How may systemic lupus erythematosus affect the heart?

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease of unknown etiology characterized by the production of various autoantibodies, including antibodies directed against nucleic acids and (deoxy)ribonucleoproteins, cell membrane epitopes (blood cells, neurons), and phospholipids. Clinical manifestations result from deposition of immune complexes or through the interaction of antibodies that directly interfere with cellular or coagulation function.

The most common cardiac manifestation of SLE is pericarditis, which is found in up to 80% of postmortem examinations. Clinical manifestations of pericarditis, either characteristic pain or an auditory rub on auscultation, may be present at some time in up to 50% of patients. SLE tends to be an episodic disorder characterized by remissions and exacerbations; pericarditis associated with SLE tends to follow this general rule. Cardiac compression due to large effusions or to constrictive pericarditis has been reported but is unusual.

Congestive heart failure in the patient with SLE may be secondary to various extracardiac causes, including renal failure and hypertension. Occasionally, myocarditis due to infiltration of the myocardium by inflammatory cells may manifest clinically as congestive heart failure or dysrhythmias.

Endocarditis caused by Libman-Sacks vegetations is present in up to 75% of patients with SLE on postmortem examination. These small 1-4 mm lesions are found on the edge of the mitral and aortic valves most commonly but occasionally involve the right-sided valves, valve rings, papillary muscles, and endocardium. They are usually clinically silent but occasionally may lead to valvular compromise, embolic phenomenon, and bacterial endocarditis.

Premature coronary artery disease due to atherosclerosis is becoming a common problem as patients with SLE survive longer. Potential causes of this premature atherosclerosis include hypertension, glucocorticoid therapy, and chronic immune complex deposition within coronary artery walls.

Finally, patients with SLE and antiphospholipid antibodies may have the same manifestations as patients with primary antiphospholipid antibody disease (see question 11).

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