An updated Endocrine Society review shows men with low or high testosterone may face increased atrial fibrillation risk. Learn the safe target ranges for TRT.
Atrial fibrillation is an irregular heart rhythm associated with an increased risk of stroke. A patient sits in a clinical exam room staring at a lab report with a single flagged hormone number. The choice to begin treatment often seems like a simple math problem. You find a low number and you take medication to make it higher.
Human physiology is rarely that straightforward. A September 2026 Endocrine Society news release summarizes an updated review examining testosterone replacement therapy and this specific heart condition. The peer-reviewed article was written by Anand Reddy Maligireddy, Shumedha T. Barua, and Rajat S. Barua. It was published in the Journal of the Endocrine Society.
Trying to maintain fitness years after leaving service required a completely new mindset. The goal changed from immediate tactical readiness to healthy aging and longevity. I learned that connecting short term performance with long term health, focusing on mobility and cardiovascular function, was the real key to staying capable. Understanding the cardiovascular impact of hormone therapy is a direct extension of that mindset.
The review authors describe the available evidence as heterogeneous and conflicting rather than definitive. Their central conclusion is that the relationship between testosterone and atrial fibrillation appears to be U-shaped. Atrial fibrillation risk may be higher among men with low testosterone and among men with high testosterone. Risk appears to be lowest for men in the middle of the normal range.
To understand this conclusion, we must look at the 2023 TRAVERSE trial. This trial enrolled 5,246 men aged 45 to 80 with symptomatic hypogonadism. Participants had two fasting morning testosterone measurements below 300 ng/dL. They also had pre-existing cardiovascular disease or multiple cardiovascular risk factors.
Participants received either a daily 1.62% transdermal testosterone gel or a placebo. The mean treatment duration was 22 months. The mean follow-up period lasted 33 months. The results provided crucial data for clinicians and patients evaluating these hormone treatments.
Major adverse cardiovascular events occurred in 7.0% of testosterone-treated participants and 7.3% of placebo participants. This met the trial noninferiority criterion for the primary cardiovascular endpoint. However, incident atrial fibrillation occurred in 3.5% of the testosterone group versus 2.4% of the placebo group. This represented 91 versus 63 events respectively, with a reported P value of 0.02.
The review notes this represented an approximate 50% relative excess in atrial fibrillation. It also points out that the comparison was not adjusted for multiplicity. Furthermore, no covariate-adjusted atrial fibrillation analysis was reported in the primary trial documentation.
The TRAVERSE trial provides important data but does not paint the entire picture. The review cites a 2024 meta-analysis of 106 randomized placebo-controlled trials. This pooled analysis included 8,126 men receiving testosterone and 7,310 receiving placebo. That specific analysis found no statistically significant atrial fibrillation signal.
The meta-analysis reported an odds ratio of 1.44 with a 95% confidence interval of 0.46 to 4.46. The authors say this null pooled result does not necessarily disprove the TRAVERSE finding. The analyzed trials differed heavily in duration, patient populations, outcome ascertainment, and statistical power.
Observational evidence points in multiple directions regarding cardiovascular health. A 2017 national cohort of 76,639 U.S. veterans evaluated patients receiving hormone treatment. This study found that normalization of testosterone during treatment was associated with a significant reduction in incident atrial fibrillation. You can learn more about veteran health outcomes in our collection of military health articles.
By contrast, a post-hoc analysis of the ASPREE study followed 4,570 community-dwelling older men for a median of 4.4 years. The study recorded 286 incident atrial fibrillation events. In that analysis, atrial fibrillation risk was nearly doubled in the highest testosterone quintile versus the median quintile. The hazard ratio was 1.91 with a 95% confidence interval of 1.29 to 2.83.
A separate five-year cohort cited in the review reported a hazard ratio of 1.27. This was for atrial fibrillation among cisgender hypogonadal men receiving therapy. Additionally, a retrospective TriNetX replication of the TRAVERSE trial involved hypogonadal men with testosterone levels of 100 to 300 ng/dL. This specific replication did not reproduce the atrial fibrillation signal over three years.
The review is a structured narrative review based on searches of MEDLINE/PubMed and Embase through May 4, 2026. The authors supplemented this with reference-list searches and selected society materials. The authors did not perform a formal meta-analysis or formal risk-of-bias scoring. Therefore, the conclusions remain interpretive rather than definitive.
The review proposes different possible mechanisms at the two ends of the hormone spectrum. Co-author Rajat S. Barua is affiliated with the Kansas City Veterans Affairs Medical Center. He stated that both too little and too much testosterone appear to raise the risk of atrial fibrillation through different biological mechanisms. He argued that treatment should therefore be highly individualized and monitored.
Low testosterone may disturb calcium handling within the body. This disruption can promote delayed afterdepolarizations and triggered electrical activity. These physical changes involve the sodium-calcium exchanger, ryanodine receptor 2, and the late sodium current.
High or supraphysiologic testosterone may alter potassium currents instead. These elevated levels might shorten the atrial action-potential duration and reduce the effective refractory period. These cellular changes can make re-entry-based arrhythmias more likely to occur.
These mechanisms remain biologically plausible explanations rather than clinically proven diagnostic pathways. They cannot reliably predict an individual patient risk profile. The authors clearly state that the optimal on-treatment testosterone range for atrial electrophysiology has not been prospectively established.
The proposed treatment target is approximately 350 to 550 ng/dL total testosterone. The review authors recommend this specific middle range rather than pushing for the high end of the reference range. The authors emphasize that this range is inferred entirely from observational evidence. It has not yet been prospectively tested as an atrial fibrillation prevention target.
The clinical position is not that all hormone therapy should be stopped entirely. Instead, the review recommends risk-stratified prescribing for men with confirmed testosterone deficiency. Clinicians should aim for physiologic mid-range levels. They should actively avoid efforts to push levels toward upper-normal or supraphysiologic concentrations.
Total testosterone can be misleading when sex hormone-binding globulin is abnormal. The review recommends using calculated free testosterone in that specific diagnostic situation. Conditions such as obesity, diabetes, liver disease, or older age may alter sex hormone-binding globulin.
The TRAVERSE trial tested only one specific product formulation. That product was a daily 1.62% transdermal gel. Its findings cannot automatically be generalized to every product or dosing schedule on the market. The authors identify comparative studies of gels, long-acting preparations, short-acting injections, and oral formulations as a critical research priority.
The review also raises pharmacokinetic concerns about short-acting intramuscular testosterone injections. These injections can produce supraphysiologic peaks within 24 to 72 hours after administration before declining toward a trough. Direct randomized evidence comparing formulations for irregular heartbeat risk remains very sparse.
For men with cardiovascular or arrhythmic risk, the authors favor stable-pharmacokinetic formulations over short-acting formulations. That preference is based on mechanistic and clinical reasoning rather than definitive head-to-head trials. You can find more context on these therapy options in our collection of testosterone and hormone articles.
Low testosterone may also be a marker of underlying illness rather than the sole cause of arrhythmia risk. The review notes that obesity, metabolic disease, and sleep apnea independently affect atrial fibrillation risk. Hypertension and heavy alcohol use also play significant roles in this process. These overlapping lifestyle factors can complicate attempts to isolate the exact effect of the hormone.
The article recommends addressing modifiable risk factors before and during treatment. Patients should work with their doctors to manage severe hypertension and abnormal lipids. You can read more about comprehensive physical restoration in our veteran health research library.
Structured monitoring should cover testosterone status and hematocrit levels. Clinicians should also track blood pressure, renal function, hepatic function, and cardiac rhythm. The review calls maintaining a normal hematocrit the principal dose-limiting safety constraint. It identifies erythrocytosis as the most frequent dose-limiting adverse effect of the therapy.
The review also discusses men with an existing atrial fibrillation diagnosis. It advises avoiding the therapy in men with unstable or highly symptomatic atrial fibrillation. However, treatment may be considered in stable cases through careful shared decision-making and conservative targeting.
This is the proposed clinical approach of the review authors. It is not a substitute for individual guidance from a qualified medical clinician. The headline finding should not be presented as absolute proof that testosterone therapy causes this heart condition in every man.
The evidence may not generalize equally to all men or all younger veterans. TRAVERSE enrolled older, higher-cardiovascular-risk men with documented hypogonadism. Younger, healthier men, men using testosterone for nonmedical performance enhancement, and men receiving other products may have completely different risk profiles.
Veterans and service members must consult a qualified physician or VA provider before self-diagnosing or altering any medical protocol. Do not self-adjust, escalate, or discontinue prescribed medication based solely on a headline. The evidence is mixed, and the current medical review supports individualized treatment plans.
Confirm that your treatment is being used for a documented medical indication. The review focuses strictly on symptomatic hypogonadal men. It does not establish that hormones used for bodybuilding, performance enhancement, or appearance are safe. Discuss your specific formulation and dosing pattern with your provider.
Seek urgent medical attention for chest pain, fainting, severe shortness of breath, or sustained palpitations. This is especially vital for individuals with known heart disease or a prior rhythm disorder. Veterans should note that the article explicitly states its contents do not represent the views of the U.S. Department of Veterans Affairs or the U.S. government.
Understanding how hormones impact cardiovascular performance requires a shift in how we view physical restoration. Patients should recognize possible atrial fibrillation symptoms, including a racing or irregular heartbeat, unexplained fatigue, and reduced exercise tolerance. Maintaining open communication with your provider ensures these markers are properly evaluated.
The key takeaway is that testosterone treatment requires careful individualization and monitoring to restore levels to the safe middle range, preventing both low and high extremes that may threaten heart rhythm. Stay objective, manage your complete health profile, and keep your long-term capability firmly in your own hands.
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