Inflammation of the heart, medically termed carditis, occurs when the body’s immune response attacks one or more layers of the cardiac structure. While acute carditis often resolves, the condition becomes chronic when inflammation persists, recurs, or causes irreversible damage over an extended period. This sustained damage fundamentally alters the heart’s anatomy and physiology. Understanding chronic carditis involves recognizing how this progression affects the heart’s ability to function, often leading to complications.
Defining Chronic Carditis and Its Forms
Carditis is defined by the specific layer of the heart tissue affected by inflammation.
Myocarditis involves the myocardium, the muscular layer responsible for the heart’s pumping action. Inflammation of this muscle tissue over time significantly weakens the heart’s contractile ability.
Endocarditis affects the endocardium, the inner lining of the heart chambers and the heart valves. Chronic endocarditis often results from persistent infection, causing growths (vegetations) that damage the valves.
Pericarditis is the inflammation of the pericardium, the thin sac surrounding the heart.
The designation of “chronic” is applied when the inflammatory process or its symptoms last for more than six months. Chronic carditis is defined by a prolonged state where initial damage continues to remodel the heart structure, especially through the development of scar tissue, distinguishing it from acute episodes.
Underlying Causes and Risk Factors
The progression to chronic carditis is driven by underlying etiologies that lead to a sustained inflammatory or damaging response within the heart.
Infectious and Post-Infectious Damage
One primary pathway is through infectious persistence or post-infectious damage. Certain bacterial infections, such as those causing Lyme disease or rheumatic fever, can trigger a delayed, harmful immune response that targets heart tissue, leading to chronic inflammation. Other long-term bacterial or fungal infections, particularly in endocarditis, may require prolonged antibiotic courses to eradicate, and the resulting damage to the valves remains a chronic problem.
Autoimmune Conditions
Another significant group of causes involves autoimmune and systemic inflammatory conditions, where the body’s immune system mistakenly attacks its own healthy heart tissue. Diseases like systemic lupus erythematosus, rheumatoid arthritis, or sarcoidosis can cause inflammation across all layers of the heart, frequently leading to chronic forms of carditis. These conditions result in an ongoing cycle of immune-mediated damage that requires long-term management to suppress the inflammatory response and prevent progressive heart injury.
Environmental and Toxic Exposures
Environmental and toxic exposures also contribute to chronic cardiac damage by causing cumulative cellular injury over time. Exposure to certain medications, including some chemotherapy agents or drugs used for seizures or irregular heart rhythms, can initiate inflammation in susceptible individuals. Furthermore, high-dose radiation administered for the treatment of cancers in the chest area can induce inflammation and fibrosis in the pericardium and myocardium, leading to chronic carditis years after the initial exposure.
Long-Term Impact on Heart Function
The most significant long-term consequence of chronic carditis is the development of fibrosis and scarring within the heart layers. Chronic inflammation triggers the deposition of fibrous tissue, replacing healthy, functional heart cells with stiff, non-contractile scar tissue. In the muscular layer, this scarring is known as myocardial fibrosis, which directly impairs the heart’s ability to stretch and contract effectively, reducing its pumping efficiency.
This structural remodeling frequently progresses into chronic heart failure, often manifesting as a form of cardiomyopathy. Chronic myocarditis, for instance, can lead to dilated cardiomyopathy, where the heart chambers become enlarged and weakened, unable to pump enough blood to meet the body’s needs. Conversely, chronic pericarditis can result in constrictive pericarditis, where the scarred and thickened pericardial sac tightens around the heart, physically restricting the ventricles from filling properly.
Chronic endocarditis primarily results in severe valvular disease, as the persistent infection and inflammation cause holes, tears, or excessive scarring on the valve leaflets. This damage leads to either regurgitation, where the valve leaks blood backward, or stenosis, where the valve opening narrows and obstructs forward blood flow. Over time, the heart must work harder to compensate for these faulty valves, accelerating the onset of heart failure.
Scattered scar tissue within the muscle also disrupts the heart’s electrical signaling pathways, which are necessary for coordinated beating. This disruption leads to the formation of arrhythmias, or irregular heart rhythms. These electrical instabilities can range from relatively benign palpitations to life-threatening ventricular arrhythmias that increase the risk of sudden cardiac arrest.
Management and Therapeutic Strategies
The management of chronic carditis targets both the underlying cause of the inflammation and the consequences of the resulting structural damage. For cases driven by persistent infection, such as specific forms of endocarditis, prolonged courses of intravenous antibiotics are often necessary to fully clear the causative microorganisms. If the chronic inflammation is linked to an autoimmune disorder, treatment focuses on using immunosuppressive and anti-inflammatory medications to dampen the immune system’s attack on the heart.
For chronic or recurrent pericarditis, long-term use of anti-inflammatory agents like nonsteroidal anti-inflammatory drugs (NSAIDs) and colchicine is common to control symptoms and prevent recurrence. Managing the irreversible damage involves medications used for heart failure, such as beta-blockers and angiotensin-converting enzyme (ACE) inhibitors, which reduce the workload on the damaged muscle and help prevent further deterioration.
In cases where the electrical system is compromised, anti-arrhythmic drugs may be prescribed, or an implantable cardioverter-defibrillator (ICD) may be necessary to correct dangerous heart rhythms. When structural damage becomes severe, surgical intervention is often required to restore heart function. This can include valve repair or replacement for endocarditis, or a pericardiectomy, which is the surgical removal of the constrictive pericardial sac. Ultimately, for patients with end-stage heart failure due to extensive chronic damage, a heart transplant may be the only remaining viable therapeutic option.