My blood panels go back 6 years. I track inflammation markers obsessively because chronic low-grade inflammation is the silent tax on every cardiovascular outcome I care about. So when a study drops showing that an untreated bacterial infection can raise your stroke risk by 92% and your death risk by nearly 6x, I stop everything and read it twice.

The Tulane study published April 15 in JAMA Network Open is not a small signal. Researchers analyzed 1,469 adults with syphilis against 7,345 matched controls across 15 years of New Orleans hospital data. They excluded anyone with prior cardiovascular disease. The results are not subtle: ischemic stroke at 10.3% vs. 5.7% in controls, hemorrhagic stroke at 2.0% vs. 0.8%, aortic aneurysm at 3.3% vs. 1.3%. Heart attack risk ran 31% higher. Death risk ran 5.8 times higher overall, and in tertiary syphilis specifically, 6.93 times higher.

The Inflammation Tax Nobody Is Billing For

The mechanistic story here is not complicated. Treponema pallidum, the bacterium behind syphilis, triggers chronic systemic inflammation when left untreated. Chronic inflammation is exactly what drives atherosclerosis, arterial stiffness, and plaque instability. I have spent years trying to suppress my hsCRP through diet, sleep, and cold exposure because I understand what sustained inflammation does to vessel walls over a decade. Syphilis, in its later stages, is essentially running that same inflammatory process at scale, and most people carrying it have no idea.

The critical detail: none of these cardiovascular risks showed up in early-stage infection. Primary and secondary syphilis, caught and treated quickly, did not produce the same signal. The damage accumulates when the infection goes latent and untreated for over a year. That is the window where the cardiovascular stack starts compounding against you.

Dr. Alex Chen will correctly point out that this is observational data and cannot prove causation. Fair. The retrospective design cannot rule out confounders, and the PAD numbers in the study look like a reporting error worth scrutinizing. But the hazard ratios here are not marginal. A 92% increase in hemorrhagic stroke and a 2x aortic aneurysm risk are not noise. When mechanistic plausibility is strong and the signal is this large, waiting for a randomized controlled trial is its own kind of risk management failure.

This Is a Screening Problem, Not a Research Problem

U.S. syphilis cases have been climbing for years, concentrated heavily in Southern states, which is exactly where the Tulane data came from. The infection is treatable with penicillin. The cardiovascular damage it causes is not reversible once it accumulates. That asymmetry should be making every cardiologist and primary care provider rethink their intake protocols.

Right now, syphilis screening is not a standard part of cardiovascular risk assessment. It should be, at minimum, for any high-risk patient presenting with unexplained inflammation markers or early atherosclerosis. Lead author Eli Tsakiris put it plainly: providers treating high-risk patients need to be aware of this association. I would go further. The CDC and cardiology societies should issue joint guidance adding syphilis serology to CVD risk workups for relevant populations.

The optimization math here is almost insultingly simple. A syphilis test costs less than a copay. A course of penicillin costs almost nothing. An aortic dissection costs you everything. If you are a provider reading this and you are not screening high-risk patients for syphilis before their next echocardiogram, you are leaving a treatable variable completely unaccounted for in your cardiovascular risk model.