main Results:

  • Testosterone therapy in transgender men shortened QTc and QTp, and increased TAmp.
  • Antiandrogen therapy in transgender women prolonged QTc and QTp, and decreased TAmp.
  • QTc changes mirrored sexual dimorphism observed in cisgender populations.

Conclusions:

  • GAHT significantly impacts cardiac repolarization in transgender individuals.
  • Testosterone and antiandrogen therapies induce opposite effects on QTc, QTp, and TAmp.
  • These findings highlight the need for attention to GAHT's cardiovascular effects, especially in those also taking QTc-prolonging drugs.