How Ankylosing Spondylitis Affects the Heart

Ankylosing spondylitis raises your risk of heart problems well beyond what most people with the condition realize. Population studies show that people with AS face roughly 35-40% higher odds of dying from a vascular cause compared with the general population, and the excess risk traces to several distinct cardiac complications rather than just one.¹ The connection involves more than garden-variety heart disease: AS can directly inflame the aorta and its valve, scramble the heart’s electrical signals, stiffen the heart muscle, and speed up the artery-clogging process that leads to heart attacks. Understanding which of these problems to watch for, and what can be done about them, matters for anyone managing this diagnosis.

Why AS Affects the Heart at All

The link between a spinal condition and the heart comes down to chronic inflammation. AS keeps your immune system in a sustained state of activation, and many of the inflammatory molecules circulating in your blood do not confine their damage to the spine. Over time, those molecules injure the inner lining of blood vessels, a process called endothelial dysfunction, which is considered a first step toward atherosclerosis.² But AS also causes a form of cardiac inflammation that looks different from ordinary heart disease. The aorta itself can become inflamed (aortitis), the tissue around the aortic valve can thicken and scar, and the electrical wiring of the heart can be damaged by inflammatory deposits. These are AS-specific problems that do not depend on cholesterol levels or blood pressure.

A useful way to think about it: AS creates two overlapping streams of cardiac risk. One is the accelerated atherosclerosis you would expect from any chronic inflammatory condition, raising your chance of heart attacks and strokes. The other is direct inflammatory damage to the heart’s structures, particularly the aortic root, the aortic valve, and the conduction system. Both streams are at work, and they can appear together or independently.³

Aortic Root and Valve Damage

The most distinctive cardiac signature of AS involves the aortic root, the first section of the main artery leaving the heart, and the aortic valve sitting inside it. Inflammation can thicken the aortic valve cusps, widen the root itself, and produce a characteristic ridge of scar tissue just below the valve. When that happens, the valve may stop closing properly, letting blood leak backward into the heart with every beat. That backward flow is called aortic regurgitation, and in severe cases it forces the heart to work harder and can lead to heart failure.

Echocardiography studies going back decades have found subtle signs of this process even in AS patients who had no cardiac symptoms. Researchers in one early study detected thickened cusps and small fibrous ridges below the valve in patients who were otherwise asymptomatic, suggesting that the inflammatory changes begin long before they produce a noticeable leak.⁴ More recent work has connected these changes to HLA-B27, the gene strongly associated with AS. Patients who carry HLA-B27 tend to have wider aortic roots and are more likely to develop root dilation than those who do not.⁵ That matters because wider roots are a setup for worsening regurgitation over time.

The HLA-B27 Connection

HLA-B27 deserves special attention because its cardiac effects can show up even when the typical spinal symptoms of AS are mild or absent. In roughly half of patients found to have HLA-B27-related conduction problems or aortic regurgitation, a formal rheumatic disease had not previously been diagnosed.⁶ In other words, some people develop the cardiac complications before anyone suspects they have AS. This has led researchers to describe an “HLA-B27-associated cardiac syndrome” in which aortic regurgitation and serious conduction abnormalities travel together. One study found HLA-B27 in 88% of men who had both aortic regurgitation and severe conduction problems, whether or not they had obvious joint disease.⁷

For practical purposes, this means that if you have been diagnosed with unexplained aortic regurgitation or an unusual heart block, it may be worth asking about HLA-B27 testing, especially if you also have back stiffness or other joint symptoms you have been dismissing.

Heart Rhythm and Conduction Problems

The heart’s electrical system runs through tissue that sits close to the aortic root, which is exactly where AS-related inflammation tends to concentrate. Scarring in this area can slow or block the electrical signals that keep the heart beating in a coordinated rhythm. In cross-sectional studies of AS patients, conduction disturbances have been found in roughly 10 to 33% of patients depending on the criteria used, most commonly first-degree heart block and widened electrical impulses through the ventricles.⁸ A small number required pacemakers.

Follow-up data over five years found that about 18% of AS patients had a conduction disturbance at some point. Men were affected much more often than women, with about 20% of all men developing a detectable problem compared with 5% of women. A history of anterior uveitis, the eye inflammation commonly associated with AS, and higher disease activity at the start both predicted who would go on to develop conduction issues.⁹

Beyond conduction blocks, AS also raises the risk of atrial fibrillation. A meta-analysis found the risk of atrial fibrillation was roughly 85% higher in people with AS, and the risk of atrioventricular block was more than threefold higher.¹⁰ A nationwide study added a sobering detail: among younger AS patients under 40, the risk of developing new atrial fibrillation was about three times higher than in people of the same age without AS.¹¹ Atrial fibrillation in a 30-something is unusual enough that clinicians should consider AS-related inflammation as a possible contributing factor.

Coronary Artery Disease and Heart Attacks

The accelerated atherosclerosis side of AS translates into a measurably higher risk of coronary artery disease. A meta-analysis pooling data from multiple studies estimated that AS patients carry about 41% more risk of coronary artery disease than the general population.¹² That number held across different study designs.

The picture gets more nuanced when you look at heart attacks specifically. One population-based study found that AS patients were slightly more likely to have ischemic heart disease at baseline, but after excluding people who already had heart disease and adjusting for risk factors, the added risk of a new heart attack was not clearly elevated overall. Where the risk did stand out was in women with AS, who had a notably higher rate of developing ischemic heart disease. The researchers found that much of this excess risk in women was tied to NSAID use, a finding with interesting implications discussed below.¹³

Young patients deserve particular mention. A population-based study following newly diagnosed young AS patients found a roughly 47% higher risk of developing ischemic heart disease compared to age-matched controls, even after adjusting for other medical conditions.¹⁴ That finding matters because young adults are rarely screened for heart disease, and AS itself tends to be diagnosed in the twenties and thirties.

How the Heart Muscle Itself Gets Involved

Even before coronary arteries narrow or valves start leaking, the heart muscle in AS patients often shows signs of stiffening. A meta-analysis found that AS patients consistently have worse markers of diastolic relaxation, the phase when the heart fills with blood between beats. Studies combining multiple measures of this relaxation found diastolic dysfunction in anywhere from 9% to 45% of AS patients, compared with 0% to 18% of controls.¹⁵ The progression likely follows a cascade: systemic inflammation activates the lining of the heart’s small blood vessels, triggering immune cell infiltration, collagen buildup, and increased stiffness of the heart muscle cells themselves.¹⁶

Newer imaging techniques can pick up even subtler changes. Speckle tracking echocardiography, which measures how the heart muscle deforms during each beat, has detected impaired strain in AS patients who had normal results on standard echocardiography. Researchers have suggested this could serve as an early warning of cardiac involvement before symptoms develop.¹⁷

The NSAID Paradox

One of the more counterintuitive findings in AS cardiology involves nonsteroidal anti-inflammatory drugs. In the general population, long-term NSAID use is associated with increased cardiovascular risk, and regulatory agencies have issued warnings about it. But in AS patients, the relationship looks different. A large study found that long-term NSAID use raised cardiovascular risk by about 64% in people without AS, but in AS patients the same long-term use showed essentially no increase in cardiovascular risk at all.¹⁸

The leading explanation is that in AS, the anti-inflammatory benefit of NSAIDs offsets the cardiovascular harm they would otherwise cause. Because so much of the cardiac risk in AS comes from chronic inflammation itself, reducing that inflammation with NSAIDs may be protective on balance, even though the drugs carry cardiovascular risk in other contexts. Some studies have even suggested that NSAIDs are associated with lower cardiovascular risk in inflammatory arthritis patients compared to those not taking them, a stark reversal of the pattern seen in the broader population.¹⁹ This does not mean you should take more NSAIDs than prescribed, but it does mean the standard cardiovascular warnings about these drugs apply differently when chronic inflammation is the driving problem.

Biologic Therapies and Heart Protection

Tumor necrosis factor inhibitors, the biologic drugs widely used to treat AS, appear to offer cardiovascular benefits alongside their anti-inflammatory effects. A study found that AS patients on TNF inhibitor therapy had about 28% lower risk of heart attack or stroke compared to those not on biologics, after adjusting for traditional cardiovascular risk factors. The benefit was consistent across subgroups. Congestive heart failure risk, however, did not differ between users and nonusers.²⁰

Newer biologics targeting interleukin-17, such as secukinumab, have also been studied for their cardiometabolic effects. Available evidence suggests that IL-17 blockade does not worsen traditional cardiovascular risk markers like cholesterol or blood sugar, and may be associated with fewer cardiovascular events.²¹ The evidence here is still accumulating, but so far the picture is reassuring. Effective disease control through biologics appears to be good for the heart, not just the joints.

Sex Differences in Cardiovascular Risk

The cardiac profile of AS looks different in men and women in ways that are easy to overlook. In a large multicenter study of over 900 patients, women with AS had fewer traditional cardiovascular risk factors and less visible artery damage overall. But the story changed at the high end of the risk spectrum. Among patients already categorized as high or very high cardiovascular risk, women actually had more carotid plaques than men, and those women were characterized by worse functional impairment and higher disease activity scores.²²

The biological mechanisms behind this divergence also show sex-specific patterns. In men, higher levels of inflammatory markers were associated with lower “good” cholesterol, while in women, inflammation tracked more closely with higher triglycerides. Only women showed a clear relationship between insulin resistance and disease activity.²³ The practical takeaway is that using a single cardiovascular risk framework for all AS patients may miss risk in women with active disease, precisely the group that might be assumed to be at lower cardiac risk based on traditional scoring.

Cardiovascular Risk Assessment in Practice

Standard cardiovascular risk calculators were not designed with chronic inflammatory disease in mind, and they tend to underestimate risk in AS patients. One study applied Dutch, European, and American guidelines to a group of AS patients and found that only about 7-12% were flagged as high risk using standard age-based criteria. But when researchers added 15 years to the patients’ ages, a rough proxy for the extra burden of inflammation, the proportion classified as high risk jumped to 22-29%.²⁴ Some European rheumatology guidelines already recommend applying a multiplication factor to the calculated risk score for patients with inflammatory joint diseases, though this is not yet universally adopted.

What this means in practice is that if you have AS, standard risk scores may falsely reassure you or your doctor. Discussing your inflammatory disease status when getting cardiovascular screening is worth doing, even if the screening tools do not explicitly ask about it.

Exercise and Arterial Stiffness

High-intensity exercise has shown a specific cardiovascular benefit in AS patients that goes beyond general fitness. A randomized controlled trial found that AS patients assigned to a high-intensity exercise program had meaningful reductions in arterial stiffness compared to a control group, along with improvements in peak oxygen consumption, resting heart rate, and body fat.²⁵ Arterial stiffness is considered an early marker of cardiovascular risk, and the fact that exercise can reduce it in AS patients suggests that the vascular changes driven by inflammation are at least partly reversible. Traditional cholesterol and blood pressure numbers did not change significantly in the same trial, reinforcing the idea that the cardiovascular benefit of exercise in AS works through different channels than in the general population.²⁶

When Cardiac Problems Start Early

Juvenile-onset AS raises concerns about heart involvement beginning well before adulthood. A study of children with HLA-B27-associated juvenile arthritis found inflammatory aortic regurgitation in four patients and none in controls, along with evidence of cardiac muscle involvement during exercise stress testing. The authors concluded that HLA-B27 is a risk factor for cardiac damage even when joint disease is short-lived and mild.²⁷ This finding reinforces that cardiac screening should not wait until adulthood in patients with early-onset spondyloarthritis.

Amyloidosis as a Rare but Serious Complication

In a small number of AS patients with long-standing, poorly controlled disease, a secondary condition called AA amyloidosis can develop. This happens when years of inflammation cause the body to produce and deposit an abnormal protein (amyloid) in organs including the kidneys, thyroid, and heart. Cardiac amyloidosis causes the heart walls to thicken and stiffen, leading to heart failure that is difficult to treat. AA amyloidosis has been estimated to occur in about 5% of patients with poorly controlled chronic inflammatory diseases including AS.²⁸ Case reports describe patients with decades of AS who developed cardiac amyloidosis confirmed by biopsy, sometimes presenting with heart failure as the first sign that something beyond the spine was involved.²⁹ This is rare enough that most AS patients will never encounter it, but it underscores why keeping systemic inflammation under control matters for reasons far beyond back pain.