[Ischemic heart disease in the elderly].
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Biomedical subjects
Publications and source records attributed to S Furuta.
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A case of thyroid cancer causing right ventricular outflow tract obstruction is described. A 72-year-old woman was admitted because of shortness of breath, some ecchymoses, and marked anasarca. Her liver was palpable four fingerbreadths below her costal margin. Laboratory findings included leukocytosis, marked thrombocytopenia, and an increase in fibrinogen degradation products due to disseminated intravascular coagulopathy. Two-dimensional echocardiography demonstrated a solid mass in the right ventricle, which protruded into the right atrium and main pulmonary artery. Right ventricular outflow tract obstruction and tricuspid regurgitation were demonstrated by contrast echocardiography. These findings were confirmed by CT scans, RI angiography, and contrast angiography. The mass was partially resected from her right ventricle and her tricuspid valve was replaced successfully, but she died of sepsis three weeks after surgery. At autopsy, undifferentiated thyroid cancer and cardiac metastasis were verified. To date, only eight cases with initial symptoms of congestive heart failure due to right ventricular outflow tract obstruction caused by metastatic intracavitary tumors have been reported. Very rarely have cardiac tumors resulted in disseminated intravascular coagulopathy.
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The sensitivity and specificity of the two-dimensional (2D) echocardiographic criteria for diagnosing ruptured mitral chordae tendineae (RCT) were assessed in 52 cases with non-rheumatic mitral regurgitation undergoing mitral valve prostheses. At surgery, chordal rupture was confirmed in 38 cases (RCT group), but not in 14 cases (non-RCT group). Four presumptive and three definite findings for diagnosing mitral chordal rupture using 2D echo were evaluated. Mitral valve prolapse with incomplete coaptation of the mitral leaflets in the long-axis view was observed in 32 cases in the RCT group and in four cases in the non-RCT group (sensitivity 84%, specificity 80%). In the short-axis view at the level of the mitral orifice, delayed closure of the involved mitral leaflet was observed in four cases in the RCT group but in none of the non-RCT group (sensitivity 11%, specificity 100%), delayed protodiastolic opening of the involved leaflet in 15 cases of the RCT group and in one of the non-RCT group (sensitivity 39%, specificity 92%), and finally, increased excursion of the involved valve in 27 cases of the RCT group and in three cases of the non-RCT group (sensitivity 71%, specificity 79%). The following three echocardiographic findings were regarded as direct evidence of mitral chordal rupture: Fine echoes with abnormally rapid transverse and/or oblique motion around the mitral orifice in the short-axis view were observed in 13 cases of the RCT group (sensitivity 34%, specificity 100%); echoes with abnormal whip-like motion in the long-axis view in 10 cases (sensitivity 26%, specificity 100%).(ABSTRACT TRUNCATED AT 250 WORDS)
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For the studies on the mechanism of induction of peroxisomal beta-oxidation enzymes and biogenesis of the organelle, we have isolated cDNA clones for rat peroxisomal enoyl-CoA: hydratase-3-hydroxyacyl-CoA dehydrogenase bifunctional enzyme. On blotting experiments with liver RNA, the cDNAs hybridized to a 3.0-kilobase RNA which was increased 5-7-fold by the administration of di-(2-ethylhexyl)phthalate to rats. Nucleotide sequencing was carried out for four cloned cDNAs and one obtained by a primer extension method. By overlapping these sequences with each other, we identified 20 nucleotides of 5'-noncoding, 2,166 nucleotides of coding, and 910 nucleotides of 3'-noncoding regions. The deduced amino acid sequence of the enzyme is composed of 722 residues, and the composition agrees with that of the protein data. The sequence was confirmed by the amino acid compositions and sequence analyses of some of the tryptic peptides. The molecular weight of the mature enzyme is calculated to be 78,511 from the predicted amino acid sequence. The enzyme has no terminal peptide extension as a signal for translocation into peroxisomes.
In order to elucidate the functional states of the pancreas in the asymptomatic latent stage of chronic alcoholic pancreatitis, 45 chronic alcoholics with no obvious pancreatic structural abnormalities judged by endoscopic pancreatography were studied by pancreozymin-secretin test. We found three patterns of exocrine pancreatic function in alcoholics with or without cirrhosis: normal secretion (40%), hyposecretion (29%) and hypersecretion (31%). In the hyposecretory group, the amylase output proved to be impaired more frequently. In the hypersecretory group increases were observed in one or more of the following parameters, volume, bicarbonate output and amylase output. However, increase in volume was a fundamental condition in this hypersecretion. This study confirmed that exocrine pancreatic hyposecretion and hypersecretion were almost equally frequent in asymptomatic chronic alcoholics with no obvious pancreatographic abnormalities. These results suggest that ongoing exocrine pancreatic dysfunctions exist in the subclinical stage of chronic alcoholic pancreatitis.
Antibody to hepatitis B core antigen of immunoglobulin A class was determined in the serum of patients infected with hepatitis B virus by a sandwich-type solid-phase radioimmunoassay with monoclonal antibodies. The antibody, as defined by a sample to normal ratio greater than 2.1, was detected in all of 39 patients with acute hepatitis, with titers varying widely depending on the time of blood sampling. In persons with persistent infection, the antibody was detected in only 2 (4%) of 46 asymptomatic carriers of the virus, contrasting with the positivity in as many as 15 (41%) of 37 patients with chronic persistent hepatitis, in 45 (94%) of 48 patients with chronic active hepatitis, and in 40 (87%) of 46 patients with liver cirrhosis with or without hepatocellular carcinoma. The mean +/- SE titer of antibody in chronic persistent hepatitis (3.8 +/- 0.9) was significantly lower than those in chronic active hepatitis (13.8 +/- 3.2) and cirrhosis with or without carcinoma (25.6 +/- 6.1) (p less than 0.001). Based on the results obtained, the antibody may reflect hepatic injury in the persistent hepatitis B virus infection.
The contact Nd-YAG laser system with ceramic rods which has been developed by us was applied to animal experiments and clinical practice. It was confirmed that: 1) this method can be performed at low power of 6 to 8 W in contact laser incision of soft tissue and at 3 to 4 W in localized laser hyperthermia; 2) it permits accurate and precise incision because mis-shots of laser irradiation can be eliminated in the target tissue; 3) it causes less bleeding with minimal damage to adjacent tissue; and 4) it has remarkably high controllability. The contact Nd-YAG laser systems are very useful as one of the new modalities for surgical procedures as well as localized laser hyperthermia in head and neck tumors.
Rat hepatocytes were cultured for 72 h with or without the addition of 0.5 mM clofibric acid. The activities of individual enzymes of the peroxisomal beta-oxidation pathway (acyl-CoA oxidase, enoyl-CoA hydratase-3-hydroxyacyl-CoA dehydrogenase bifunctional protein, and 3-ketoacyl-CoA thiolase) decreased in the control culture, but markedly increased synchronously in the clofibric acid-treated culture. The levels of mRNAs coding for these enzymes and the rates of synthesis of the enzymes were also elevated in the clofibric acid-treated culture, although no proportional relationship was observed between the time-dependent changes of these parameters. The increase in mRNAs was much higher than the increase in the rate of synthesis of the enzymes. The activity of catalase, its mRNA level and the rate of its synthesis were slightly affected. The effects of clofibric acid on the peroxisomal beta-oxidation enzymes and catalase in primary cultured hepatocytes were very similar to those observed in vivo. These results, therefore, suggest that primary culture of hepatocytes should provide a useful means for investigating the mechanism of induction of peroxisomal enzymes and the mechanism of action of peroxisome proliferators.
In order to search for some parameters that would make it possible to predict a potentially high risk of evolution from liver cirrhosis to hepatocellular carcinoma (HCC), the DNA content of hepatocytes in patients with liver cirrhosis with or without development to HCC was investigated by means of microspectrophotometry in Feulgen-stained specimens. In patients without development of HCC in more than 5 years of follow-up, 90% or more of tested hepatocytes were diploid, whereas in patients with liver cirrhosis who developed HCC within 3 years the frequency histogram of nuclear DNA content was widely spread from diploid to hyperpolyploid with a small peak of triploid. Furthermore, in the latter group of patients, many of the binucleate cells had different DNA contents in each paired nucleus. In non-cancerous portions of HCC, the ploidy histogram of nuclear DNA content was widely spread from diploid to polyploid with different DNA contents of each paired nucleus in binucleate cells, without the small peak of triploid. These results suggest that the deranged cell kinetics of hepatocytes in cirrhosis may be considered to be a state of potentially high risk for the evolution of HCC, and that a patient with liver cirrhosis with such an abnormal hepatocyte DNA content should be followed up carefully for the early diagnosis of HCC.
Forty-two patients with hepatitis Be antigen (HBeAg)-positive chronic hepatitis were treated by intramuscular injections with OK-432, an immunopotentiator possessing interferon-inducing activity. They were monitored with serial measurements of virological parameters to evaluate therapeutic effectiveness, and compared with a group of seventy-five untreated patients (natural course group). In the group receiving OK-432 therapy, twenty-seven patients (64.3% of the forty-two patients) became negative for HBeAg in an average observation period of 20.1 months. Of these, fourteen patients (33.3% of the forty-two patients) underwent seroconversion from HBeAg to anti-HBe antibody (anti-HBe). In the natural course group, twenty-three patients (30.7% of the seventy-five patients) lost HBeAg reactivity in a mean follow-up period of 32.3 months, and thirteen patients (17.3% of the seventy-five patients) became seroconverted. Thus, the drug group showed significantly higher percentages of patients with disappearance of HBeAg and seroconversion, notwithstanding the shorter duration of the follow-up. Young males and females, females generally, or patients with high serum GPT levels were more likely to respond to the therapy. The serum GPT level tended to stabilize more in patients receiving OK-432.
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Recently, the frequency of nonrheumatic aortic regurgitation (AR) has apparently increased, accompanied by a decrease in frequency of rheumatic fever. The purpose of the present study was to ascertain the echocardiographic features of nonrheumatic AR. We had 24 surgically- or autopsy-proven cases of nonrheumatic AR admitted during a two year period. These were 10 cases of infective endocarditis (IE), five with ventricular septal defect of type I, three with syphilis, and two with prosthetic valve malfunctions, and the remainder five were difficult to diagnose clinically. These five were three men and two women, whose ages ranged from 40 to 67 years and averaged 50 years, and their final diagnoses were annulo-aortic ectasia (AAE), Behcet's disease, and the aortitis syndrome (Takayasu's arteritis), and two other cases were of unknown etiology. The echocardiographic manifestations were compared with the operative, autopsy, and pathological findings. Echocardiographically, there were few or no increased intensities of aortic valvular echoes, and aortic roots had a tendency to dilate, leading to the failure of coaptation of valve leaflets, for a relative lack of valvular surface area to cross-sectional area of the aortic ring. Three of the five had flail aortic valves and three had associated MVP. Three were diagnosed as floppy aortic valves at the time of surgery. Excised valves revealed little hyperplasia or sclerosis grossly. Fibrinoid necrosis or mucoid degeneration were noted by light microscopy. Some specimens of aortic walls also revealed cystic medial necrosis or disruption of elastic fibers. All these findings were based on degenerative processes of connective tissue, and not on inflammatory processes. These pathological findings and the coexistence of mitral valve prolapse (MVP), which were not regarded as coincidental, suggest that connective tissue fragility--congenital or acquired--may play an important role in the genesis of nonrheumatic AR.
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The purpose of the present study was to determine the usefulness of two-dimensional echocardiographic measurements of the surgical aortic ring diameters (ARDs) in predicting correct sizes of the prosthetic valves and in determining the mechanisms of aortic regurgitation. Forty patients with aortic regurgitation who underwent prosthetic valve surgery, and 20 normal controls were selected for the study. The 40 patients consisted of 21 with rheumatic aortic regurgitation (RHD group), and 19 with non-rheumatic non-inflammatory aortic regurgitation (non-RHD group). Aortic regurgitation due to annuloaortic ectasia with or without the stigmata of Marfan's syndrome and bicuspid aortic valves were excluded from the non-RHD group. Echocardiographic estimates of the ARDs proved to be useful for predicting prosthetic valve sizes considering the good correlation between the echocardiographic and direct measurements (r = 0.814), despite a slight tendency to echocardiographic underestimation. The ARDs was 24.7 +/- 3 mm in the RHD group, 28.8 +/- 2.9 mm in the non-RHD group and 21.8 +/- 1.7 mm in the normal controls. The ARDs in the RHD group was significantly larger than that of the normal controls (p less than 0.001), and the ARDs of the non-RHD group was significantly larger than that of the RHD group (p less than 0.001). There were loose correlations between the ARDs and left ventricular end-diastolic dimension, and between the ARDs and left ventricular end-systolic dimension in the RHD group (r = 0.549 and r = 0.455, respectively), but there were no correlations between these two parameters in the non-RHD group. In four patients with aortic regurgitation in the non-RHD group, mitral regurgitation coexisted. Both the ARDs and the mitral ring dimension were markedly increased in these patients. It is concluded that in the non-RHD group, marked dilatation of the ARDs appears to be one of the cause of aortic regurgitation.
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