The changes produced by acute pericardial tamponade were examined. Tamponade produced the expected hemodynamic alteration; namely, depression on cardiac output, left ventricular pressure and LV dp/dt and elevation of right atrial and intrapericardial pressures. The mechanism of the hemodynamic disturbance was that the elevation of the intrapericardial pressure produced a negative atrial transmural pressure and disturbed atrial and ventricular filling producing the vicious cycle: diminished venoatrial gradient→decreased cardiac output→attenuated effect of ventricular systole on atrial filling, and so forth. The myocardial contractility was not impaired in cardiac tamponade.

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(1) In large pericardial effusion, echography showed a revolving motion of the heart. This characteristic motion was interfered by the pericardial adhesion. Real time cross-sectional scanning was useful for detecting the adhesion, especially the localized one. When excessive cardiac motion coexisted with techycardia, alternation of the heart position accompanied by electrical alternans was observed. Based on the results, the mechanism for the alternation of the heart position was discussed. (2) Echogram suggesting the pericardial thickening was found in about a half of patients with constrictive pericarditis. Another findings, which may reflect the anatomical and functional changes in constrictive pericarditis, were also presented. Although each of them is not pathognomonic, concurrence of them may suggest the presence of constrictive pericarditis. (3) Inflow velocity in jugular vein was markedly decreased in cardiac tamponade. The inspiratory increase in the inflow velocity was observed in mild cardiac tamponade, but not in severe one. Flow velocity pattern of jugular vein in constrictive pericarditis was characterized by the appearance of the reverse flow being coexistent with rapidly deceralating inflow in diastole.

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1) Thirty-eight cases of idiopathic pericarditis in our institutes were analyzed and were classified into 3; group A: clinical picture of pericarditis, group B: clinical picture of peri-myocarditis and group C: dominant clinical picture of chronic pericardial effusion. 2) All cases of group A showed a good clinical course. 3) In group B cases with complete A-V block continued to have heart block with significant myocardial changes, and the prognosis may not be good. 4) Many cases of group C belonged to elderly female and the etilogy was unclear. 5) Viral pericarditis was proven in only one case.

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A total of 87 cases of pericardial heart disease (73 of pericarditis and 14 of hemopericardium) among 870 consecutive autopsies of aged patients was studied. Fibrinofibrous pericarditis was found in 80.8% of pericarditis, neoplastic in 13.7% and purulent in 5.5%. Representative cases of each type of pericarditis were illustrated. Among fibrinofibrous pericarditis, idiopathic was the most common and the other causes included irradiation, myocardial infarction, renal failure, rheumatoid arthritis and hypothyroidism. Frequent association of congestive heart failure or anasarca with mild to moderate fibrinofibrous pericarditis was noted. Clinical and morphologic evidences of pulmonary tuberculosis were present in nearly one third of cases with fibrinofibrous pericarditis, but actual incidence of tuberculous pericarditis could not be determined. Incidence of clinical signs and symptoms of acute pericauditis was evaluated with the stress on the relatively high incidence of supraventricular tachyarrhythmias, especially in cases with histological evidences of sinus node involvement in aged cases.

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1. The clinical study of 24 patients with pericarditis has been presented. 2. In this series the patients were predominantly female. 3. Collagen disease was the most common cause followed by idiopathic pericarditis. Rheumatic and tuberculous pericarditis were rare. 4. Rheumatic anc tuberculous pericarditis were rare. 5. Three cases of constrictive pericarditis were presented in this series. Two were with atrial septal defect and one was tuberculous pericarditis. 6. Recognition of the right ventricular "dip" and platear curve by cardiac catheterization is necessary for the diagnosis of constrictive pericarditis. 7. In constrictive pericarditis right ventricular "dip" and platear curve remained longer after the operation of pericardiectomy. 8. THe typical physical findings were fever, cardiomegaly, hepatomegaly and tachycardia. 9. Right side cardiac faulure was more common than left side failure. 10. Friction rub, distant cardiac sound and paradoxical pulse were less common than it has been thought. No specific laboratory finding was present. 12. None of the cases revealed elevated virus titer. 13. Most of the patients revealed enlarged cardiac silhouette in chest X-ray. 14. The electrocardiographic changes were low voltage, ST segment elevation and T wave abnormality. 15. The ST segment elevation was seen in all standard leads, especially in aVF and from V₂ to V₆. 16. The abonormal T wave vector oriented to superiorly posteriorly and to right or left. 17. The presence of abonormal T wave suggests myocardial involvement. 18. In some cases T wave abonormality persists after the echocardiographic disappearance of pericardial fluid. 19. Arrhythmia was rare except constrictive pericarditis.

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Electrophysiologic disorders in 17 patients with sick sinus syndrome (SSS) were assessed by recording of intracardiac electrograms, atrial overdrive pacing and extrastimulus technique. Significant suppression of the sinoatrial node (SAN) by overdrive pacing (maximum corrected SAN recovery time of longer than 560 msec) was noted in 14 of 16 patients studied. In nine patients, scanning with atrial extrastimuli, sinus rest was defined in all. In one patient there was a longer interpolation zone. Calculated sinoatrial conduction time (SACT) in individual patients varied considerably. The mean SACT was over 110 msec in 5 of 9 patients (56%). Sinus echo was demonstrated in 3; one manifested SAN re-entrant tachycardia with rates of 72 to 77 beats/min. AV nodal echo was demonstrated in 3, two of them manifested AV nodal re-entrant tachycardia. Intracardiac electrograms revealed prolonged AV conduction time in 2 of 15 patients and prolonged His-Purkinje system conduction time in 2 of 17 patients studied. Two patients disclosed what we thought to be manifestation of intraatrial conduction disturbance. Both had considerable time interval between pacing impulse and atrial response. In one of them Mobitz type 1 and 2:1 intraatrial blocks were observed on atrial pacing and a possible internodal tract depolarization was also recorded. It is concluded that the electrophysiologic manifestations of patients with SSS cover a wide spectrum .The machanism of tachycardia can be due to either SAN or AV nodal re-entry.

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