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

The fear started with observational studies, and that matters because observational studies cannot randomly assign people to treatments, which means the men who ended up on TRT in those early studies were already different from the men who did not, often sicker, older, or carrying more metabolic risk, and when those men had worse cardiovascular outcomes the data made it look like testosterone caused the problem when the real issue was that the sickest patients were the ones most likely to get prescribed it in the first place. That kind of bias has a name in research: confounding. And it poisoned the conversation around TRT for over a decade.

To actually answer the question of whether testosterone raises heart attack risk, you need a randomized controlled trial, which means you flip a coin and assign people to the treatment or the placebo so that both groups start equal and any difference in outcomes at the end can actually be attributed to the intervention.

That trial was run and it was called TRAVERSE.

5,246 men with confirmed low testosterone, all of them carrying existing risk factors for heart disease like hypertension, diabetes, or prior cardiovascular events, were randomized to either testosterone replacement therapy or a placebo gel and followed for an average of nearly three years. This was the largest randomized controlled trial ever conducted specifically on TRT and cardiovascular outcomes, and it was designed precisely because the question had never been answered cleanly.

The primary outcome they were tracking was something called MACE, which stands for major adverse cardiovascular events and refers to the combined rate of heart attack, stroke, and cardiovascular death, the three things that most people are actually afraid of when they worry about TRT.

Over the course of the trial, the TRT group had a MACE rate of 7.0% compared to 7.3% in the placebo group. That difference was not statistically significant, meaning it falls within the range of normal random variation, but the direction of the data matters: the men on testosterone did not do worse. In a population that already had elevated cardiovascular risk, three years of TRT produced no increase in heart attacks, strokes, or cardiovascular death.

A meta-analysis published in the Journal of the American College of Cardiology then pooled TRAVERSE together with every other randomized controlled trial on TRT and cardiovascular outcomes and reached the same conclusion across a broader dataset, and an expert review published in 2026 in the journal Andrology, which synthesized both TRAVERSE and the wider body of evidence, confirmed that finding again. Three separate analyses of the best available evidence are pointing the same direction.

So where does that leave the original fear? Largely without support, at least when testosterone is used appropriately in men with confirmed deficiency.

But there is a part of the TRAVERSE data that the conversation around TRT tends to skip over, and it is the part that actually matters for anyone managing a real protocol.

TRAVERSE did find two areas where TRT produced elevated rates of adverse events compared to placebo. Atrial fibrillation occurred in 3.5% of the testosterone group versus 2.4% in the placebo group. Pulmonary embolism, which is a blood clot in the lungs, occurred in 0.9% of the testosterone group versus 0.5% in placebo. Neither of these findings overturns the primary cardiovascular safety finding, but both of them are mechanistically explained by something that happens in almost every man who goes on TRT: the rise in hematocrit.

Hematocrit is the percentage of your blood volume that is made up of red blood cells, and testosterone stimulates the production of those cells through a hormone called erythropoietin, which signals the bone marrow to ramp up red blood cell output. More red blood cells means thicker blood, and thicker blood moves more slowly and clots more easily, which is exactly the mechanism behind the elevated pulmonary embolism signal in TRAVERSE and a plausible contributor to atrial fibrillation as well.

The clinical threshold most practitioners use is 54%. Below that number, the thickening of the blood is generally considered manageable. Above it, you are meaningfully increasing clotting risk, and that risk is not theoretical, it is the documented mechanism behind real adverse events in real patients.

This is why hematocrit is not optional monitoring. It is the primary safety variable in any well-managed TRT protocol, and it needs to be checked at minimum every six months, more frequently in the first year when the body is still calibrating to the new hormonal environment. If hematocrit is trending upward and approaching that 54% threshold, the clinical options include reducing the dose, increasing the injection frequency to flatten the peaks, donating blood, or in some cases therapeutic phlebotomy.

The lipid picture with TRT is more nuanced. Testosterone tends to lower HDL, which is the cholesterol particle associated with cardiovascular protection, but it also tends to lower triglycerides and in some cases improves LDL particle behavior, and the net effect on actual cardiovascular outcomes in TRAVERSE was neutral. The mechanism for why HDL drops on TRT relates to how the liver processes androgens and their effect on an enzyme called hepatic lipase, which accelerates HDL clearance from circulation. Whether that HDL reduction is clinically meaningful given the overall neutral MACE finding is genuinely unsettled, but it is a reason to keep lipids in your regular lab panel rather than ignoring them.

The practical failure mode that shows up repeatedly in clinical practice is not that TRT causes heart attacks. It is that men start TRT, feel better, and then treat the injection as a replacement for the behaviors that actually drive cardiovascular health. The testosterone is not doing cardioprotective work on its own. What it can do is increase training capacity, support body composition, and improve energy in ways that make it easier to do the things that protect your heart, but only if you actually do those things.

A man who starts TRT, improves his body composition, maintains his aerobic fitness, keeps his hematocrit monitored, and manages his lipids is in a genuinely different risk category than a man who starts TRT, lets his diet slide because he feels invincible, stops doing cardio because his energy is better, and skips his six-month labs.

The injection does not know which of those men you are. The outcome does.

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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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