Bodies are busy ecosystems. Millions of cells and countless chemical processes are constantly interacting to keep us alive and in motion. Most of these exchanges go unnoticed, yet we feel their results – a rash that heals, a muscle that flexes, a breath that steadies.
Inflammation is one of those unseen activities, an essential protective mechanism that goes into action when we’re confronted with an injury or infection. When tissue is injured or threatened, the immune system launches a rapid inflammatory response to contain damage and begin repair, known as acute inflammation. It might show up as a fever, swelling, or redness as the body’s visible proof that it’s working. Typically, it’s short-term, purposeful, and necessary for healing.
But when that response goes haywire, it becomes chronic: a low-grade, persistent activation that can gradually harm rather than help. Chronic inflammation touches nearly every biological process, from metabolism and immunity to cellular repair and organ function. And that includes the heart. Over time, this ongoing immune activation can alter vascular integrity, disrupt electrical signaling, and heighten vulnerability to rhythm disorders such as atrial fibrillation.
When the body’s natural defense becomes the source of collateral damage, what happens to the rhythm meant to sustain life itself?
Inflammation on a Granular Level
Chronic inflammation can persist for months, or even years. Unlike acute inflammation, which flares up quickly to heal injuries or fight infection, chronic inflammation lingers; the severity and effects depend on both the cause of the trigger and the body’s ability to repair itself.
The triggers for chronic inflammation are varied. Sometimes it results from a residual infection, like tuberculosis or certain parasites, that the body cannot fully eliminate. It can also result from irritants that the body can’t break down, such as silica dust or industrial chemicals. Autoimmune disorders, in which the body mistakenly attacks healthy tissue, are another common cause. Sometimes it’s due to defects in the cells that regulate immune response, recurrent episodes of acute inflammation, or biochemical stressors like free radicals (unstable molecules that can damage cells), oxidized lipoproteins (fats that have reacted with oxygen, promoting tissue injury), or advanced glycation end products, or AGEs (molecules formed when sugar binds to proteins, contributing to oxidative stress and tissue damage).1
Whatever the trigger, chronic inflammation is marked by a shift in the immune system’s response. Neutrophils (the immune system’s “first responders”) dominate the acute phase, and as the cascade continues and cycles, chronic inflammation starts recruiting more macrophages (cells that engulf debris and pathogens), lymphocytes (immune cells that coordinate and target responses), and plasma cells (antibody-producing cells) to the affected tissue. These cells instigate inflammatory cytokines (messenger molecules that orchestrate immune activity), growth factors, and enzymes that start promoting tissue damage, fibrosis, or granuloma formation (clusters of immune cells that wall off persistent irritants). Over time, this ongoing activity can overwhelm the body, leaving organs vulnerable to dysfunction – including the heart.
Several factors increase the likelihood of developing chronic inflammation. Aging, obesity, metabolic syndrome, and a diet high in saturated fat, trans fats, or refined sugars all contribute to elevated inflammatory markers. Smoking, low levels of sex hormones, chronic stress, and disrupted sleep can further amplify the body’s inflammatory response.
Signs of chronic inflammation can be subtle but widespread: persistent fatigue, joint or muscle pain, mood disturbances, gastrointestinal issues, and changes in weight. Because there aren’t laboratory tests for chronic inflammation, per se, it often goes unnoticed until it manifests through associated chronic conditions, like type 2 diabetes or heart disease.1
Habitually unchecked immune responses, and the unhealthy patterns we indulge in, can disrupt nearly every system in the body. Understanding inflammatory mechanisms, and how everyday lifestyle choices can contribute, can help us take a proactive role in preventing more serious disease.
Cellular Saboteurs and Cardiac Disruption
Chronic inflammation doesn’t stay confined to an aggressively regenerative process in a siloed area of the body; it can promote actual remodeling of the body tissue itself, which is orchestrated by tiny, multi-protein signaling platforms called inflammasomes. These specialized complexes act like sentinels that detect danger signals from pathogenic molecules, and they help coordinate a defense response.
A particular inflammasome, NLRP3, is showing up in recent research as a key player in cardiac arrhythmias, including atrial fibrillation and other rhythm disorders. When NLRP3 activates within heart cells (cardiomyocytes) or in fibroblasts (the structural support cells of the heart), it sets off a cascade of biochemical alarms. Remember the cytokines? They’re released to instruct neighboring cells to respond. While essential and protective in the short term, their prolonged presence reshapes the heart over time.2
Immune cells, including macrophages and T-lymphocytes, infiltrate atrial tissue in response to the inflammatory signals, releasing additional cytokines and perpetuating a local inflammatory cycle. This creates a feedback loop: inflammation alters tissue structure and electrical activity, which, in turn, sustains immune activation. Over time, the heart’s rhythm becomes increasingly fragile, vulnerable to both subtle and overt arrhythmic events.
Structurally, chronic inflammation destabilizes the heart through fibrosis, the formation of scar-like tissue. Fibroblasts, normally the heart’s structural caretakers, respond to prolonged inflammasome signaling by transforming into myofibroblasts, cells with enhanced contractile and collagen-producing abilities. This remodeling thickens and stiffens heart tissue, disrupting the normal architecture that allows electrical impulses to flow smoothly. The result is a proarrhythmic environment where electrical signals can misfire, collide, or loop back on themselves, creating the conditions for abnormal rhythms.3
Cardiomyocytes rely on tightly regulated calcium signaling to initiate each contraction. NLRP3 activation alters calcium handling, producing erratic waves that destabilize a coordinated heartbeat. Add oxidative stress to the mix, another byproduct of chronic immune activation, and the heart’s cellular environment becomes even more unpredictable, amplifying the risk of arrhythmias.
Autonomic dysregulation (the imbalance between the sympathetic “fight or flight” and parasympathetic “rest and digest” systems of the nervous system) is another consequence of chronically hyperactive immune response. Cytokines can interfere with these regulatory pathways, causing the heart to respond inappropriately to stress, activity, or rest. Combined with structural remodeling and electrical misfires, this imbalance further heightens arrhythmic risk, particularly in conditions like heart failure where sympathetic overactivation is already present.
A Strategic Reset
If we go on not paying attention, the very mechanisms meant to protect us can instead undermine our health and wellbeing. Actively reducing exposure to inflammation is one of the most accessible and effective ways to protect your heart. Our lifestyle choices – what we eat, how we move, when we rest, and how we manage stress – all influence our inflammatory load. Basic yet foundational strategies are all you need.
Physical Activity
There’s no way around weight management: excess adipose tissue releases inflammatory molecules, so maintaining an optimal weight is one of the most effective ways to reduce chronic inflammation. Regular exercise not only helps maintain a healthy weight by reducing the pro-inflammatory burden of adipose tissue, but also independently lowers inflammatory molecules, strengthens the cardiovascular system, and supports muscular and skeletal health.
Diet
Minimizing refined carbohydrates, sugary beverages, trans fats, and hydrogenated oils helps prevent the triggers that fan the fire of inflammation.
A diet rich in anti-inflammatory foods provides both protection and repair. Fatty fish like salmon supply omega-3s that temper inflammatory cytokines. Fruits and vegetables like blueberries, cherries, kale, broccoli, and Brussels sprouts deliver antioxidants, polyphenols, and fiber, which help keep inflammatory mediators in check. Nuts, sesame oil, and curcumin (from turmeric) offer additional anti-inflammatory benefits, while micronutrients like magnesium, vitamin D, vitamin E, zinc, and selenium shield tissues from chronic immune overactivation.4
Sleep and Stress Management
Restorative sleep is another pillar. Seven to eight hours of quality sleep each night stimulates hormones that aid tissue repair and maintain balanced immune activity. It also helps combat chronic stress that can amplify inflammatory responses, disrupt hormonal balance, and compromise the body’s natural defenses. Mind-body practices like yoga, meditation, and mindful breathing can reduce stress-driven inflammation and protect heart function.
Gut Health
Believe it or not, the intestinal microbiome also plays a part. Overuse of antibiotics, antacids, or NSAIDs can disrupt gut health, leading to low-grade intestinal inflammation that spills into the rest of the body.4 Preserving healthy gut microbiota with the help of healthy foods and probiotics helps reduce systemic inflammatory signaling.
By making better lifestyle choices, we can reduce chronic inflammation and support the integrity of both heart tissue and electrical rhythm. These strategies may not reverse existing damage, but they lower the ongoing assault on the heart, giving rhythm, structure, and resilience a fighting chance.
Always consult your healthcare provider before making changes to biological routines like diet or exercise, especially if you have a history of heart rhythm or other health issues.
Dr. Tordini is a part of Florida Medical Clinic Orlando Health
- Pahwa, R., Goyal, A., & Jialal , I. (2023, August 7). Chronic Inflammation. National Library of Medicine; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK493173/.
- Karakasis, P., Pamporis, K., Theofilis, P., Milaras, N., Vlachakis, P. K., Grigoriou, K., Patoulias, D., Karamitsos, T., Antoniadis, A. P., & Fragakis, N. (2025). Inflammasome Signaling in Cardiac Arrhythmias: Linking Inflammation, Fibrosis, and Electrical Remodeling. International journal of molecular sciences, 26(13), 5954. https://doi.org/10.3390/ijms26135954.
- Obeagu E. I. (2025). Inflammatory cytokines and cardiac arrhythmias: from pathogenesis to potential therapies. Annals of medicine and surgery (2012), 87(9), 5607–5613. https://doi.org/10.1097/MS9.0000000000003499.
- Pahwa, R., Goyal, A., & Jialal , I. (2023, August 7). Chronic Inflammation. National Library of Medicine; StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK493173/.
