Sum of two vectors having an included angle greater than ninety degrees.

If the angle between two vectors is acute an increase in either vector will increase the resultant. If the angle is obtuse, however, an increase in one vector may either decrease or increase the resultant. A mathematical derivation and a simple geometric construction are presented. The theory is applied to vectors in the horizontal plane in right ventricular hypertrophy. It is shown that as the right ventricular vector is increased from a small value, the resultant vector may first decrease and then increase again with a continuous clockwise rotation.     

Changes in the microvasculature with age

The microvasculature of various organs of the rat and of the mesentery of the cat were examined for histochemical changes as a function of age, using the periodic acid-Schiff (PAS) reaction. Arterioles, minute arteries, and nonmuscular venules were histochemically unchanged to approximately 17 months of age in the rat and 8 years in the cat. Subsequently, focal areas of PAS-positive material developed in the media of arterioles and small arteries and increased in extent and severity with age. The adventitia of nonmuscular venules normally stains slightly positive due to the mucopolysaccharide coating of collagen fibers. With age this adventitial layer becomes more intensely PAS-positive. In the 26-month-old rat and 19-year-old cat, the media of arterioles and small arteries were extensively hyalinized. Lesions of arteriosclerosis were not present. These observations, in consort with prior observations of others in various mammals, indicate that there is a regular systematic alteration of various elements of the microcirculation with age. A possible relationship between these anatomical changes and tissue exchange is considered.     

Nodular regenerative hyperplasia of the liver associated with macroglobulinemia: A clue to the pathogenesis

Nodular regenerative hyperplasia of the liver is an infrequent condition characterized by transformation of the hepatic parenchyma into nodules with only mild fibrosis. Little is known about the etiology except that there is usually an underlying chronic disease, such as Felly's syndrome, which antedates the development of clinical liver disease. It is poorly understood how the associated diseases contribute to the pathogenesis of nodular regenerative hyperplasia. Presented are four cases of nodular regenerative hyperplasia in which macroglobulinemia was also present. This new association suggests to us a hypothesis for the pathogenesis of nodular regenerative hyperplasia.

Histologic examination of the livers in these and other cases of nodular regenerative hyperplasia reveals widespread obliteration of the small portal veins. Postmortem angiography of one liver in the present series demonstrated that the nodules were well perfused and that the atrophic areas were poorly perfused with portal blood. This supports the view that atrophy of lobules results from a lack of portal blood supply and that nodules develop from lobules well supplied with portal blood. In each of the clinical conditions associated with nodular regenerative hyperplasia, including macroglobulinemia, inflammatory or thrombotic vascular lesions are found in many organs. Therefore, nodular regenerative hyperplasia may be the hepatic expression of a more widespread vascular disease.     

Prevalence of sleep apnea syndrome among patients with essential hypertension

The purpose of this study was to investigate the prevalence of sleep apnea syndrome (SAS) among patients with essential hypertension. Sixteen of 50 patients with essential hypertension were suspected of having SAS based on their responses to a sleep questionnaire. Whole-night polysomnographic recordings revealed that 11 of the 16 patients, which is 22% of the initial sample, had SAS as defined by the occurrence of at least 10 apneas lasting 10 seconds each per hour of polygraphically defined sleep. The preponderant finding of SAS in this group indicates that the possibility of the syndrome should be taken into consideration in the clinical evaluation of these patients.     

T cell subsets and cellular immunity in end-stage renal disease

The T lymphocyte population was studied by immunofluorescent staining with monoclonal antibodies and laser flow cytometry in the blood of 50 patients with end-stage renal disease undergoing long-term maintenance intermittent hemodialysis. The absolute number of T cells was lower in patients receiving dialysis for more than one year (p less than 0.001), as was the absolute count of helper T cells (p less than 0.005). In patients under 30 years of age, the absolute number of helper T cells was markedly reduced, whereas the number of suppressor/cytotoxic T lymphocytes was not changed. In patients between the ages of 30 and 60 years, both helper and suppressor cells were significantly reduced. In patients over 60 years of age, only the number of helper T cells was reduced. The in vitro response of patients' lymphocytes was reduced both in the mixed lymphocyte reaction (p less than 0.01) and after phytohemagglutinin stimulation (p less than 0.001). Natural killer cytotoxicity of patients' peripheral blood mononuclear cells, however, was unaffected.     

Uremic pulmonary edema

Pulmonary edema fluid analyses and hemodynamic evaluations were performed in two uremic patients with acute pulmonary edema. The colloid osmotic pressure of the pulmonary edema fluid ranged from 57 per cent to 93 per cent that of the serum. Although cardiac function was normal in both patients, the serum colloid osmotic pressure--pulmonary artery wedge pressure gradients were markedly reduced. Uremic pulmonary edema is the result of alterations of pulmonary intravascular Starling forces and increases in pulmonary capillary membrane permeability, allowing for the efflux of protein-rich fluid from the capillaries into the lung.     

Follow-up catheterization of patients with myocardial infarction during coronary artery bypass surgery.

Of 197 consecutive patients having aortocoronary bypass grafts over a 30 month period, 38 (19 per cent) had ECG evidence of myocardial infarction. The infarctions occurred more commonly in patients receiving multiple grafts. The infarctions were usually in areas supplied by grafted vessels. The infarctions occurred most often in the inferior wall, even when multiple vessels were grafted. Eleven patients with intraoperative infarction have had repeat postoperative coronary arteriograms. Seven had all grafts patent; three of these patients had hypokinesis of the infarcted wall. Four of the 11 patients had one or more occluded grafts; three of these patients had an area of hypokinesis. We conclude that intraoperative myocardial infarction is a common problem in aortocoronary bypass surgery and is not necessarily caused by graft occlusion.     

Immunoglobulin and autoantibody response in acute and chronic liver disease

Serum immunoglobulin and nonorgan-specific autoimmune responses (autoantibody response) were studied in 269 patients with a variety of acute and chronic liver disease. A majority of patients with hepatitis B antigen (HB Ag)-positive and HB Agnegative acute viral hepatitis showed a mild elevation in total globulin, gamma globulin, immunoglobulin G (IgG) levels and a moderate elevation in immunoglobulin M (IgM) levels during the first 2 weeks of illness; these levels began to subside by the 8th week of illness and were completely normal by the 12th week, concomitant with the return of normal transaminase values. Serum complement (C₃) levels were low in 20 per cent of the patients with acute viral hepatitis, during the first 2 weeks of illness and returned to normal thereafter. Of the 80 patients with acute viral hepatitis, 42.5 per cent had smooth muscle antibody (SMA), 20.5 per cent had mitochondrial antibody (MA), 10 per cent had rheumatoid factor (RA), and none had antinuclear antibody (ANA); these nonorgan-specific autoimmune markers were only transiently present (mean, 2 weeks) and became undetectable as the patient's condition improved. There was no difference in these immunologic responses between patients with HB Ag-positive and HB Ag-negative acute viral hepatitis. High levels of gamma globulin and IgG were seen in chronic active liver disease, either of viral or alcoholic etiology. Serum immunoglobulin A (IgA) levels were elevated only in those with alcoholic liver disease, whereas IgM levels were high in those with liver disease associated with an active hepatocellular damage either of alcoholic or viral etiology. HB Ag-positive blood donors with asymptomatic mild liver disease had normal immunochemistry values.     

Anaplastic plasma cell myeloma and immunoblastic lymphoma. Clinical, pathologic, and immunologic comparison

To test whether highly anaplastic myeloma and immunoblastic lymphoma are truly identical disease processes, simultaneous series were compared in respect to cytomorphologic features, immunoglobulin content or secretion, clinical and laboratory findings, and patient survival. Although the series partially overlapped in each studied feature, different trends served to distinguish them. Of the 14 patients with myeloma, all were dead at two years, whereas six of the 22 patients with lymphoma were disease-free at 35 to 78 months. Only 50 percent of patients with myeloma received intensive chemotherapy, whereas all 19 patients with stage III or IV lymphoma received such therapy. Myelomas secreted predominantly IgA heavy chain rather than IgG and lambda light chain rather than kappa. Lymphomas contained predominantly IgM rather than IgG and kappa rather than lambda. There were no IgM myelomas and no IgA lymphomas. The shorter survival of patients with the extremely anaplastic form of myeloma, as compared with patients who had immunoblastic lymphoma, may relate, in part, to prior therapy for previous lower grade myeloma; however, intrinsic differences in the nature of these two disease processes are reflected in their disparate immunologic characteristics.     

Arthropathy,hypouricemia and normal serum iron studies in hereditary hemochromatosis

A patient manifesting the arthropathy of hemochromatosis without abnormal serum iron studies is described. Hemochromatosis was confirmed by liver biopsy. This case serves to emphasize the diagnostic value of the characteristic arthropathy of hemochromatosis. Our observations in this patient support the hypothesis that the pathogenesis of hereditary hemochromatosis differs from that of acquired iron overload states. The concurrent presence of hypouricemia is explored in this patient and in 18 other patients with hereditary hemochromatosis. Men with hereditary hemochromatosis were found to have lower serum uric acid levels than expected. In our patient, a renal defect in tubular reabsorption of uric acid appears responsible for hypouricemia.The apparent association of hemochromatosis and hypouricemia deserves further investigation.