Biomedical subjects

O Sunagawa

Publications and source records attributed to O Sunagawa.

13 recordsLinked to original sources

PubMed2001

Significant association between the progression of coronary artery calcification and dyslipidemia in patients on chronic hemodialysis.

Quantification of coronary artery calcification (CAC) determined by electron-beam computed tomography (EBCT), known as the CAC score (CACS), correlates with total plaque amount and coronary risk factors and strongly associates with maximal stenosis in the epicardial arteries. However, data are limited concerning the CACS in chronic dialysis patients, although atherosclerotic vascular disease is the most frequent complication. We examined the relation between coronary risk factors, metabolic factors of calcium and other minerals, and CACS progression in 24 dialysis patients. The mean patient age was 53 +/- 14 (SD) years, and mean duration of dialysis was 64 +/- 69 months. In each patient, the CACS was measured twice, with a mean interscan period of 17 +/- 3 months. The mean CACS progressed from 449 +/- 605 to 669 +/- 894 overall, and the mean change in CACS (DeltaCACS) was 220 +/- 78. Patients were divided into two groups: slow progressors, with DeltaCACS of 7.5 +/- 31 (n = 12), and rapid progressors, with DeltaCACS of 432 +/- 458 (n = 12). Triglyceride concentrations (198 +/- 65 versus 103 +/- 50 mg/dL; P < 0.001) were high, and high-density lipoprotein cholesterol (HDL-C) concentrations (46 +/- 11 versus 60 +/- 18 mg/dL; P < 0.05) were low in rapid progressors. Rapid progression of CAC was associated with high triglyceride and low HDL-C concentrations. The clinical significance of these observations remains to be determined.

Adult↗

PubMed2001

Risk factors for stiffness of the wall of the thoracic aorta in patients with mild atherosis.

Previous studies have suggested that aging is associated with progressive arterial stiffness and widening of the pulse pressure, and pulse pressure has been found to be a risk factor of cardiovascular diseases. However, the effects of age, blood pressure (including pulse pressure) or atherogenic factors on thoracic aortic wall stiffness in patients with mild atherosis are unclear, so the present study used transesophageal echocardiography to examine 103 consecutive patients with various cardiovascular diseases. The extent of atherosis was evaluated in terms of intima-medial thickness (IMT), and 2 indices of wall stiffness in the aorta were calculated: elastic modulus and stiffness parameter (beta). In subjects with mild atherosis (IMT <1.0mm), age, body mass index, systolic blood pressure, pulse pressure, triglyceride level, and hypertension were factors significantly associated with high wall stiffness, and multiple logistic stepwise analysis revealed that age, pulse pressure, and triglyceride level were particularly significant.

Adult↗

PubMed2001

Arrhythmogenic right ventricular dysplasia presenting as regression of left ventricular dysfunction: a case report.

Arrhythmogenic right ventricular dysplasia is considered to be a slowly progressive disease in which left ventricular dysfunction and congestive heart failure usually appear at the end stage. The initial clinical presentation of this 56-year-old Japanese woman was left-sided heart failure, and the diagnosis was dilated cardiomyopathy, but her left ventricular size and ejection fraction regressed during 10 years of treatment, whereas her right ventricular parameters showed no change.

Arrhythmogenic Right Ventricular Dysplasia↗

PubMed2001

[Giant-cell myocarditis without a symptom of heart failure seen in a patient with myasthenia gravis and concurrent Hashimoto's disease].

A 69-year-old Japanese woman initially noticed difficulty in squatting in the last two years, followed by nasal voice, fatiguability in mastication, and blepharoptosis. On admission to our hospital, in addition to these neurological findings, we detected ectopic arrhythmia and Levine II systolic murmur at the apex region, without any subjective symptoms. The serum titer of anti-acetylcholine receptor antibody was elevated to 28 nmol/l (normal: < 0.2), and she responded to repetitive nerve stimulation at a frequency of 3 Hz showing 13% waning, she had positive test for edrophonium administration, and was diagnosed as having myasthenia gravis (MG). There was no thymoma by radiographic examination. She also had Hashimoto's disease confirmed by the laboratory findings. Chest X-p revealed dilatation of the heart, and 24-hour Holter ECG revealed non-sustained ventricular tachcardia (VT). Ventriculography revealed prominent dilatation of the left ventricle and diffuse hypokinetic ventricular wall motility. Endomyocardial biopsy revealed muscle fiber degeneration, cellular infiltration, and scattered multinucleated giant cells, confirming a diagnosis of giant cell myocarditis (GCM). Quadriceps muscle biopsy revealed a small number of muscle fibers with giant nuclei, but no giant cells were seen. Immunological study revealed elevation of CD4/CD8 ratio and memory CD4 cells. Antibody to anti-cardiac and anti-striate muscle were strongly positive in the serum. Four months later, she developed dyspnea on effort and hypoxia, accompanied by severe bradycardia leading to sinus arrest. For acute cardiac deterioration, steroid pulse therapy was started followed by oral predonisolone and azathioprine, which aggravated myasthenic symptoms. The patient was ventilated for respiratory hypercapnia. During immunoabsobent therapy, she developed VT which caused a cardiac arrest, leading to fatal outcome. In case of MG, especially overlapped with other autoimmune diseases, evaluation of cardiac function should be conducted to detect GCM.

Aged↗

PubMed2000

Differences between coronary hyperresponsiveness to ergonovine and vasospastic angina.

The objective of the present study was to investigate the differences between coronary hyperresponsiveness without ischemia and vasospastic angina in an ergonovine provocation test using multivariate analysis. We have sometimes experienced a more than 50% narrowing response of vascular diameter without ischemia in a coronary response to ergonovine. We studied 107 patients with less than 50% stenosis in a coronary arteriogram. Their vascular responses to ergonovine were measured and the patients were divided into three groups, as follows: Group 1 had 50% or less vascular narrowing response without ischemia; Group 2 had a vascular hyperresponsiveness of more than 50% narrowing response without ischemia; and Group 3 experienced a hyperresponsiveness with ischemia. The degree of coronary response was found to be related to smoking, inpaired glucose tolerance (IGT) and the Gensini score by multiple regression analysis. A multiple logistic analysis revealed that the Gensini score and smoking were significant predictive factors for Group 3 (odds ratio: 1.20 and 8.97). The only factor different between Group 2 and Group 1 was gender. The coronary hyperresponsiveness to ergonovine without ischemia differs from vasospastic angina in the degree of coronary atherosclerosis and smoking habits. The patients with hyperresponsiveness had similar characteristics to those with atypical chest pain rather than vasospastic angina, except for a gender difference.

Aged↗

PubMed1999

[Apical hypertrophic cardiomyopathy followed by midventricular obstruction and apical aneurysm: a case report].

A 72-year-old man presented with apical hypertrophic cardiomyopathy followed by midventricular obstruction and apical aneurysm. Doppler echocardiography revealed an abnormal blood flow from the apical aneurysm to the left ventricular outflow through the obstructive lesion during diastole. Myocardial perfusion scintigraphy showed no ischemic change in the apex. This case suggests that apical aneurysm may not be caused by ischemia, although previous reports showed ischemic degeneration or fibrosis may be a cause of an apical aneurysm.

Aged↗

PubMed1996

Headache as a manifestation of myocardial infarction.

We report a 64-year-old man who complained of headache without chest pain at the onset of acute myocardial infarction (AMI). He had no history of chest pain or headache. Severe headache in this case was the first symptom of AMI. The headache was reproduced during stress test. During the angioplasty procedure, he also complained of headache without vasospastic change in the coronary artery. These findings suggest that the headache which accompanied AMI or myocardial ischemia in this case was due to referred pain rather than a generalized vasospastic disorder.

Angioplasty, Balloon, Coronary↗

PubMed1996

[Athlete's heart].

Explore the source record for details and available documents.

Cardiomegaly↗

PubMed1995

Alterations of alpha 1-adrenergic receptor densities in right and left ventricles of spontaneously hypertensive rats.

To clarify whether alpha 1-adrenergic receptors contribute to cardiac hypertrophy, we examined alpha 1-adrenergic receptor densities in the right and left ventricles of 5- and 20-week-old spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) using [3H]prazosin. Also, we analyzed a pharmacologically distinct subtype of alpha 1-adrenergic receptors by pretreatment with chloroethylclonidine. The ratio of right ventricular weight to body weight as well as left ventricular weight to body weight was higher in SHR than in WKY at 5 weeks of age. At 20 weeks of age, only the left ventricular weight to body weight ratio was higher in SHR. At 5 weeks of age, the right and left ventricular alpha 1-adrenergic receptor densities in SHR were greater than those in WKY (LV 1760 vs. 1275, RV 2543 vs. 1521 fmol/mg protein). At 20 weeks of age, only right ventricular alpha 1-adrenergic receptor density remained higher in SHR (1425 vs. 885 fmol/mg protein). The percentage of pharmacologically distinct alpha 1A receptor was higher in the right ventricle of SHR than in that of WKY at 5 weeks of age (25% vs. 18%). There were no significant differences in the dissociation constants among the alpha 1-adrenergic receptor assays. These findings suggest that an increase in alpha 1-adrenergic receptors might be involved in cardiac hypertrophy in the early phase of hypertension in SHR.

Adrenergic alpha-Antagonists↗

PubMed1995

Alpha 2-adrenoceptors in brain and kidney during development of hypertension in Dahl-Iwai salt-sensitive rats.

BACKGROUND: Both renal and extrarenal factors have been considered to contribute to the development of hypertension in Dahl salt-sensitive rats, but contents of both factors have not been established precisely. AIM: To clarify the role of those factors in the sympathetic nervous system, we examined the regulation of alpha2-adrenoceptors in the lower brainstem and the renal tubular basolateral membranes simultaneously during the development of salt-induced hypertension in Dahl-Iwai salt-sensitive rats. METHODS: Dahl-Iwai salt-sensitive or resistant rats were fed a high (8.0% NaCl)- or low (0.3%)- salt diet from 4 to 6 or 10 weeks of age. At 4, 6 and 10 weeks of age, the plasma membranes of the lower brainstem and the renal tubular basolateral membranes were obtained simultaneously and alpha 2-adrenoceptors were quantified by a radioligand binding assay using 3H-rauwolscine. RESULTS: In the salt-sensitive rats, systolic blood pressure was significantly higher in those fed a high-salt diet than in those fed a low-salt diet. In the salt-resistant rats, both the high- and the low-salt groups showed similar blood pressure levels. At 6 weeks of age, alpha 2-receptor densities of the salt-sensitive rats fed a high-salt diet were lower in the lower brainstem and higher in the renal basolateral membranes than those fed a low-salt diet. In contrast, in the salt-resistant rats, both the high- and the low-salt groups had similar densities. At 10 weeks of age, the difference between the high- and the low-salt groups in the salt-sensitive rats disappeared in both the brainstem and the renal basolateral membranes. CONCLUSIONS: Alpha 2-adrenoceptor regulation in the brainstem and the renal basolateral membranes differs between Dahl-Iwai salt-sensitive and salt-resistant rats. The modulation of alpha 2-adrenoceptors by a high salt intake may be essential particularly in the early phase of the development of salt-induced hypertension.

Animals↗

PubMed1992

Hypertension in an adult with unilateral renal dysplasia.

We report a 29-year-old Japanese female with severe hypertension and unilateral renal dysplasia, which is rarely found in adults. The involved kidney was surgically removed and then the blood pressure fell to borderline levels without any changes in plasma renin activity or plasma aldosterone concentration. Histological examinations revealed typical renal dysplasia without hyperplasia of the juxtaglomerular apparatus. Unilateral renal dysplasia may be a cause of secondary hypertension in adults, though the mechanisms are still unknown.

Adult↗

PubMed1991

Low-sodium diet and alpha-adrenoceptors of renal basolateral membrane in spontaneously hypertensive rats.

To clarify the effect of dietary sodium restriction on the mechanism regulating sodium and water in the development of hypertension, we determined the number of the alpha-adrenoceptors in renal basolateral membrane in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. The rats had been fed a low-sodium (0.5%) or normal-sodium (0.4%) diet from 3 weeks of age. The experiments were performed at 6, 8 and 20 weeks of age in both rat groups. Renal basolateral membranes were prepared using Percoll and radioligand binding studies were performed using 3H-prazosin and 3H-rauwolscine. Systolic blood pressure in SHR was already elevated at 6 weeks of age compared with that in WKY rats and rose to hypertensive levels at 8 weeks of age. The sodium balance in WKY rats on both diets decreased at 8 weeks of age, but that of SHR decreased at 20 weeks of age. The maximum number (Bmax) for the alpha 1-adrenoceptor did not differ in any groups of the WKY rats or SHR. Bmax for the alpha 2-adrenoceptors increased at 8 weeks of age in the low-sodium SHR compared with normal-sodium SHR, but did not increase in WKY rats. The data show that the increases in blood pressure in the SHR occur prior to significant increases in the alpha 2-adrenoceptor density of renal basolateral membrane, and that the modulation of alpha 2-adrenoceptor density in SHR differs from that in WKY rats under sodium restriction. The results suggest that renal alpha 2-adrenoceptors in SHR could relate the regulatory mechanism to sodium reabsorption under sodium restriction rather than to the primary cause of the development of hypertension in SHR. There may be the possibility of an abnormality in renal alpha 2-adrenoceptor mechanism in SHR.

Animals↗

PubMed1990

[Exercise-induced thallium-201 myocardial perfusion defects in angina pectoris without significant coronary artery stenosis].

We performed exercise thallium-201 myocardial scintigraphy in 32 patients with angina pectoris to study the incidence of perfusion defects, who had no significant organic stenosis on coronary angiography. None of them had myocardial infarction or cardiomyopathy. Thallium-201 myocardial scintigraphy and 12-lead ECG recording were performed during supine bicycle ergometer exercise. Perfusion defects in thallium-201 scintigrams in SPECT images were assessed during visual analysis by two observers. In the coronary angiograms obtained during intravenous infusion of nitroglycerin, the luminal diameter of 75% stenosis or less in the AHA classification was regarded as an insignificant organic stenosis. Myocardial perfusion defects in the thallium-201 scintigrams were detected in eight (25%) of the 32 patients. Six of these eight patients had variant angina documented during spontaneous attacks with ST elevations in standard 12-lead ECGs. Perfusion defects were demonstrated at the inferior or inferoposterior regions in six patients, one of whom had concomitant anteroseptal defect. The defects were not always accompanied by chest pain. All but one patient demonstrating inferior or inferoposterior defects showed ST depression in leads II, III and aVF on their ECGs, corresponding to inferior wall ischemia. The exception was a case with right bundle branch block. Thus, 25% of the patients with angina pectoris, who had no evidence of significant organic stenosis on their coronary angiograms, exhibited exercise-induced perfusion defects in their thallium-201 scintigrams. Coronary spasms might have caused myocardial ischemia in these patients.

Adult↗