Yes. Extracardiac manifestations of subacute bacterial endocarditis (SBE) may be due to circulating cytokines, deposition of immune complexes, or embolic phenomena. Since SBE is an inflammatory process, cytokines may be elaborated into the circulation and result in symptoms such as fever, fatigue, malaise, anorexia, and weight loss, findings common in primary rheumatologic disorders. Circulating immune complexes due to the chronic antigenemia are common; these may deposit in a variety of end organs such as the kidney where they may lead to acute glomerulonephritis, also a common finding in a variety of rheumatologic disorders. This mechanism likely also contributes to the arthritis which may be present in SBE. Additionally, direct infection of joints (septic arthritis) may occur secondary to the chronic bacteremia. Embolic disease may result in infarction of a variety of end organs, including the brain and heart. To make the situation even more confusing, 24-50% of patients with SBE are rheumatoid factor positive due to the chronic antigenemia. Therefore, blood cultures should be obtained in every patient with fever and arthritis to exclude the possibility of SBE.
Rheumatoid arthritis rarely affects the heart. True or false?
Rheumatoid arthritis (RA) is a systemic autoimmune disease of unknown etiology that manifests predominantly as a chronic, symmetric, inflammatory synovitis of the peripheral joints. Extraarticular manifestations are quite variable and usually mild but occasionally severe and life-threatening. Extraarticular manifestations are usually due to vasculitis of small blood vessels or to granulomatous infiltration in end organs.
Although only 2% of patients with RA manifest symptoms of pericarditis, evaluation of patients by echocardiography or during postmortem examination reveals evidence of pericardial inflammation in approximately 30% of patients. Most patients with symptomatic pericarditis respond to treatment with nonsteroidal anti-inflammatory drugs (NSAIDs). Pericardial tamponade and constrictive pericarditis are unusual but well-described complications.
Like pericarditis, focal or diffuse granulomatous infiltration of the myocardium, endocardium, and valves is a fairly common pathologic finding that rarely manifests clinically. Microscopically, this finding resembles the rheumatoid nodule, with which it likely shares a common pathologic origin. Clinical manifestations, when they occur, include congestive heart failure, valvular dysfunction, and dysrhythmias.
Inflammation of the coronary arteries is demonstrable in approximately 20% of patients on postmortem examination but, like the other cardiac manifestations of RA, rarely manifests clinically as myocardial ischemia.