The relationship of abnormal regional myocardial performance to left ventricular (LV) function 2-12 months following transmural myocardial infarction was investigated in 25 patients by quantitative biplane angiocardiography. Abnormally contracting segments (ACS) (akinetic or dyskinetic) of the LV were identified in 24 patients. Their sites correlated with the electrocardiographic locations of infarction. ACS were expressed as a percentage (ACS%) of the end-diastolic ventricular circumference, and the percentages obtained correlated with ejection fraction (EF) (r = —0.838, P = 0.0001) using a quadratic regression equation. The group of patients (N = 8) with heart failure (paroxysmal nocturnal dyspnea and/or ventricular gallop sound) demonstrated a significantly lower mean value for EF ( P = 0.0003) and a significantly larger mean value for ACS% ( P = 0.0041) than the group of patients (N = 16) without heart failure. EF sharply separated the two groups. ACS% was a poor separator because in the majority of patients in both groups it was between 14 and 38%. Since EF sharply separated the heart failure and non-heart failure groups but ACS% did not, a theoretic model was developed to assess the contribution of the remaining myocardium to LV function. The curve described by the model did not differ significantly from the curve derived from the quadratic regression equation. Data from heart failure and non-heart failure patients were generally separated by a point (EF = 0.30, ACS = 23%) on the theoretic curve. Abnormal function of the nonakinetic myocardium was considered to be present when observed EF was lower than predicted EF for the observed ACS%. Thus, within the year following transmural myocardial infarction, the relative size of an abnormally contracting region of the ventricle was quantitatively related to impairment of LV function. The spherical model not only provided a framework for relating the clinical status of a patient to both ventricular function and size of the ACS, but also offered a means of estimating the function of the myocardium that appeared angiographically to be nonakinetic.

In plasma, thyroxine is avidly bound to specific proteins present in low concentration, particularly the so-called thyroxine-binding globulin (TBG) and thyroxine-binding pre-albumin (TBPA) (1-4). Several observations indicate that such protein-hormone interactions are of physiological importance. In vitro, the ability of cellular systems to accumulate thyroxine from suspending media is conditioned by the thyroxine-binding potency of the proteins within the media (5, 6). In addition, the volume of distribution and rate of turnover of thyroxine in vivo resemble those of certain plasma proteins (7, 8)'. Finally, abnormal thyroxine-binding by TBG and TBPA has been observed in a variety of states in which the peripheral metabolism of thyroid hormone is disturbed (9-12). It therefore seemed possible that interactions with plasma proteins might in part regulate the peripheral utilization and degradation of thyroxine.An ideal test of this hypothesis would be provided by studies of hormonal metabolism performed before and during the administration of large quantities of purified binding protein. However, adequate quantities of these materials are not yet available. Therefore, it. has been necessary to assess the effects of alterations in thyroxinebinding induced by pharmacological means. Large

A group of 13 normal subjects were evaluated for their extrathyroidal thyroxine distribution. The method employed the measurement of the acute plasma disappearance of a thyroxine-'311 tracer and its concomitant uptake into the liver and forearm. The analysis of these prameters allowed the theoretical construction of a four compartmental mathematical model system comprised of the plasma, extracellular fluid, hepatic, and extrahepatic thyroxine pools. The results of this analysis revealed that the exchange of thyroxine from the plasma into the hepatic and extrahepatic cellular fluid spaces appeared, in general, to be rapid, while the uptake into the extrahepatic tissues was relatively slow. The calculated distribution of thyroxine at equilibrium was estimated to be 14%o in liver, 34%o in extrahe'atic tissues, and 26%o each in the plasma and extracellular fluid pools in this group of normal subjects.

No abstract