Serum lactic dehydrogenase level as a diagnostic test for carditis in rheumatic fever.

a case of rheumatic fever, at least one of its five chief manifestations must be recognized, namely, mitral valvulitis, aortic valvulitis, partial heart block, pericarditis, and cardiac failure. It is doubted that there are other manifestations of rheumatic carditis. Sinus tachycardia is not disproportionate to fever, anxiety, pericardial effusion, or heart failure. Gallop rhythm in a child is difficult to distinguish from a normal third heart sound. Technical and laboratory procedures are of little help to the clinician in this respect. Enlargement of the heart shadow rarely if ever occurs in the absence of advanced valvular disease, heart failure, or pericardial effusion. The electrocardiogram shows no obvious changes other than those of partial heart block, pericarditis, or the consequences of advanced valvular disease, and a normal tracing does not exclude active carditis. Considerable doubt has been thrown on the value of prolongation of the Q-T interval,' as found by Taran and Szilagyi2 and Abrahams.3 The Creactive protein, leukocyte count, and the erythrocyte sedimentation rate4 may provide good evidence of rheumatic activity, but they fail to identify carditis. Hence the importance of searching for a diagnostic test of active carditis in rheumatic fever is clear. The serum glutamic oxaloacetic transaminase (SGOT) level was found to be elevated in myocardial infarction.5 Nydick et al.6 found significant elevation of SGOT activity in 65 per cent of their cases with clinically active carditis. Lactic dehydrogenase (LDH) is an enzyme that catalyzes the interconversion of lactate and pyruvate. It has a wide tissue distribution and is particularly abundant in the myocardium, skeletal muscle, liver, and kidney. Necrosis, degeneration, or inflammation results in an increased rate of release of the enzyme from the cells and a rise of its level in the serum. Since necrotic, degenerative, and inflammatory changes are all features of the pathologic picture of rheumatic carditis, and since in myocardial infarction, the concentration of serum lactic de-