This article describes how infectious agents, inflammation, and autoimmunity contribute to the development of heart disease.
Autoimmune heart disease refers to several different heart conditions that have an autoimmune origin. Some of these disorders such as constrictive pericarditis are unique disorders. Other autoimmune heart ailments occur when the heart is one of the organs targeted in people who have systemic autoimmune disorders, for instance the cardiac involvement that can occur in systemic lupus erythematosus (SLE). Other autoimmune disorders such as Hashimoto's thyroiditis are associated with hemodynamic changes that lead to congestive heart failure over time if thyroid hormone levels are too low for the body's needs.
INFECTIOUS TRIGGERS
The development of autoimmune disease is caused by a combination of genetic and environmental factors. Viral and bacterial infections are known to trigger a number of different autoimmune diseases. Studies show that infection with Coxsackievirus B3 causes immune system changes, specifically activated mast cells and innate cytokines, which promote the development of autoimmune heart disease, a condition that can affect young as well as older adults.
The Coxsackie virus can cause myocarditis, which is an inflammation of heart muscle. Myocarditis is a principal cause of heart disease and sudden cardiac death in young adults. Researchers at Johns Hopkins University have found that complement, an innate immune system component, directs a series of events in Coxsackie infection that lead to the development of autoimmune myocarditis.
In Chlamydia infection, a surface protein on the bacterial surface mimics the heart's myosin protein. In infection, the immune system produces antibodies against the Chlamydia protein. Through a process of molecular mimicry these same antibodies react with the myosin protein in heart cells, causing inflammatory heart disease.
CONSTRICTIVE PERICARDITIS
Constrictive pericarditis (inflammation of the pericardial sac surrounding the heart) represents a serious hemodynamic syndrome that can lead to heart failure without surgical intervention. Pericarditis can be caused by tuberculosis, radiation therapy, malignancies, open-chest surgery, and autoimmune disorders. Autoimmune pericarditis may result from an ongoing inflammatory process involving other layers of the heart, particularly the myocardium in conditions such as rheumatic pancarditis and viral perimyocarditis. Decreased cardiac performance in pericarditis is mainly caused by diastolic dysfunction.
THE INFLAMMATORY PROCESS
Inflammation is recognized as a contributing factor in heart disease. At the Second Conference of the Heart, Rheumatism and Autoimmunity, held in Italy in May 2005, researchers reported that a growing body of evidence supports the view that autoimmune mechanisms are involved in the development of cardiovascular disease. With improved treatments for systemic lupus, most of the serious consequences are related to heart, kidney, or lung complications. SLE is a significant risk factor for accelerated atherosclerosis and premature coronary heart disease. Lupus patients have a 5-6 fold increased risk of developing coronary heart disease, and in younger patients the risk is even higher.
Inflammation in lupus is suspected of increasing cardiac risk factors such as earlier menopause, hypertension, elevated blood lipids, and causing the production of lupus anticoagulant antibodies that increase the risk of blood clots. The use of corticosteroid therapy increases the risk for these factors.
In patients with Graves' disease, myxedematous deposits of mucin and glycosaminoglycan can surround the heart and contribute to congestive heart disease. These changes are most likely in patients with pretibial myxedema and thyroid eye disease as part of the EMO syndrome (exophthalmos, myxedema, ophthalmopathy).
REDUCING INFLAMMATION
While many medications, including corticosteroids and non-steroidal anti-inflammatory agents, are designed to reduce inflammation, they often have undesirable side effects. Lifestyle changes can also reduce inflammation. Dietary changes, particularly reducing saturated fats and sugar, and adding more antioxidant-rich fruits and vegetables, can reduce inflammation. Anti-inflammatory herbs can also be incorporated into healing protocols. Stress promotes inflammation, and stress-reduction techniques such as yoga, exercise, mediation, sleep, prayer, social support, and biofeedback, reduce the effects of chronic stress, including a reduction in inflammation related to a reduction of the stress hormone cortisol.
Resources:
Afanasyeva, Marina; Rose, Noel; FairWeather, DeLisa, Novel Model of Constrictive Pericarditis Associated with Autoimmune Heart Disease in Interferon-Gamma-knockout Mice, American Heart Association, 2004.
Berger Abi, Autoimmune reaction links Chlamydia to heart disease, British Medical Journal, March 6, 1999.
Fairweather D, Rose N, Mast cells and innate cytokines are associated with susceptibility to autoimmune heart disease following Coxsackievirus B3 infection, Autoimmunity, March 2004; 37(2): 131-45.
Sternberg, Esther, The stress response and autoimmune disease-what have we learned? InFocus Publication of the Autoimmune Diseases Association, June 2006.
