Sometimes, a study on one topic can reveal important issues in another. Case in point: A recent Lancet study explored what a person’s life was like before they developed chronic pain — the diseases they had, whether they were lonely, and whether they had depression.

Looking beyond the socioeconomic responses, it was also apparent that compared with the study’s no pain control group, 50% of the pain group reported some form of cardiovascular disease and one quarter reported arthritis.

Medscape Medical News thought it was important to connect those dots, so we turned to Gregg Fonarow, MD, interim chief of UCLA’s Division of Cardiology and director of the Ahmanson-UCLA Cardiomyopathy Center, to answer a few questions. “There is an important intersection of neurobiology and preventive cardiology,” he said in an email. “Regardless of etiology, neuropathic, inflammatory, musculoskeletal pain should be considered a cardiometabolic risk factor.”

Is the type of pain associated with cardiovascular diseases more acute than chronic?

Cardiovascular diseases can manifest with a variety of pain types, depending on the underlying pathology and affected structures. Most pain syndromes associated with cardiovascular disease are acute or intermittent rather than chronic.

Atherosclerotic coronary artery disease (angina) can result in chest pain. This pain is frequently experienced as pressure, squeezing, or heaviness rather than sharp pain. This pain may radiate to the left arm, jaw, neck, or back. Angina may occur during exertion and is relieved by rest.

The patient with acute myocardial infarction may present with intense, crushing chest pain that can radiate like angina pain. There may be associated symptoms like nausea, diaphoresis, and shortness of pressure. However, some individuals experience more subtle pain with acute myocardial infarction. Peripheral artery disease can cause claudication that may be sensed as cramping or aching pain in the legs during walking; it is relieved by rest.

While cardiovascular disease does not usually cause chronic pain syndromes, individuals with chronic pain syndromes due to other causes have been found to be at an increased risk for cardiovascular events in a number of studies. (In a 2024 study of nearly 160,000 people, the more chronic pain sites someone had, that person’s index for increased arterial stiffness went up.)

Chronic pain can exacerbate cardiovascular risk through increased sympathetic nerve activity, elevated blood pressure and heart rate, reduced physical activity, and higher prevalence of modifiable risk factors, like smoking and poor diet. Further chronic inflammation can also contribute to the initiation and progression of cardiovascular disease.

In the Lancet study, 32.1% of the pain group reported having hypertension. What type of pain can high blood pressure cause?

High blood pressure (hypertension) does not typically cause pain directly. Many individuals with high blood pressure do not experience any noticeable symptoms. However, when blood pressure becomes severely elevated or leads to complications, pain can emerge as a secondary symptom.

Some individuals who experience out-of-control blood pressure can have headache-related pain, particularly in cases of hypertensive crisis, in which some may experience severe headaches due to increased intracranial pressure.

High blood pressure, particularly during hypertensive emergencies, can contribute to chest pain, with anginal symptoms or even acute coronary syndromes. In the case of aortic dissection — an infrequent but life-threatening complication of uncontrolled hypertension — there can be a sudden, severe, tearing pain in the back.

Pain symptoms caused by hypertension usually resolve with improved blood pressure control. In the case of aortic dissection, this is a medical or surgical emergency.

Overall, 25% of the Lancet study pain group reported having arthritis pain. Is there some connection between arthritis and heart disease that could explain this high percentage?

There are important connections between arthritis and cardiovascular disease. While arthritis is often viewed as a joint-specific condition, many forms, particularly inflammatory arthritis, have systemic effects that directly affect cardiovascular health.

Arthritis can be characterized by chronic inflammation. Rheumatoid arthritis (RA), lupus, and psoriatic arthritis are autoimmune diseases marked by persistent inflammation. This chronic inflammation accelerates atherosclerosis, destabilizes plaques, and promotes endothelial dysfunction, increasing the risk for acute coronary events, strokes, peripheral vascular disease, and heart failure.

Individuals with RA have a 50%-70% higher risk for cardiovascular disease than the general population. Psoriatic arthritis also increases the likelihood of coronary artery disease.

Even osteoarthritis can contribute to cardiovascular disease risk via risk factors like obesity, inactivity, and nonsteroidal anti-inflammatory drug (NSAID) use. Treatments used in arthritis, like NSAIDs and corticosteroids, can raise blood pressure, cholesterol, and glucose levels, compounding heart risks, though helpful for reducing pain.

Depression and loneliness both scored as significant factors in the Lancet pain group. What are your thoughts on these findings?

Depression and loneliness are common in individuals with chronic pain. Depression and loneliness are also important contributors to cardiovascular disease. These conditions can influence the onset, progression, and outcomes of the other. Depression is associated with elevated inflammatory markers (eg, C-reactive protein, interleukin 6, and TNF-alpha), which accelerate atherosclerosis and endothelial dysfunction. There is autonomic dysregulation with chronic pain and with depression. Increased sympathetic activity and reduced heart rate variability heighten arrhythmia and ischemia risk. Depressed individuals often have more activated platelets, increasing the likelihood of thrombosis.

Importantly, chronic pain syndromes, depression, and loneliness can impair self-care — contributing to poor medication adherence, sedentary lifestyle, smoking, and unhealthy diet. These, in turn, contribute to cardiovascular disease onset and clinical events.

Yet cardiovascular disease itself can contribute to the onset of depression and loneliness. Studies have reported that 20%-30% of patients develop depression after a cardiac event. Fear of recurrence of cardiovascular events, reduced physical capacity, and loss of independence contribute to emotional distress and loneliness. Cardiac injury can alter neurochemical pathways, affecting mood regulation.

Depression and loneliness are independent predictors of mortality in patients with cardiovascular diseases, even after adjusting for other established risk factors. There are guideline recommendations for screening for depression, and when identified, appropriate treatment and referral in cardiology settings, especially in post-myocardial infarction and heart failure management.

Because chronic pain can activate the sympathetic nervous system, thereby initiating the development of cardiovascular disease, it would seem that paying attention to a patient’s pain level, regardless of the source, is very important.

There is an important intersection of neurobiology and preventive cardiology. Chronic pain can be a persistent stressor that reshapes autonomic balance, promoting sustained sympathetic activation, vascular remodeling, and inflammatory signaling — all of which heighten cardiovascular risk.

The clinical implications of this suggest that there should be routine pain assessment in patients with and at a risk for cardiovascular disease. Regardless of etiology, neuropathic, inflammatory, and musculoskeletal pain should be considered a cardiometabolic risk factor. Combining pharmacologic, psychological, and lifestyle interventions may reduce sympathetic tone and improve cardiovascular outcomes. There is an important need for collaborative care. The integration of cardiology, pain management, and behavioral medicine may help foster patient-centered care.

Can the way physicians assess a patient’s pain be improved?

Many cardiologists primarily focus on pain that may be cardiac in origin. However, they may also assess pain more broadly when it informs diagnosis, risk stratification, or patient management. If pain appears musculoskeletal, gastrointestinal, or psychological in origin, cardiologists may still evaluate it to rule out cardiac causes or refer to other specialists.

There is research supporting the use of pain scales and opportunities to apply these into clinical practice. Numeric rating scales or descriptive tools may be used to gauge severity and monitor changes over time. But the opportunity exists for greater recognition that chronic pain contributes to cardiovascular risk and the importance to modify that risk.

Having collaborative care plans between cardiologists, primary care physicians, pain management specialists, and psychologists or psychiatrists can be very valuable. Shared decision-making emphasizes involving patients in the discussion regarding their symptoms, including pain, to integrate their preferences in guiding testing and therapy.

Can you discuss your patient population and their pain issues?

We have a multidisciplinary care team involved in the assessment and management of patients with heart failure. Patients, their family members, and their caregivers also are involved in the discussion. These patients often have comorbid conditions that can contribute to chronic pain. As NSAIDS can greatly increase the risk of worsening heart failure, we collaborate closely with the patient, their other clinicians, and pharmacists to identify pain control strategies that avoid the use of NSAIDs but still effectively address their pain.