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Biomedical subjects

M Hiroe

Publications and source records attributed to M Hiroe.

At least 73 records · Page 4Linked to original sources
PubMed1997

Proliferation of smooth muscle cells in acute allograft vascular rejection.

OBJECTIVES: To determine whether immune injury during acute cardiac rejection induces phenotypic modulation of arterial smooth muscle cells and lesion formation, we studied the expression of embryonic myosin heavy-chain isoform and degrees of intimal proliferation in aortas and coronary arteries of allografted rabbit hearts. Modulation of phenotype in arterial smooth muscle cells during acute vascular injury is a widely reported phenomenon, and proliferation and migration of medial smooth muscle cells contribute to development of intimal hyperplasia of arteries in response to immune injury. METHODS: Rabbit hearts were heterotopically transplanted to the neck without immunosuppression. Hearts were harvested at 2, 5, 7, and 10 days after transplantation. Proliferation of smooth muscle cells was assessed by bromodeoxyuridine labeling. Staining for immunohistochemical indicators was done with use of monoclonal antibodies that recognize T lymphocytes and all types of smooth muscle cells (SM1), adult type of smooth muscle cells (SM2), and embryonic myosin heavy-chain isoform. Intimal thickening and luminal narrowing were assessed with a computer-assisted video image analysis system. RESULTS: Intimal thickening and luminal narrowing in aortas and coronary arteries gradually increased in a time-dependent manner. The neointima thus formed consisted of proliferating smooth muscle cells positive for both SM1 and embryonic myosin heavy-chain isoform and massive T lymphocyte accumulation. Intimal proliferation was more prominent in aortas and large epicardial coronary arteries than in the intramyocardial small coronary arteries. CONCLUSIONS: These findings suggest that allogeneic immune injury facilitates phenotypic modulation of smooth muscle cells, which may contribute to subsequent transplantation-associated atherosclerosis.

Animals↗
PubMed1997

Longitudinal dissociation in the his bundle: a possible mechanism of two distinct cycle lengths in atrioventricular reentrant tachycardia.

Two wide QRS tachycardias with identical morphology but different cycle lengths (CLs) developed in a 63-year-old man. Electrophysiological study demonstrated inducible atrioventricular reentrant tachycardia (AVRT) due to a concealed left posterior accessory pathway (AP), which was successfully ablated by radiofrequency application. Neither dual AV nodal pathways nor other APs were documented. Splitting of the His-bundle electrogram was shown, and programmed stimulation induced sudden prolongation of intra-hisian conduction time. These results suggest longitudinal dissociation in the His bundle may be responsible for two distinct CLs in AVRT without dual AV nodal physiology.

Bundle of His↗
PubMed1997

Adenosine-sensitive atrial reentrant tachycardia originating from the atrioventricular nodal transitional area.

INTRODUCTION: Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 +/- 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unaffected after successful ablation. CONCLUSION: There may be an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can be ablated without disturbing AV nodal conduction from the right atrial septum.

Adenosine↗
PubMed1997

Radiofrequency catheter ablation of posteroseptal atrioventricular accessory pathways--location-specific electrographic characteristics of successful ablation sites.

The electrographic features of successful sites of radiofrequency catheter ablation were analyzed in 33 cases of posteroseptal accessory pathways and compared with those from 155 cases of free wall accessory pathways. The atrioventricular intervals in the posteroseptal cases were significantly longer than in the free wall cases (posteroseptal vs left and right free wall; 38 vs 33 and 26 msec, respectively; p < 0.05), and the incidences of continuous electrograms (42 vs 63 and 79%; p < 0.01) and PQS-pattern unipolar electrograms (50 vs 76 and 78%; p < 0.05) were significantly lower in the posteroseptal cases. The V-delta intervals in the posteroseptal cases were significantly longer than in the left free wall cases (17 vs 13 msec; p < 0.05), but shorter than in the right free wall cases (17 vs 23 msec; p < 0.05). No statistically significant difference in the incidence of Kent potentials among the 3 groups was observed. In radiofrequency ablation of posteroseptal pathways, the length of the atrioventricular interval and the incidences of continuous electrograms and PQS-pattern unipolar electrograms may be unsatisfactory even at the appropriate target site, but the V-delta interval and Kent potential are good indicators of suitable target sites.

Adolescent↗
PubMed1997

Porphyria cutanea tarda with constrictive pericarditis in a family.

Two cases of familial porphyria cutanea tarda (PCT) with constrictive pericarditis are described. A 50-year-old woman and her 48-year-old younger brother were admitted because of right ventricular heart failure. Constrictive pericarditis was diagnosed by RV pressure waveform and echocardiogram. The patients were diagnosed as PCT based on clinical symptoms, histologic findings and elevated urinary excretion levels of uroporphyrin. Even to this day, over 40% of the etiology of constrictive pericarditis remains unknown. There is a possibility of overlooking porphyria cutanea tarda in constrictive pericarditis patients. This report describes the first documented cases of familial PCT with constrictive pericarditis.

Coproporphyrins↗
PubMed1997

Cardiomyopathy in a case of Crow-Fukase syndrome.

Crow-Fukase syndrome or POEMS syndrome is a variant of plasma cell dyscrasia that is characterized by polyneuropathy, organomegaly, endocrinopathy, the presence of M-protein in serum, and dermatological changes. A 60-year-old man presented with features of Crow-Fukase syndrome, such as the presence of M-protein in serum, dermatological changes, and osteosclerotic changes, but did not have polyneuropathy. To our knowledge, this is the first case of Crow-Fukase syndrome in which the presence of hypertrophic cardiomyopathy has been confirmed by a left endomyocardial biopsy. The findings suggest that hypertrophic cardiomyopathy may be a manifestation of organomegaly in patients with Crow-Fukase syndrome.

Cardiomyopathy, Hypertrophic↗
PubMed1997

A left atrial myxoma complicated with acute myocardial infarction.

A 43-year-old female, admitted because of acute infero-posterior myocardial infarction, showed angiographic findings of 100% occlusion of left circumflex artery. Echocardiographic findings showed inferior hypokinesis, while a large left intraatrial tumor was also observed. The coronary angiography on the 17th hospital day showed complete reperfusion of the culprit lesion without stenosis. On the 21st hospital day, the removal operation of the tumor was performed. Pathological findings showed typical cardiac myxoma, and the etiology of the occlusion at the culprit vessel was presumed to be closely related to the existence of the left atrial tumor.

Adult↗
PubMed1997

Distribution of inducible nitric oxide synthase in ulcerative colitis.

OBJECTIVE: To investigate reports that the biosynthesis of nitric oxide (NO) is increased in the colonic mucosa of patients with active ulcerative colitis (UC), which suggests that serum NOx levels may be an important indicator of UC activity. METHODS: To determine the role of NO within the colon, we purchased polyclonal antibodies against human-inducible NO synthase (iNOS). We then examined the distribution of iNOS-reactive cells in UC colon tissues. RESULTS: In specimens from 12 UC patients, iNOS-positive neutrophils and macrophages were observed at the base of the ulcer but not in distant areas in the active stage. iNOS expression in colon mucosa was virtually absent during the inactive stage of UC and within the colon of patients with non-UC colitis. CONCLUSIONS: We conclude that NO in colonic mucosa may play a potential role in the pathogenesis of UC.

Adult↗
PubMed1997

Calcitonin gene-related peptide (CGRP) and hypertrophy of cardiomyocytes.

We studied whether calcitonin gene-related peptide (CGRP), a neuropeptide secreted from the sensory nervous supply to the myocardium, induces hypertrophy of cardiomyocytes in culture. CGRP increased the cell surface area of neonatal rat cardiomyocytes; the surface area of the cells was almost doubled by treatment with CGRP for 48 h. Furthermore, CGRP up-regulated mRNA expression for skeletal alpha-actin and atrial natriuretic peptides, which are genetic markers for cardiac hypertrophy. These results indicate that CGRP is a potent hypertrophic factor for cardiomyocytes.

Animals↗
PubMed1997

Effect of training program based on anaerobic threshold in the early phase after acute myocardial infarction.

We devised a new physical training program on the basis of anaerobic threshold for rehabilitation in the early phase of acute myocardial infarction. Forty-four patients were divided into two groups, control and training. We measured the left ventricular ejection fraction using nuclear stethoscopy during the treadmill test and calculating radioactive cardiac output. In the training group, anaerobic threshold and exercise time to the anaerobic threshold point were significantly increased, and stroke volume at rest measured by the dye dilution method increased significantly. Radioactive cardiac output during exercise also increased after the exercise therapy. These results indicate that the rehabilitation program consisting of physical training based on the anaerobic threshold is effective.

Adult↗
PubMed1996

Relation between oxygen uptake and carbon dioxide output during constant work rate exercise in patients with mild congestive heart failure.

The gas exchange (anaerobic) threshold, a useful index of exercise capacity, is determined as the oxygen uptake (VO2) value at which the ratio of the increase in carbon dioxide output (VCO2) to the increase in VO2 becomes > 1 during incremental exercise (V-slope method). However, this method has not been applied to the constant work rate exercise. We evaluated whether a similar threshold phenomenon (i.e., the gas exchange threshold) could be detected during exercise performed at a constant work rate. Thirty-seven patients with a variety of cardiovascular diseases and 27 normal subjects performed symptom-limited incremental exercise and 6 minutes of 50 W constant work rate exercise. The gas exchange threshold could be determined during both symptom-limited incremental exercise (GETi) and constant work rate exercise (GETc) in all subjects, except for 3 normal subjects, by using the V-slope method. There was a significant correlation between GETc and GETi (r=0.80, p<0.0001). GETc was significantly correlated with peak VO2 obtained during the incremental exercise test (r=0.69, p<0.0001). The results suggest that the gas exchange threshold during constant work rate exercise, which does not require the subject's maximal effort, is a useful measure of exercise capacity in patients with cardiovascular disease.

Adult↗
PubMed1996

Heparin and heparan sulfate block angiotensin II-induced hypertrophy in cultured neonatal rat cardiomyocytes. A possible role of intrinsic heparin-like molecules in regulation of cardiomyocyte hypertrophy.

BACKGROUND: Heparan sulfate, one of the primary components of extracellular matrix, is a potent antigrowth factor in certain types of cells. To elucidate a possible role of endogenous heparin-like molecules in regulating cardiomyocyte hypertrophy, we investigated the effects of heparin and heparan sulfate on angiotensin (Ang) II-induced hypertrophy in cultured neonatal rat cardiomyocytes. METHODS AND RESULTS: Competitive [3H]heparin binding assay showed that cardiomyocytes had specific binding sites for heparin. In situ [3H]heparin binding assay demonstrated that heparin, which rapidly bound to the cardiomyocyte surface, was subsequently accumulated around the nuclei, suggesting that heparin might work in the nucleus. Cotreatment with heparin (20 micrograms/mL) completely inhibited increased cell surface area by Ang II (10(-6) mol/L). Increased [3H]leucine incorporation by Ang II was reduced by heparin dose-dependently. The inhibitory effect of heparin on Ang II-induced cardiomyocyte hypertrophy also was confirmed by Northern blot analysis: heparin dose-dependently inhibited skeletal alpha-actin and atrial natriuretic peptide gene expression, genetic markers for cardiomyocyte hypertrophy. Heparan sulfate showed similar inhibitory effects on cell surface area, [3H]leucine incorporation, and skeletal alpha-actin gene expression. Treatment with heparinase I or III, which specifically digests the disaccharide chains of endogenous heparin-like molecules, upregulated protein synthesis and skeletal alpha-actin and atrial natriuretic peptide gene expression in cardiomyocytes. CONCLUSIONS: Our findings in this study strongly suggest that heparin and heparan sulfate are potent inhibitors of cardiomyocyte hypertrophy and that endogenous heparin-like substances negatively regulate cardiomyocyte hypertrophy.

Angiotensin II↗
PubMed1996

Endothelin-3 induces hypertrophy of cardiomyocytes by the endogenous endothelin-1-mediated mechanism.

We have recently reported that endothelin-1 (ET-1) mediates angiotensin II-induced hypertrophy of cardiomyocytes as an autocrine/paracrine factor. In the present study, we examined whether endothelin-3 (ET-3) induces hypertrophy of cultured neonatal rat cardiomyocytes and whether endogenous ET-1 mediates this effect. ET-3 (10(-7) M) increased the cell surface area of cardiomyocytes after 48 h. ET-3 dose dependently (10(-9)-10(-7) M) stimulated protein synthesis as evaluated by [3H]leucine incorporation; the maximum response was 1.4-fold increase over the control at 10(-7) M. Since the response of cardiac hypertrophy is characterized by enhanced expression of fetal isoforms of muscle specific genes, the effect of ET-3 on steady state levels of mRNA for skeletal alpha-actin was evaluated by Northern blot analysis. ET-3 (10(-9)-10(-7) M) increased mRNA level for skeletal alpha-actin with a maximum response after 6 h. ET-3-induced [3H]leucine incorporation, skeletal alpha-actin mRNA and cell surface area were inhibited by a synthetic ETB receptor antagonist (BQ788). Interestingly, ET-3-induced skeletal alpha-actin gene expression and [3H]leucine incorporation were inhibited by a synthetic ETA receptor antagonist (BQ123) as well as by antisense oligonucleotides against peproET-1 mRNA. ET-3 (10(-7) M) transiently increased mRNA levels for ET-1 peaking at 30 min and stimulated the release of immunoreactive ET-1 from cardiomyocytes. These results suggest that endogenous ET-1 locally generated and secreted by cardiomyocytes may contribute to ET-3-induced cardiac hypertrophy as an autocrine/paracrine factor.

Actins↗
PubMed1996

Mild hypoxia induces hypertrophy of cultured neonatal rat cardiomyocytes: a possible endogenous endothelin-1-mediated mechanism.

Hypoxic or ischemic stresses on cardiomyocytes may cause a variety of compensatory responses including cell hypertrophy. In this study, we examined whether hypoxia induces hypertrophy of cardiomyocytes in vitro and whether hypoxia-induced hypertrophy is inhibited by an endothelin A receptor antagonist (BQ123). Neonatal rat cardiomyocytes were cultured in 10% O2/85% N2/5% CO2 or 95% N2/5% CO2 to produce a mild or severe hypoxic condition, respectively. Cardiomyocytes exposed to severe hypoxia revealed degenerative morphological changes and a decrease of cell number, suggesting the toxicity of severe hypoxia on cardiomyocytes. In contrast, cardiomyocytes with mild hypoxia developed hypertrophy; cell surface area of cardiomyocytes as evaluated by an image analyser system increased by 1.6-fold over control after 48 h. [3H]leucine incorporation into the cells was significantly increased by mild hypoxia but decreased by severe hypoxia, mRNA level of skeletal alpha-actin, a genetic marker of cardiac hypertrophy, up-regulated after 6-24 h by mild hypoxia. A transient increase of preproET-1 mRNA and a time-dependent increase of ET-1 protein in the culture medium were also observed in cardiomyocytes exposed to mild hypoxia. BQ123 partially inhibited either hypoxia-induced [3H]leucine incorporation or skeletal alpha-actin mRNA in a dose-dependent manner. These data suggest that mild hypoxia induces hypertrophy of cardiomyocytes and that activation of endogenous ET-1 may, at least in part, mediate this hypertrophic responses as an autocrine/ paracrine factor.

Actins↗
PubMed1996

Cardiac sarcoidosis: diagnostic, prognostic, and therapeutic considerations.

Cardiac involvement in patients with sarcoidosis is an important consideration for those who are concerned with this strange disease. Sarcoidosis is not an acute malignant disease but may be noticed at the time of sudden, expected death as fatal myocardial sarcoidosis at autopsy. Even with modern advances in our ability to diagnose heart disease, cardiac sarcoidosis is still often overlooked because of its subclinical disease progression. In view of this, an extensive review of previously published literature and of our own case analyses has been carried out because of the authors' long-term experience with performing Konno's endomyocardial biopsy, which was originally developed in 1962 at the author's institution. However, the sensitivity of endomyocardial biopsy in detecting sarcoid granuloma is low (20-30%), and, instead, various kinds of nongranulomatous pathologies are often seen. During the course of our research it was found that there might exist a racial difference in cardiac sarcoidosis. Cardiac death was much more frequent in Japanese patients. The possibility that heart disease in sarcoidosis is caused by cor pulmonale due to advanced pulmonary fibrosis should be reevaluated because only a limited amount of background data is available. The author's review clarified the fact that cardiac sarcoidosis is caused by myocardial or pericardial involvement, resulting in various kinds of bradyarrhythmias or tachyarrhythmias and/or congestive heart failure. Electrocardiographic (ECG) and Holter monitor readings provide a simple and effective method for early detection of this disease. The incidence of ECG abnormalities in a total of 963 sarcoidosis patients was 22.1%, which was more frequent than that of the sex- and age-matched healthy control subjects (17.9%; p < 0.025). Echocardiography and radionuclide studies also provide useful clinical information. Careful follow-up and early corticosteroid administration followed by small maintenance doses may prevent the progression of the disease and improve prognosis. Owing to the progress in antiarrhythmic drugs and pacemaker implantation, the primary cause of death in cardiac sarcoidosis has changed from sudden death (1976 report) to congestive heart failure (1985 report).

Adrenal Cortex Hormones↗
PubMed1996

Apolipoprotein(a) and pentanucleotide repeat polymorphisms are associated with the degree of atherosclerosis in coronary heart disease.

To evaluate whether a high level of lipoprotein(a) (Lp(a)) is a risk for the development of coronary heart disease (CHD), 94 Japanese patients and 64 age-matched Japanese controls, diagnosed after coronary angiography (CAG), were analyzed with special reference to the relations between the degree of atherosclerosis, Lp(a) levels and the apolipoprotein(a) (apo(a)) genotypes. the degree of atherosclerosis was evaluated based on CAG findings in the following three ways: the number of diseased vessels, the Gensini score, and the presence or absence of vascular ulcers and/or irregular outlines of coronary stenotic lesions. Apo(a) protein sizes and the pentanucleotide (TTTTA) repeat polymorphism in the 5' control region of the apo(a) gene were analyzed. Multivariate predictors for the number of diseased vessels were, in decreased order of significance, plasma Lp(a) levels, history of smoking, hypertension, diabetes mellitus, and body mass index (BMI). Independent factors associated with the Gensini score were Lp(a) levels, BMI, hypertension, and diabetes mellitus. A negative association of Lp(a) levels with apo(a) protein sizes, and higher Lp(a) levels in those homozygous for an allele with 8 8 (TTTTA)-repeats, was found in both the controls and patients. In decreasing order of significance, apo(a) protein sizes, the degree of atherosclerosis, the genotype of the pentanucleotide repeat, and gender were independent predictors of Lp(a) levels in stepwise regression models. Apo(a) protein sizes were a significant predictor, and the genotype homozygous for the 8 (TTTTA)-repeats was a possible predictor, for the degree of atherosclerosis in CHD. These findings support the notion that a high Lp(a) level is a risk for the development of atherosclerosis in CHD.

Alleles↗
PubMed1996

Does appropriate endurance exercise training improve cardiac function in patients with prior myocardial infarction?

OBJECTIVE: The objective of the present study was to determine whether appropriate endurance exercise training improves cardiac function in patients with prior myocardial infarction. METHODS: Twenty-nine patients with prior myocardial infarction were divided into three groups (Group 1: control, Group 2: low-intensity training, Group 3: high-intensity training). Low and high training intensities were determined according to the gas exchange threshold of each patient. The patients in Groups 2 and 3 performed 15 min of home-based physical training safely, twice a day, 5 days a week for 2 months. Prior to and following this training, each patient performed two constant work rate tests (moderate and heavy intensity) and a symptom-limited incremental exercise test. RESULTS: Heart rates at rest and during exercise were decreased significantly after 2 months in all three groups. Stroke volume at rest increased significantly after 2 months only in Group 3. Stroke volume after 6 min of heavy-intensity exercise increased significantly in Groups 2 and 3. However, the ejection fraction at 6 min of heavy-intensity exercise increased significantly only in Group 3. The maximal work rate attained during incremental exercise testing increased significantly in Groups 2 and 3. This parameter did not significantly change in the control group. CONCLUSIONS: Effects of physical training on maximal exercise capacity were noted in both exercise training groups. However, improvement in cardiac function (such as stroke volume), both at rest and during exercise, was noted only in the high-intensity training group. Our results suggest that relatively high-intensity training may improve exercise capacity and cardiac function of patients with prior myocardial infarction.

Adult↗