No abstract

Multifocal atrial tachycardia, also designated "chaotic atrial tachycardia," was identified in the records of 31 patients. It was particularly noted that the arrhythmia progressed to atrial fibrillation or flutter in 17 cases (55%). Unifocal or multifocal premature atrial contractions preceded the arrhythmia in 20 cases (64%). The arrhythmia developed during an acute illness in 18 cases (58%). However, it occasionally occurred in paroxysms without an apparent cause in patients with chronic disease. Significant acute or chronic pulmonary disease was present in 12 cases (39%). The arrhythmia was not associated with digitalis toxicity or with rhythm disturbances known to occur in digitalis intoxication such as paroxysmal atrial tachycardia with block. In general, digitalis therapy seemed to have little effect on the course of the arrhythmia, but in some cases it appeared to be beneficial, especially if atrial fibrillation supervened. In several patients there seemed to be a transition from multifocal premature atrial contractions through chaotic atrial tachycardia to atrial fibrillation. These observations suggested that chaotic atrial tachycardia might be a forewarning of atrial fibrillation and that the two arrhythmias may have a similar mechanism.

In studies of coagulation of the arterial and venous blood of relatively young normal subjects, there were statistically significant arteriovenous differences in some of the tests employed. These differences, however, were not all in the same direction, in that some indicated increased and some decreased coagulation activity of the arterial blood. In patients with coronary heart disease, these arteriovenous differences were absent or less marked. It was suggested that this change in arteriovenous difference in such patients could possibly be attributed to the surface effect of the diseased arterial wall on the coagulation mechanism. It was recognized, however, that a number of other factors could contribute to, or entirely account for, this phenomenon. There was some evidence of increased coagulation activity in the venous blood of patients with coronary heart disease as compared to matched controls. This was indicated by a more rapid generation of thromboplastin with the addition of inosithin (platelet substitute), and a more rapid generation as well as a greater yield of thromboplastin without the addition of inosithin. Fibrinolytic activity was significantly lower in the arterial blood compared to the venous in both the normal subjects and patients with atherosclerosis. This arteriovenous difference was greater in the atherosclerotic group and it was widely variable. Because of this variability, venous fibrinolysis determinations could not be taken as an indicator of the level of fibrinolytic activity in the arterial blood. Hence, it was suggested that in studies of fibrinolysis as related to atherosclerosis, arterial blood samples should be routinely used. Fibrinolytic activity of the blood in the atherosclerotic group as a whole was lower than that in the normal group on both the arterial and the venous sides. The difference between the two groups was greater in the arterial than the venous blood. In the group with atherosclerosis, the subgroup with coronary heart disease and that with occlusive disease of the peripheral arteries were separately analyzed. The subgroup with coronary heart disease exhibited a significantly lower fibrinolytic activity compared to normal subjects only in the arterial blood, whereas the subgroup with occlusive disease of the peripheral arteries showed a lower fibrinolytic activity in both the arterial and the venous blood. In the subgroup with occlusive disease of the peripheral arteries, it was particularly note-worthy that the younger patients had a very low fibrinolytic activity. It was thought that one could only speculate as to whether this low fibrinolytic activity in such young patients is in any way causally related to the disease process. It appeared that in patients with coronary heart disease the delicate balance of coagulation and fibrinolysis was tipped in the direction of clot formation. It was not clear, however, whether the changes in blood coagulation and fibrinolysis observed in such patients were etiologic in the pathogenesis of the disease process, associated with it, or simply a secondary phenomenon. Moreover, it was recognized that in vitro demonstration of such changes in blood coagulation and fibrinolysis does not necessarily imply in vivo hypercoagulability. No correlation was found between the level of serum cholesterol and plasma fibrinolytic activity.