Gout is a painful form of inflammatory arthritis caused by the accumulation of excess uric acid, which leads to crystal deposits in the joints. While its most noticeable symptom is the sudden, intense pain of a joint flare, often in the big toe, the disease is far from just a joint issue. Research shows that gout has a significant connection to overall cardiovascular health. The underlying mechanisms that drive gout—high uric acid levels and systemic inflammation—actively contribute to damage within the heart and blood vessels.
The Systemic Link: Uric Acid, Inflammation, and Cardiovascular Risk
The root cause of gout is hyperuricemia, defined by high levels of uric acid in the blood, typically above 6.8 mg/dL. This excess uric acid is independently associated with dysfunction in the body’s vascular system. High uric acid levels promote oxidative stress, which damages the delicate lining of blood vessels known as the endothelium. This endothelial dysfunction is recognized as an early step in the development of atherosclerosis, the hardening and narrowing of arteries.
Gout is characterized by acute inflammatory attacks, but even between flares, patients experience chronic systemic inflammation. This inflammation acts as a primary bridge linking gout to heart disease. Inflammatory markers, such as high-sensitivity C-reactive protein (hsCRP), are often elevated in gout patients, signaling ongoing activity that contributes to vascular damage. The sustained inflammation accelerates the buildup of plaque in the arteries, increasing the risk for cardiovascular events.
Specific inflammatory molecules, like interleukin-1 (IL-1), trigger acute gout flares and contribute to systemic inflammation affecting the heart. Studies show that patients who experience a gout flare have a temporarily increased risk of heart attack or stroke in the following months. This suggests that the intense inflammatory response of a flare can destabilize existing plaque deposits within the coronary arteries, contributing to acute cardiovascular events.
Specific Heart and Vascular Conditions Linked to Gout
People with gout face a higher risk of developing specific heart and vascular problems. One common connection is to hypertension, or high blood pressure, with more than 70% of gout patients also having this condition. High uric acid levels are thought to contribute to hypertension by activating the renin-angiotensin system and impairing the ability of blood vessels to relax, which restricts blood flow.
The risk of coronary artery disease (CAD), which involves blockages in the heart’s major vessels, is also elevated. Gout patients are more likely to suffer a myocardial infarction (heart attack) or die from cardiovascular disease. There is also a strong link between gout and heart failure, a condition where the heart muscle cannot pump blood efficiently. Individuals with gout have been found to be up to 64% more likely to develop heart failure than those without the condition.
Vascular damage caused by chronic inflammation and hyperuricemia also extends to the brain, increasing the likelihood of stroke. Studies suggest that patients with gout are at an elevated risk for stroke, consistent with the accelerated atherosclerosis seen in major arteries. These increased cardiovascular risks are often proportional to both the severity and the duration of the gout condition.
Managing Gout to Protect Cardiovascular Health
Because the mechanisms that cause gout also threaten the heart, effective gout management is viewed as a form of cardiovascular protection. The primary goal of treatment is to achieve and maintain a serum uric acid level below 6 mg/dL, which is necessary to dissolve crystal deposits. Uric acid lowering therapy (ULT) with medications like allopurinol prevents gout flares and may also improve outcomes for certain heart conditions, such as heart failure.
Lifestyle modifications are a foundational component of a comprehensive treatment plan for both conditions. Maintaining a healthy weight is particularly important, as obesity increases the risk of both gout and poor cardiovascular metrics. Weight reduction has been shown to lower uric acid levels and reduce the number of gout attacks. Dietary changes should focus on limiting foods high in purines, such as red meat and certain seafood, and reducing the intake of high-fructose corn syrup and alcohol, which can raise uric acid.
Adopting a heart-healthy eating pattern, such as the Mediterranean diet or the Dietary Approaches to Stop Hypertension (DASH) diet, benefits both gout and cardiovascular risk factors. These diets emphasize fruits, vegetables, whole grains, and low-fat dairy while limiting saturated fats. Gout patients should work closely with their primary care physician, a rheumatologist, and a cardiologist to ensure that treatment for one condition complements the management of the other.