Newer aspects of diagnostic and therapeutic management of acute idiopathic pericarditis.

Acute pericarditis continues to present a challenge to the clinician from the point of view of etiology and differential diagnosis as well as treatment. Acute pericarditis occurring in the course of myocardial infarction, neo-plastic diseases and advanced renal disease with uremia may be accepted as directly related to these disorders. It poses, however, an etiologic and differential diagnostic problem when it is encountered not only in the so-called idiopathic or non-specific form but even in the case of so-called rheumatic or primary tuberculous pericarditis. It has been noted by many observers f. i. how rarely isolated rheumatic pericarditis is followed by subsequent recurrence of acute rheumatic fever or any valvular defects. The diagnosis of so-called primary tuberculous pericarditis rests also usually on circumstantial evidence since bacteriological proof of tuberculosis is obtained only rarely. Clinically these three types of pericarditis resemble each other markedly, There are, however, considerable differences in treatment and also prognosis. At times, the clinical picture of pericarditis resembles closely that of acute myocardial infarction. Whether it occurs in a middle-aged or older individual the differential diagnosis bears greatly upon the immediate and long term management. 1. Pericarditis: Etiologic and differential diagnostic considerations. The dissatisfaction with the laboratory procedures currently available for this purpose have prompted a search for additional laboratory aids. Of these the fibrinogen polymerization (F.P.) test of Losner and Volkt held particular promise. Having noted its highly specific nature in active rheumatic fever and arthritis2 we explored its usefulness in pericarditis and found it to be positive in a preliminary group of patients with acute rheumatic and non-specific pericarditis.3 ' We have since followed a total of 20 patients with pericarditis with systematic serial studies of the F.P. test as well as the conventionally used acute phase reactants including the C-reactive protein (CRP), the erythrocyte sedimentation rate (ESR), plasma fibrinogen concentration and antistreptolysin-0 (ASO) titer. In cases where myocardial infarction had to be considered we have also employed the serum GO-transaminase test. Our experience is summarized in Table I. Some of the observations recorded here have been reported elsewhere.5 The additional observations made since have confirmed the previous ones.