Cardiovascular Involvement in Systemic Lupus Erythematosus

Abstract

Cardiovascular involvement in systemic lupus erythematosus (SLE) was first reported by Kaposi in 1872 of cardiac irregularity and dyspnea. In 1924, Libman and Sacks reported verrucous endocarditis but ironically did not recognize the association of verrucous endocarditis with SLE. (Petri, 2004) In the last decade, newly recognized clinical entities have been described with the introduction of very sensitive, non-invasive and semiinvasive cardiac imaging techniques.(Turiel, 2005) With the use of very sensitive methods of cardiovascular investigations, it has been found the prevalence of cardiac involvement to be >50%. (Petri, 2004) Several autoantibodies such as antiDNA, anti-phospholipid antibodies (apl), antiSSA (Ro antibodies) and antiendothelial cell antibodies present in patients with SLE can mediate cardiac damage. These autoantibodies can directly affect the heart tissue or, alternatively, trigger mechanisms able to cause heart damage for example, apl can contribute to cardiac damage enhancing atherosclerosis phenomena, causing thrombosis of coronary arteries or starting an immune-complex mediated reaction and deposition at the valve level. Consequences of autoantibody damage has been reported in several heart structures such as the valves, myocardium, pericardium, conduction tissues and cardiac arteries in patients suffering from SLE, antiphospholipid syndrome (APS), Sjogrens syndrome and other autoimmune rheumatic diseases(ARD). (Tincani et al, 2006) Overall improvements in medical care including the availability of antibiotics, antihypertensive, and renal replacement therapy coupled with the judicious use of glucocorticoids, antimalarial and immunosuppressive drugs have led to improved survival of SLE patients in the past 50 years. (Nikpou, 2005) In 1976, Urowitz first described the ‘bimodal mortality pattern’ of SLE. This observation was based on SLE deaths early in the course of the disease were due to active SLE and use of high dose steroids associated with complications such as infection and sepsis. Later in the disease course (›5 years after diagnosis) deaths were frequently associated with inactive SLE, long duration of prednisolone therapy and myocardial infarction (MI) due to atherosclerotic heart disease. (Urowitz, 1976) Cardiac disease has recently been acknowledged as a primary cause of morbidity and mortality in SLE as well as APS, and numerous factors leading to accelerated