Does TRT Raise Heart Attack Risk? What the New Research Actually Shows

May 20, 2026
Does TRT Raise Heart Attack Risk? What the New Research Actually Shows

The fear around testosterone replacement therapy and heart attacks did not come from nowhere. It came from a string of observational studies published in the early 2010s that showed men on TRT had higher rates of cardiovascular events, and those studies got a lot of attention, triggered FDA warnings, and shaped how physicians thought about prescribing testosterone for the better part of a decade.

The problem is that observational studies cannot tell you what caused what. They can only tell you what happened in a group of people who made their own choices, and the men who were being prescribed TRT in those studies were already sicker, older, and had more underlying heart disease than the men who were not being prescribed it, so of course they had more events. That is called confounding, and it is exactly why you run a randomized controlled trial instead.

So that is what researchers did. They ran the largest randomized controlled trial ever conducted on testosterone replacement therapy and called it TRAVERSE, published in the New England Journal of Medicine in 2023.

Here is how it worked. They took 5,246 men who had low testosterone, confirmed by labs, and who already had or were at elevated risk for cardiovascular disease, which is important because this was not a group of healthy younger men. These were the exact men that physicians were most worried about putting on TRT. They randomized half of them to a daily testosterone gel targeting a level between 350 and 750 nanograms per deciliter, and they randomized the other half to a placebo gel, and they followed both groups for an average of nearly three years while tracking major cardiovascular events, specifically heart attacks, strokes, and cardiovascular death.

The outcome was that TRT did not increase risk. The rate of major cardiovascular events was 7.0 percent in the testosterone group and 7.3 percent in the placebo group, a difference that was statistically negligible and within the non-inferiority margin the trial was designed to detect. The men taking testosterone actually had a slightly lower event rate numerically, though that gap is small enough that you would not hang your hat on it as a benefit claim. What the trial definitively established is that in men with pre-existing cardiovascular risk, testosterone replacement therapy over roughly three years does not make things worse.

Then researchers took TRAVERSE and pooled it with every other randomized controlled trial on TRT that had been conducted, and the meta-analysis published in JACC in 2024 confirmed the same finding across the full body of evidence. And an expert review published in Andrology in 2026 drew the same conclusion after integrating the TRAVERSE data with the broader mechanistic and clinical literature.

That is a randomized controlled trial of over 5,000 men, a meta-analysis, and an expert synthesis all pointing the same direction.

Now here is where the story gets more nuanced, because the trial also found things that do matter and that do require monitoring.

TRT raised hematocrit, which is the percentage of your blood that is made up of red blood cells. The body responds to higher testosterone by producing more of something called erythropoietin, a hormone your kidneys release that signals bone marrow to produce more red blood cells, and that is actually why testosterone was historically used to treat anemia. But when hematocrit climbs too high, the blood becomes thicker and harder to pump, and the risk of clotting goes up with it.

In TRAVERSE, elevated hematocrit was significantly more common in the testosterone group, and 22.4 percent of men in the testosterone arm developed a hematocrit above 54 percent compared to 1.7 percent in the placebo group. The threshold of 54 percent is not arbitrary. Above that level the evidence for increased clotting risk becomes clinically meaningful, and it is why hematocrit is one of the primary labs you track when someone is on TRT. Catching it early means you can adjust the dose, donate blood, or take a temporary break from injections before it becomes a problem.

Atrial fibrillation, which is an irregular heart rhythm that increases stroke risk, was also more common in the TRT group, occurring in 3.5 percent of men on testosterone versus 2.4 percent on placebo. That difference is meaningful enough to warrant awareness, particularly in men who already have risk factors for arrhythmia.

There were also higher rates of acute kidney injury and pulmonary embolism in the testosterone group in TRAVERSE, though those signals were smaller and require more research to fully interpret. The expert review noted them as areas that need continued follow-up rather than established causal conclusions.

So what does this all mean practically for someone on TRT or considering it.

The cardiovascular boogeyman that scared physicians and patients for years does not have strong evidence behind it when TRT is used appropriately in men with actual testosterone deficiency. The TRAVERSE trial was specifically designed with high-risk men to test the worst-case scenario, and even there the primary outcome was non-inferior to placebo.

But non-inferior does not mean consequence-free. There are real physiological changes happening when you raise testosterone, and some of them require monitoring. The hematocrit issue is the most consistently documented and the most directly manageable, and a hematocrit check every six months is not optional, it is the mechanism by which you catch the one side effect with the clearest clotting implications before it causes harm.

The other piece that the research cannot account for is behavior. A clinical trial controls for the intervention, but in real life the men who start TRT sometimes stop doing everything else, because they feel better and the motivation to stay disciplined about diet, cardio, and lipids can fade when the symptoms that were driving that discipline go away. Testosterone does not lower LDL. It does not reduce visceral fat on its own. It does not undo years of metabolic dysfunction. What it does is restore a hormone to a physiological range, and if the cardiovascular risk factors that existed before TRT are still present and unmanaged, the hormone itself is not going to offset that.

The men in TRAVERSE who had events had them because they had serious cardiovascular disease at baseline, not because testosterone caused it.

That is the actual picture the research paints. TRT does not appear to be the cardiovascular villain the early observational data suggested it was, and it also is not a cardiovascular protector that replaces the work of managing the underlying risk factors that will determine how your heart does over decades.


References

  1. Lincoff AM, et al. 2023. "Cardiovascular Safety of Testosterone-Replacement Therapy." New England Journal of Medicine. Source
  2. Zitzmann M, et al. 2026. "Cardiovascular Safety of Testosterone Therapy: Insights from the TRAVERSE Trial and Beyond." Andrology. Source
  3. Hudson J, et al. 2024. "Long-term Cardiovascular Safety of Testosterone-Replacement Therapy in Middle-Aged and Older Men: A Meta-Analysis of Randomized Controlled Trials." JACC. 04050-6 Source

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