Syncope masquerading as a panic disorder: role of the subcutaneous loop recorder in eliciting the appropriate diagnosis.

The present case describes a 49-year-old woman with apparent panic disorder in whom the Reveal Plus, a newly developed subcutaneous loop recorder, was used to show that the panic attacks were secondary to prolonged episodes of ventricular asystole.

Plasma beta-thromboglobulin in acute myocardial infarction with ventricular arrhythmias.

Patients with myocardial infarction, complicated by ventricular arrhythmias (Lown grade greater than or equal to 2), had higher (p less than 0.05) plasma beta-thromboglobulin level than that found in patients with uncomplicated infarction. This indicates higher platelet activation in the former group than in the latter. Such data provide rationale for clinical trial of antiplatelet drugs in cases of myocardial infarction complicated by severe arrhythmias.

Formation of prostacyclin-sensitive platelet aggregates in human whole blood in vitro. Part II. The occurrence of the phenomenon in males suffering from acute myocardial infarction.

The de-aggregatory effect of prostacyclin (PGI2) and the rate of spontaneous platelet aggregation (SPA) were studied in vitro in whole blood of 24 males with acute myocardial infarction (MI) and 18 males, patient controls (PC). The de-aggregatory effect of PGI2 and the rate of SPA (measured as a percentage of changes in free platelet number in whole blood) were higher (p less than 0.01) in MI than PC. The de-aggregatory effect of PGI2 in whole blood was higher (p less than 0.05) on the first day of MI than on day 14 following MI. The highest de-aggregatory effect of PGI2 was found in whole blood of patients with MI complicated by ventricular fibrillation. In neither of the groups did the de-aggregatory effect of PGI2 correlate with patients' age, haematocrit, erythrocyte and leucocyte counts, triglycerides, HDL, LDL or total cholesterol levels. In the MI group, de-aggregatory effect of PGI2 was correlated with free platelet concentration (r = -0.59, p less than 0.05), elevation of glutamic oxalacetic transaminase (r = 0.53, p less than 0.05) and creatinine phosphokinase (r = 0.69, p less than 0.001). The de-aggregatory effect of PGI2 in blood of patients with evolving MI did not differ from that in PC. It is concluded that the increased rate of SPA and formation of PGI2-sensitive platelet aggregates in vitro in whole blood of MI patients are secondary to myocardial necrosis.