Changing patterns of fracture in the dorsal and lumbar spine.

Myocardial Infarction-Ardlie et al. MDCBOURNAL 891 1959), a finding which we have confirmed in this study. This elevation could either wholly or partly account for the longer and heavier thrombi found in patients with myocardial infarction. We do not know whether the factor or factors responsible for the development of large thrombi were present before infarction or merely reflect the results of infarction. It appears that the latter is more likely. Nevertheless, it is interesting to speculate whether this propensity to abnormal in vitro thrombosis after myocardial infarction might be associated with the tendency of these patients to subsequent thrombotic episodes. Our results clearly indicate that there is a significant increase in the incidence of platelet abnormalities in patients with myocardial infarction when compared with control subjects over the age of 40 years. Again we cannot be sure whether these findings relate to a state existing before infarction or are wholly or in part a sequel to myocardial necrosis. However, we have demonstrated that there is a definite tendency for both the frequency of spontaneous platelet aggregation and thrombus size to increase with age in apparently healthy subjects. These findings suggest that the factor or factors responsible for these phenomena are present to some extent before the clinical event, and that coronary thrombosis could result from an exaggeration of this trend. The overall frequency of platelet abnormality was similar in patients with myocardial infarction whether or not they were receiving anticoagulant therapy (Table II). Two explanations for this finding should be considered. First, it could be that in anticoagulated patients the initial overall frequency of platelet abnormality was greater, and that this frequency has in fact been reduced by therapy. Alternatively, anti-coagulants may have had little or no effect on platelet aggrega-tion. On the other hand, there was a trend, though not statistically significant (Table II), for the snowstorm phenomenon to occur more often in anticoagulated patients (11.5%) than in those not receiving anticoagulant therapy (4.7%). At first sight this might suggest that anticoagulant therapy had enhanced platelet aggregation. This trend may, however, merely reflect the fact that those patients selected for anti-coagulant therapy differed from those not given anticoagulants, possibly on the basis of more extensive infarction. It is apparent that the effect of oral anticoagulants on platelet aggregation in this in vitro system is inconclusive. Summary Fifty healthy subjects and 52 patients with myocardial infarction were investigated, the …