Miller, Richard

Abstract A double antibody radioimmunoassay (RIA) was developed to measure IgD in serum and secretions. One IgD myeloma protein was used as radiolabeled antigen and standard with antiserum to a second IgD myeloma protein. The IgD standard and normal sera yielded parallel inhibition curves in the RIA and inhibition was produced by IgD and not by any of the other immunoglobulins. The assay had a lower limit of sensitivity of 0.01 International Unit (I.U.)/ml and modifications increased the sensitivity to 0.0008 I.U./ml. Measurable IgD levels were found in all 112 normal adult sera assayed (geometric mean 13.0 I.U./ml, arithmetic mean 30.1 I.U./ml, median 14.8 I.U./ml, range 0.10 to 202 I.U./ml, 95% of values between 0.19 and 156 I.U./ml. The distribution of IgD in the 112 normal sera appeared trimodal with modes at approximately 0.25 I.U./ml, 5 I.U./ml, and 35 I.U./ml. IgD was measurable in nasal and bronchial washes and human milk, but could not be detected in parotid fluid.

The purpose of this investigation was to study the incidence and location of systemic arterial occlusion and pulmonary embolism in a consecutive series of cases of fatal acute myocardial infarction. Another consecutive series of cases in which healed myocardial infarction was demonstrated at necropsy was similarly studied. In none of the cases included in this study had anticoagulant therapy been employed. Massive pulmonary embolism was the most frequent fatal thrombo-embolic complication found among the cases of acute myocardial infarction. Cerebral infarction was the most frequent fatal thrombo-embolic complication found among the cases of healed myocardial infarction. Cerebral infarction was the most frequent fatal systemic arterial thrombo-embolic lesion in both groups. Acute splenic and renal infarcts were frequently demonstrated but with one exception appeared to play an incidental role in the clinical course of the patients. Although systemic arterial occlusion was frequently found in association with intracardiac mural thrombi, there were many other cases in which evidence of systemic arterial occlusion was found in the absence of intracardiac mural thrombi. A positive correlation existed between the presence of pulmonary and systemic arterial occlusion and the occurrence of congestive cardiac failure.

This is a study of the location and incidence of intracardiac thrombi in acute and in healed myocardial infarction. In myocardial infarction intracardiac thrombi occur predominantly in the left ventricle. Anterior myocardial infarcts are more commonly associated with mural thrombi than posterior myocardial infarcts. Large myocardial infarcts and congestive failure are factors which predispose to the formation of left ventricular mural thrombi in myocardial infarction.