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Biomedical subjects

Y Shigematsu

Publications and source records attributed to Y Shigematsu.

At least 109 records · Page 6Linked to original sources
PubMed1995

Relation between postpacing T wave changes and myocardial scintigraphic characteristics in patients with ventricular demand pacemaker.

The aim of this study was to elucidate the cause of T wave changes after ventricular pacing using thallium 201 single photon emission computed tomography (Tl-SPECT). Tl-SPECT was performed in 20 patients with sick sinus syndrome who had negative T wave after ventricular pacing and had had a ventricular demand pacemaker (VVI) implanted. Patients who have stenotic coronary arteries were excluded from the study. From the analysis of Tl-SPECT, extent score was calculated as the ischemic region. Data in patients with SSS were compared with those in 20 normal controls (NC). Thallium perfusion defects in patients with VVI were observed and distributed mainly in apex and inferior regions on the polar map. The extent score in patients with VVI was significantly higher than that in NC (56.4 +/- 21.6% vs 3.2 +/- 6.4%, P < 0.01). The washout rate of thallium 201 in the defect area was significantly lower in patients with VVI than in NC (27.4 +/- 10.2% vs 46.8 +/- 12.3%, P < 0.01). These results suggest that T wave changes after ventricular pacing are closely related to myocardial ischemia.

Aged↗
PubMed1995

Mechanism of atrial fibrillation and increased incidence of thromboembolism in patients with hypertrophic cardiomyopathy.

To elucidate the morphologic characteristics of the left ventricle in patients with hypertrophic cardiomyopathy who developed atrial fibrillation, we studied left ventricular geometry by two-dimensional echocardiography in 92 patients with hypertrophic cardiomyopathy. These patients were divided into two groups; 24 patients with transient or persistent atrial fibrillation (group I) and 68 patients with sinus rhythm (group II). Left ventricular chamber size in group I was significantly smaller than that in group II. Left ventricular chamber size was correlated positively with stroke volume, and was correlated negatively with left ventricular end-diastolic pressure. The incidence of systemic thromboembolism in group I was 7.1% per patient year. In hypertrophic cardiomyopathy, the size of the left ventricle appears to have major pathophysiologic significance in the development of atrial fibrillation. In addition, since patients with hypertrophic cardiomyopathy who develop atrial fibrillation have a potential risk of systemic thromboembolism, prophylactic anticoagulant therapy should be performed in these patients.

Adult↗
PubMed1995

[Influence of aging upon changes in symptoms and cardiac size associated with surgical repair of atrial septal defect in adults].

To elucidate the influence of aging upon the improvement of symptoms and cardiac size associated with surgical repair of atrial septal defect, clinical symptoms, cardiothoracic ratio and hemodynamic variables in older patients (group A; age at operation > or = 50 years old, n = 11) were compared with those in younger patients (group B; age at operation < 50 years old, n = 8). There were no differences in hemodynamic variables, i.e., peak systolic pulmonary pressure, pulmonary to systolic flow ratio (Qp/Qs), pulmonary to systolic vascular resistance ratio (Rp/Rs) and left to right shunt ratio between the two groups. Symptomatic benefits occurred in all patients, although 3 patients in group A who had atrial fibrillation preoperatively still displayed symptoms such as exertional dyspnea. The postoperative (after 3 months) cardiothoracic ratio improved in all patients except for 3 patients in group A who were operated at over 60 years of age. Although there was no significant difference in preoperative cardiothoracic ratio between the two groups, the postoperative cardiothoracic ratio in group B was significantly smaller than that in group A. These results indicate that operative closure of atrial septal defect is recommended for all patients aged 50 years old or older, but early improvement of symptoms and cardiomegaly in older patients is lower than that in younger patients.

Adult↗
PubMed1995

Clinical evidence for an association between left ventricular geometric adaptation and extracardiac target organ damage in essential hypertension.

OBJECTIVES: To elucidate an association between left ventricular geometric adaptation to sustained hypertension and preclinical extracardiac target organ damage in essential hypertension. We also studied the clinical significance of neurohumoral factors for cardiovascular structural changes. DESIGN: One hundred and forty patients with essential hypertension were divided into four subgroups, based on left ventricular mass index and relative wall thickness. With respect to extracardiac target organ damage, we measured the funduscopic grade of retinal changes and serum creatinine levels. RESULTS: Among the hypertensive patients, only 19 (14%) had a typical concentric hypertrophy (increase in left ventricular mass index and relative wall thickness). Hypertensive patients with concentric hypertrophy had the most advanced funduscopic abnormalities and the greatest renal involvement, and hypertensive patients without left ventricular hypertrophy had the least extracardiac target organ damage. Plasma renin activity and plasma aldosterone concentration were higher in hypertensive patients with than in those without concentric hypertrophy. In a multiple regression model there was a strongly significant correlation between the degree of left ventricular mass index and the severity of hypertensive retinopathy and renal involvement, independent of office blood pressure. CONCLUSIONS: These results clearly demonstrate that echocardiographically determined left ventricular mass and geometry stratify extracardiac target organ damage in patients with essential hypertension more closely than office blood pressure. The present study also suggests that, in addition to blood pressure load, the renin-angiotensin-aldosterone system appears to play an important role in myocardial hypertrophy and peripheral vascular damage in hypertension.

Aldosterone↗
PubMed1995

Contractile properties of left ventricular myocytes isolated from spontaneously hypertensive rats: effect of angiotensin II.

OBJECTIVE: This study was undertaken to clarify whether the myocardial dysfunction observed in the hypertensive heart is an intrinsic property of the myocyte or not. MATERIALS AND METHODS: We investigated left ventricular function and contractile function of myocytes from 30-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). We also evaluated the effect of angiotensin II on contractile function of myocytes from both rats. RESULTS: The time constant of isovolumic pressure fall was significantly greater in SHR (13.2 +/- 0.6 ms) than in WKY (10.3 +/- 0.5 ms). The extent of shortening in isolated myocytes was significantly higher in SHR (11.3 +/- 0.4%) than in WKY (9.8 +/- 0.4%, P<0.01). Both the normalized maximal velocity of shortening and the normalized maximal velocity of relengthening were significantly greater in SHR (2.12 +/- 0.08 and 2.10 +/- 0.08 s-1; both P<0.01) than in WKY (1.76 +/- 0.06 and 1.75 +/- 0.07 s-1). Angiotensin II caused significant decreases in the extent of shortening, the normalized maximal velocity of shortening and the normalized maximal velocity of relengthening in isolated myocytes from SHR, but these parameters were unchanged in WKY. CONCLUSIONS: These results suggest that left ventricular diastolic dysfunction in SHR is not due to an intrinsic abnormality of the cardiac myocytes, and that angiotensin II suppresses the function of myocytes from hypertrophied hearts.

Animals↗
PubMed1995

Effect of age on left ventricular geometric patterns in hypertensive patients.

OBJECTIVES: To investigate the effect of age on left ventricular structure and geometry in hypertensive patients, we studied the relationship between age and echocardiographic variables in patients with uncomplicated essential hypertension. PATIENTS AND METHODS: We divided 168 patients with hypertension into three groups according to age: young (<40 years), middle-aged (40-59 years) and an elderly group (> or = 60 years). They were further categorized according to relative wall thickness and the left ventricular mass index. We then evaluated the prevalence of left ventricular geometric patterns in these patients according to age. RESULTS: The left ventricular end-diastolic dimension decreased with age, both in normotensive control subjects and in hypertensive patients. The magnitude of this decrease was similar for both. The relative wall thickness and left ventricular mass index were greater in the hypertensive patients than in the normotensive control subjects, and these increased with age both in the controls and the hypertensives. The differences between normotensives and hypertensives in these variables remained unchanged with age. The prevalence of a normal left ventricle (normal relative wall thickness and left ventricular mass index) in the hypertensive patients decreased with age. Conversely, the prevalence of concentric remodeling (increased relative wall thickness with normal left ventricular mass index) and concentric hypertrophy (increased relative wall thickness and left ventricular mass index) increased with age. CONCLUSIONS: These results demonstrate that age significantly affects left ventricular structure both in normotensive control subjects and in hypertensive patients. Thus, the differences in left ventricular geometric patterns with age may have important implications in assessing left ventricular structure and geometric patterns in hypertensive patients.

Adult↗
PubMed1994

Diffuse leukodystrophy with a large-scale mitochondrial DNA deletion.

An 8-year-old girl with progressive ataxia and bulbar palsy showed diffuse white-matter lesions in the occipital to parietal lobes on magnetic resonance imaging. Since she had slightly elevated lactate in the cerebrospinal fluid, a muscle biopsy was done which revealed scattered ragged-red fibres and focal cytochrome c oxidase deficiency. Southern blot and polymerase-chain-reaction analyses revealed a large-scale mitochondrial DNA deletion, which was 6990 base-pairs in length with 6 base-pair (-TCATCG-) direct repeats at the junctions. Mitochondrial DNA mutation should be considered as one of the candidate causes for diffuse leukodystrophy in children.

Base Sequence↗
PubMed1994

cDNA sequences encoding human fructose 1,6-bisphosphatase from monocytes, liver and kidney: application of monocytes to molecular analysis of human fructose 1,6-bisphosphatase deficiency.

Fructose 1,6-bisphosphatase deficiency is an autosomal recessive inherited disorder of gluconeogenesis. We could isolate cDNAs encoding human fructose 1,6-bisphosphatase from normal monocytes, liver and kidney, but not from normal lymphocytes. The cDNAs contained an open reading frame coding for 338 amino acids, and their nucleotide sequences in monocytes and liver were identical. G644C645 nucleotides in this sequence were the same as those of cDNA from HL-60 cells, although our result differed from a previous report (M. El-Maghrabi et al. (1993) J. Biol. Chem. 268, 9466-9472) on an alteration to C644G645 nucleotides in human liver cDNA resulting in a change of Gly-214 to Ala-214 in the enzyme. The Gly-214 (GGC) residue was therefore conserved in the enzymes hitherto isolated from humans and other animals. Analysis of monocytes in seven patients with fructose 1,6-bisphosphatase deficiency showed a DNA fragment with apparent normal size in two sisters but no detectable DNA fragment in the other five patients. Monocytes were thus useful as an alternative source for mRNA from human liver for the molecular analysis of fructose 1,6-bisphosphatase deficiency.

Alanine↗
PubMed1994

Acylcarnitine profile in tissues and body fluids of biotin-deficient rats with and without L-carnitine supplementation.

Since biotin-deficient (BD) rats are a good animal model for human multiple carboxylase deficiency and have low plasma free carnitine levels, short-chain acylcarnitine profiles in biotin-deficient rats with L-carnitine supplementation (BDC rats) and BD rats were investigated by fast-atom bombardment and tandem mass spectrometry and gas chromatography/mass spectrometry. By the latter method, 3-hydroxyisovalerylcarnitine was identified in BD rats, and showed the greatest accumulation among short-chain acylcarnitines in tissues of BD rats, while the tissue levels of propionic acid were more markedly elevated than those of 3-hydroxyisovaleric acid. The tissue levels of 3-hydroxyisovaleryl-carnitine were significantly lower and those of propionyl-carnitine were somewhat higher in BDC rats than in BD rats, while the tissue levels of propionic acid and 3-hydroxyisovaleric acid in BDC rats were lower than those in BD rats. These changes were more apparent in kidney than in other tissues. The amounts of urinary excretion of acylcarnitines were markedly larger, and those of 3-hydroxyisovaleric acid were somewhat smaller in BDC rats than in BD rats, while those of propionic acid were very low in BD and BDC rats as compared with those of 3-hydroxyisovaleric acid. It seems that the relationship between the concentrations of 3-hydroxyisovalerylcarnitine and those of propionylcarnitine reflects the unique metabolism of the related metabolites in tissues, especially in kidney, which may be influenced by their urinary excretion and the availability of free carnitine. These data in biotin deficiency suggest that carnitine supplementation is possibly beneficial for patients with holocarboxylase synthetase deficiency who respond incompletely to biotin therapy.

Acetylcarnitine↗
PubMed1994

Scaphoid megalourethra with multiple urogenital anomalies.

A male infant with scaphoid megalourethra, which is a rare congenital anomaly, is presented. At birth he exhibited a grossly swollen, malformed penis and cryptorchidism. The corpus spongiosum was not palpable. The infant had congenital renal failure. Retrograde urethrography revealed a crescent-shaped dilatation of the anterior urethra, and the diagnosis of scaphoid megalourethra was made. Subsequent uroradiological examinations showed that there were also severe urogenital anomalies, i.e. renal hypoplasia-dysplasia, hydronephrosis, hydroureter and vesicoureteral reflux. This disorder is frequently associated with other urogenital anomalies. Therefore, once the diagnosis is reached, a careful investigation for other associated abnormalities should be undertaken.

Abnormalities, Multiple↗
PubMed1994

Uncooked cornstarch treatment for hepatic phosphorylase kinase deficiency.

UNLABELLED: A 5-year-old boy with short stature, hepatomegaly and motor weakness due to hepatic phosphorylase kinase deficiency is described. Laboratory data showed mild hypoglycaemia and metabolic acidosis, hepatic dysfunction, and a low insulin-like growth factor-I level. Mild hypoglycaemia, marked ketosis and insufficient growth hormone secretion were revealed at night. Serum total and free carnitine levels were low and the acyl/total carnitine ratio was high. Urinary acylcarnitine profile using fast atom bombardment and tandem mass spectrometry showed increased excretion of acetylcarnitine and dicarboxylylcarnitines. These endocrinological and metabolic abnormalities and clinical symptoms were improved with uncooked cornstarch treatment. CONCLUSION: Uncooked cornstarch treatment may be helpful in hepatic phosphorylase deficiency.

Child↗
PubMed1994

Adenosine 5'-triphosphate, phorbol ester, and pertussis toxin effects on atrial natriuretic peptide stimulation of guanylate cyclase in a human renal cell line.

We examined adenosine 5'-triphosphate (ATP), pertussis toxin (PT) and phorbol myristate acetate (PMA), a protein kinase C (PKC) activator, modulation of atrial natriuretic peptide (ANP)-stimulated cell-membrane guanylate cyclase (ANP-s-GC) activity and ANP stimulation of whole-cell cGMP accumulation (ANP-s-cGMP) in an ANP-receptor-transduction cell model, the human renal cell line (SK-NEP-1). Acute and long-term effects of PMA on PKC isotype activity are different: Acute (20-min) PMA activation of PKC inhibits ANP-s-cGMP and ANP-s-GC; whereas, long-term (36-h) PMA treatment inhibits slightly less by only partially down-regulating PKC activity, the type-III PKC isotype being 36-h resistant. Long-term 10(-7)M PMA treatment of cells neither affected membrane basal GC activity nor ANP-s-GC activity but partially inhibited ATP enhancement of ANP-s-GC. This partial inhibition was completely reversed by the PKC inhibitor H7 and a PKC inhibitory antibody but only partially reversed by the antibody to the catalytic domain of PKC type III. The EC50 for ATP and its non-phosphorylating analog ATP gamma S in the presence of acute PMA inhibition of ANP-s-cGMP was similar (approximately 10(-9)). This enhancement of PMA inhibition was two orders of magnitude more sensitive (EC50 10(-7)M) than inhibition of ANP-s-cGMP that we previously reported for acute PMA treatment of whole SK-NEP-1 cells. The three- to four-fold ATP enhancement of cell membrane ANP-s-GC was not blocked by 12-hour preincubation of cells with 150 ng/mL PT but was completely blocked if 2-x-10(-7)M PMA was then added for 20 minutes, indicating that acute activation of PKC by PMA does not require a functional "G-type" protein. Acute PMA inhibition of ANP-s-cGMP was reversed by permeabilizing SK-NEP-1 cells to a specific PKC inhibitory peptide, further confirming that PMA inhibition was mediated through PKC activation. These data demonstrated that ANP-s-GC and ANP-s-cGMP were modified through non-phosphorylating interactions with ATP, by multiple PMA activatable PKC isoforms, and that neither were affected by PT-sensitive guanine-nucleotide-binding (G)-protein(s).

Adenosine Triphosphate↗
PubMed1994

A case of familial thyroxine binding globulin excess associated with growth hormone deficiency.

A 7 years 3 months old Japanese boy with familial thyroxine binding globulin (TBG) excess associated with growth hormone (GH) deficiency is reported. The patients height was 106.4 cm (-2.86 s.d.) and his bone age was 5 years and 3 months. He had no goiter and his developmental milestones were normal. The serum thyroid stimulating hormone (TSH) was 2.8 microU/mL, triiodothyronine (T3) 3.1 ng/mL, thyroxine (T4) 23.4 micrograms/dL and free T4 1.8 ng/dL. The serum TBG level was beyond 80.0 micrograms/mL, with normal TSH response to the thyrotropin-releasing hormone (TRH) test. Familial study revealed that his grandmother, mother, uncle, younger sister and younger brother had high TBG and T3 levels, thus an X-linked co-dominant transmission was suggested. The peak GH responses to insulin and clonidine hydrochloride were 5.8 and 8.2 ng/mL, respectively. The mean nocturnal GH concentration was 2.5 ng/mL. His growth velocity increased from 4.8 to 8.4 cm/year and his serum TBG levels decreased gradually after human growth hormone (hGH) treatment.

Body Height↗
PubMed1994

Myocardial scintigraphic characteristics in patients with primary aldosteronism.

To evaluate the difference in myocardial damage between primary aldosteronism and untreated essential hypertension, we performed thallium-201 myocardial single-photon emission computed tomography in 10 patients with primary aldosteronism and 10 patients with essential hypertension who were matched for age, sex, blood pressure, and the severity of left ventricular hypertrophy for primary aldosteronism. From the analysis of thallium-201 myocardial scintigraphy, extent score was calculated. Extent score was significantly higher in primary aldosteronism than in essential hypertension (45.8 +/- 23.5% versus 9.5 +/- 7.3%, P < .01). After operation, blood pressure significantly decreased, and the precordial voltages (SV1 + RV5) and left ventricular mass indexes were significantly reduced in patients with primary aldosteronism. Extent score was also significantly improved. These results suggest that despite the same severity of myocardial hypertrophy between primary aldosteronism and essential hypertension, the myocardial damage estimated by thallium-201 myocardial scintigraphy is more severe in primary aldosteronism than in essential hypertension. Extent score was useful for evaluation of the severity of myocardial damage in hypertensive patients.

Echocardiography↗
PubMed1994

Accurate diagnosis of metastatic cardiac leiomyosarcoma with infundibular stenosis and cardiac tamponade by transesophageal echocardiography and Gd-DTPA magnetic resonance imaging--report of a case.

We present a patient with metastatic cardiac leiomyosarcoma that was diagnosed antemortem by transesophageal echocardiography (TEE) and ECG-gated magnetic resonance imaging with gadolinium diethylene triaminepentaacetic acid (Gd-DTPA MRI). TEE and Gd-DTPA MRI clearly revealed the morphological characteristics of infundibular stenosis and cardiac tamponade. Our patient has survived about 30 months after cardiac surgery. Since sarcoma is usually associated with a very poor prognosis, surgical treatment should be performed as soon as possible. TEE with color Doppler imaging and Gd-DTPA MRI are very useful diagnostic methods for determining the precise anatomical characterization of cardiac tumor, and these procedures are prerequisite to precise therapy.

Adult↗