Arnold L. Brown

Significance of calcification of the coronary arteries

Abstract The frequency of and association between calcification and occlusive disease of the coronary arteries were determined by roentgenographic and pathologic study of 200 human hearts obtained at autopsy of persons more than 30 years old. Calcification was present in 69 percent of the hearts, most frequently in the left anterior descending branch in men, and it occurred more frequently than significant narrowing, regardless of age, sex or presence of cardiac disease. The greater the degree of calcification, the more likely was the presence of significant narrowing. Absence of calcification indicated persons least likely to have significant narrowing. The presence of myocardial infarction associated with coronary artery calcification but without complete occlusion suggests that the advanced sclerosis of these vessels made them relatively insufficient to meet the needs of the myocardium.

Pathologic changes in aortocoronary saphenous vein grafts

Abstract Aortocoronary saphenous vein grafts from 40 patients (total 62 grafts) were studied at autopsy. The earliest change seen was the insudation of blood constituents into the vein intima. Occluding thrombi were seen in six grafts from short-term survivors, and one organized thrombus was seen in a graft from a long-term survivor (28 months). Various degrees of intimai thickening were seen in grafts from all patients surviving for more than a month; this had progressed to diffuse occlusion in three cases. Gross and microscopic findings correlated well with postmortem angiographic findings in the long-term survivors. Electron microscopic examination showed smooth muscle cells, collagen fibers and ground substance in the thickened intima. Fibroblasts were not a feature of this thickening. Increased permeability of the graft endothelium, due to injury or hemodynamic factors, may result in exposure of medial smooth muscle cells to certain plasma factors and thus promote smooth muscle cell hyperplasia as has been produced in certain experimental models.

Ultrastructure of the myeloma cell

An evaluation of the ultrastructure of the myeloma cell in 19 cases confirms its marked pleomorphism. It ranges from a cell indistinguishable from the normal plasmacyte or its precursors to a cell with clearly abnormal configuration. Abnormal features included abnormalities in size and shape of the cell, nucleus, nucleolus and mitochondria; nucleocytoplasmic asynchronism; disorganization, atypical location and hypertrophy of the Golgi apparatus; and the presence of multiple centrioles. Six types of arrangement of the endoplasmic reticulum were differentiated. In certain cases there were cells with seemingly intermediate features between the lymphocyte or the reticulum cell and the plasma‐myeloma cell. Intranuclear and different types of cytoplasmic dense (osmiophilic) bodies were observed. These bodies likely represent condensed protein and some may be lysosomes. Some morphologic features suggest that the Golgi apparatus plays a role in the condensing process. The myeloma cell releases its secretion mainly by clasmatosis or cytoplasmic fragmentation.

Myofibrillar Adenosine Triphosphatase Activity of Human Heart Tissue in Congestive Failure: Effects of Ouabain and Calcium

Ouabain had no effect on myofibrillar adenosine triphosphatase (ATPase) activity in normal, hypertrophic, and failing hearts with concentrations of calcium chloride varying from 0 to 5.0 mM. The quantitative effects of CaCl2 on myofibrillar ATPase were the same in all groups studied. At necropsy it was found that myofibrillar ATPase activity of heart tissue from patients with clinical and pathologic diagnoses of failure from left ventricular volume and pressure overload was significantly lower than that of normal controls. The ATPase activity in patients with failure due to right ventricular volume and pressure overload was not significantly lower than that in normal controls. There was no difference in myofibrillar ATPase activity between normal left and normal right and between failing left and failing right ventricles. The difference demonstrated at necropsy between normal and failing hearts was not a function of age or of hypertrophy per se. Myofibrillar ATPase activity of hypertrophic nonfailing surgical pulmonary infundibular tissue was the same as that of normal postmortem ventricles. The ATPase activity of failing surgical papillary muscle in a small number of experiments was in the range of that found in failing postmortem ventricles.

Anomalous origin of coronary artery from pulmonary artery masquerading as mitral insufficiency.

Abstract An adolescent boy with the presenting problem of gross mitral insufficiency was found to have the basic abnormality of a left coronary artery arising from the pulmonary artery. From the physiologic and pathologic data collected, no conclusion could be reached in regard to the direction of blood flow in the anomalous vessel. Gross and extensive myocardial fibrosis was present. The mitral incompetence appeared to be related primarily to the enlargement of the left ventricle and the mitral annulus.

Peri-infarction block: Postmyocardial-infarction intraventricular conduction disturbance

Abstract The cardiac pathology is reported in 21 adult patients in whom the angle between the mean initial and mean terminal 0.04-second QRS vectors was greater than 110 degrees, but in whom there were no Q waves of 0.04-second duration in the standard limb leads. In only one case was myocardial infarction present. It is suggested, therefore, that the term “periinfarction block” be restricted to the combination of abnormalities of the terminal QRS forces with the initial QRS deformity characteristic of infarction.

A QUANTITATIVE STUDY OF MYOCARDIAL MITOCHONDRIA IN EXPERIMENTAL CARDIAC HYPERTROPHY

In the hypertrophic heart there is a twofold demand for an increase in available energy: to meet the added work load13 that initiated the hypertrophy and to support the increase in protein synthesis that produced the h y p e r t r ~ p h y . ~ . ~ The production of this energy, in the form of adenosine triphosphate, occurs only within the mi toch~ndr ion .~ .~ The present study was undertaken to determine whether an increased demand for energy is reflected in an alteration of the fine structure in the mitochondrion of the myocardial muscle cell. The newborn heart and the adult hypertrophic heart, which represent conditions of accelerated cardiac growth, were used as the experimental models. Methods

Human Cardiac Myosin: Electron Microscopic Observations

Solutions of human cardiac myosin contain macromolecules which were visualized in the electron microscope by the shadow-casting technic. The dominant particle was observed to be rod-shaped, to have a globular expansion at one end, and to have a mean length of about 1500 Å. The molecule of human cardiac myosin was found to be morphologically similar to myosin molecules from canine cardiac muscle and rabbit skeletal muscle.

EFFECTS OF TRIPARANOL ON THE HYPERLIPEMIA OF EXPERIMENTAL NEPHROSIS.

Summary Since triparanol (MER-29) has been shown to arrest synthesis of cholesterol at the desmosterol stage and prevent an increase of serum cholesterol, we investigated whether this drug would decrease hypercholesteremia and hyperlipemia and reveal a relationship between increase of serum cholesterol and decrease of serum proteins in nephrosis. Experimental nephrosis was produced in dogs by intravenous administration of serum from rabbits sensitized to dog kidney (NTS). Triparanol was given orally in doses of 25 mg/kg of body weight per day before, during, and for 2 weeks after administration of NTS. Total serum lipids, serum cholesterol, and serum and urinary proteins were determined before, during, and for several weeks after injection of NTS. Triparanol decreased serum cholesterol markedly and serum lipids slightly, but it had no influence on hypoproteinemia and proteinuria. The histologic changes in the kidneys were the same in the dogs receiving NTS plus triparanol as in the dogs receiving NTS alone, namely endothelial proliferation in glomerular tufts, adhesion of tuft to capsule at several points, focal fibrosis of glomeruli, hyalinization of tufts with periglomerular fibrosis, irregular thickening of basement membrane, and fusion of foot processes. The tubular epithelium showed hydropic degeneration. Triparanol aggravated the course of the disease.