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Biomedical subjects

H Fukuzaki

Publications and source records attributed to H Fukuzaki.

At least 235 records · Page 13Linked to original sources
PubMed1984

Dilated cardiomyopathy. An echocardiographic follow-up of 50 patients.

To evaluate the significance of left ventricular (LV) hypertrophy in dilated cardiomyopathy (DCM), 50 patients seen between 1976 and 1983 were studied echocardiographically. Patients were classified into 4 groups according to the degree of LV dilatation and LV hypertrophy. Group I consisted of 17 patients who had mild to moderate LV dilatation without LV hypertrophy (LV end-systolic dimension: Ds less than 60 mm, LV wall thickness at end-systole: WTs less than 15 mm). Group II consisted of 12 patients who had mild to moderate LV dilatation with LV hypertrophy (Ds less than 60 mm, WTs greater than or equal to 15 mm). Group III consisted of 8 patients who had marked LV dilatation with LV hypertrophy (Ds greater than or equal to 60 mm, WTs greater than or equal to 15 mm). Group IV consisted of 13 patients who had marked LV dilatation without LV hypertrophy (Ds greater than or equal to 60 mm, WTs less than 15 mm). Twenty patients had LV hypertrophy and 30 patients were without LV hypertrophy at the beginning of this study. New York Heart Association functional classes, cardiothoracic ratio and ECG findings during the first study did not show statistically significant difference among 4 groups. During a follow-up period averaging 2.7 years, 8 patients died of congestive heart failure (CHF), including 5 of Group IV patients and 3 of Group I patients who had progressive LV dilatation. Three patients without signs of CHF expired suddenly; they were in Groups I, II and III during the initial study. Ambulatory ECG studies showed complex ventricular arrhythmias in all 32 patients studied. In conclusion, LV wall hypertrophy in DCM may be an important factor to predict their prognosis regarding CHF death. Sudden and unexpected death could occur in any patient with DCM and intensive antiarrhythmic therapy is important.

Adolescent↗
PubMed1984

Clinical significance of left ventricular hypertrophy in dilated cardiomyopathy: an echocardiographic follow-up of 50 patients.

To evaluate the significance of left ventricular (LV) hypertrophy in patients with dilated cardiomyopathy (DCM), 50 patients seen between 1976 and 1983 were studied echocardiographically. We categorized the patients as four groups according to the degree of LV dilatation or hypertrophy. Group consisted of 17 patients with mild to moderate LV dilatation without hypertrophy (LV end-systolic I dimension: Ds less than 60 mm, LV wall thickness at end-systole: WTs less than 15 mm). Group II, 12 with mild to moderate LV dilatation and hypertrophy (Ds less than 60 mm, WTs greater than or equal to 15 mm). Group III, eight with marked LV dilatation and hypertrophy (Ds greater than or equal to 60 mm, WTs greater than or equal to 15 mm), and Group IV, 13 with marked LV dilatation without hypertrophy (Ds greater than or equal to 60 mm, WTs less than 15 mm). Twenty patients had LV hypertrophy and 30 patients were without LV hypertrophy at the start of this study. New York Heart Association functional classes, cardiothoracic ratio and ECG findings at the first study did not show any statistically significant differences among the four groups. During the prospective follow-up of 2.7 years in average, eight patients died of congestive heart failure including five of Group IV, and three of Group I who had progressive LV dilatation. Three patients of Group I, II and III died suddenly. Ambulatory ECGs showed life-threatening ventricular arrhythmias in all 32 patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

[The heart in acromegaly: an echocardiographic study].

Clinical examinations including echocardiography were performed for 14 acromegalic patients (five men and nine women, whose mean age was 48.6 years). Three of these had hypertension (HT) above 160/95 mmHg, three had diabetes mellitus (DM). Their cardiac sizes and functions were correlated with the durations of disease and plasma growth hormone (GH) levels. The incidences of HT and DM were also evaluated. Three of 14 patients (22%) had increased cardiothoracic ratios (greater than 55%). Electrocardiographic abnormalities were noted in three patients including two with left ventricular hypertrophy (LVH) and one with interventricular conduction defects with abnormal Q waves. By echocardiography (Table 2), nine patients (64%) were judged to be normal. The remaining five patients (36%) had abnormal echocardiograms. These included LVH (sums of the interventricular and posterior wall thicknesses greater than or equal to 25 mm) in two (25 mm in Case 10, 30 mm in Case 11), increased left ventricular end-diastolic dimension (EDD greater than or equal to 55 mm) in one (72 mm in Case 14) and both abnormalities in two patients (Cases 12 and 13). Two patients (Case 13 and 14), whose %FS were 17% and 22%, respectively, had definite evidence of congestive heart failure. Two patients (Case 11 and 13) met the diagnostic criteria for asymmetric septal hypertrophy. One patient with echocardiographic LVH and another who had increased EDD with LVH had histories of HT (Case 11 and 12). Plasma GH levels in patients with LVH were greater than 100 ng/ml (Cases 10 and 11). The left ventricular hypertrophy and/or increased EDD observed in these patients seemed related to the duration of acromegaly but not to the presence of DM. Myocardial biopsy of the right ventricle in two patients with congestive heart failure disclosed myocardial hypertrophy, myocardial fiber disarray, interstitial fibrosis and large nuclei.

Acromegaly↗
PubMed1984

[Tl-201 single-photon emission computed tomography for clinical assessment of dilated cardiomyopathy].

In some cases of dilated cardiomyopathy (DCM) perfusion defects are demonstrable by Tl-201 imaging at rest. This study clarified the mechanism by which the Tl scan can show myocardial perfusion defects in patients with DCM by means of Tl-201 single-photon emission computed tomography (ECT) utilizing a rotating gamma camera to assess three-dimensional T1 distribution in the myocardium. Thirteen patients with DCM were studied by conventional planar and ECT imaging, and the degree of defects was determined visually. Perfusion defects were observed in 11 of 13 cases (85%) by planar imaging and in all 13 (100%) by ECT imaging. The mean defect score was higher in ECT than in planar imaging (4.15 +/- 1.46 vs 2.23 +/- 1.46, p less than 0.025). A comparative study of defect scores and left ventricular ejection fractions (EF) using gated cardiac blood pool scans established a negative correlation on ECT imaging (r= -0.64), and no correlation on planar imaging (r= -0.38). There was no statistically significant correlation between perfusion defects on planar imaging and regional wall motion abnormalities as observed by two-dimensional echocardiography (2-DE). In contrast, most of the segments with severe defects (defect score greater than or equal to 2) on ECT images showed high grade wall motion abnormalities on 2-DE. Both perfusion defects and wall motion abnormalities in DCM may be closely related to the fibrosis or scar formation in the myocardium. These results indicated that T1-201 myocardial scintigraphy, especially ECT imaging, is of great value in the clinical assessment of patients with DCM.

Adult↗
PubMed1984

[Clinical usefulness of exercise-nitroglycerin myocardial imaging using dual administration of thallium-201].

In order to differentiate transient myocardial ischemia from infarction, the delayed thallium-201 myocardial imaging (redistribution image) is widely utilized, however, the precise mechanism of redistribution remains unsolved. In the present study, we proposed a new method to elucidate myocardial ischemia on images. In normal subjects, patients with old myocardial infarction (OMI) without angina pectoris (AP) and patients with AP, 1.4 mCi of thallium-201 (Tl-201) was intravenously injected at the peak exercise, and immediately myocardial images were obtained in the three projections. Then, 0.3 mg of nitroglycerin (NTG) was sublingually given, and 0.6 mCi of Tl-201 was readministered. NTG myocardial images were analyzed in the left anterior oblique projection and evaluated visually and quantitatively. There was no significant difference in the relative activity on exercise to NTG images in normal subjects and patients with OMI, while patients with AP showed increased activity on exercise to NTG images. Furthermore, the increase in relative activity done by the exercise-nitroglycerin study was greater than that by the conventional exercise-redistribution study in patients with AP. It was concluded that a new method in the present study is able to image myocardial ischemia distinctly and could be useful in clinical studies.

Adult↗
PubMed1984

[Three-dimensional evaluation of mitral regurgitation by pulsed Doppler echocardiography: analysis of the amount and direction of regurgitant flow].

Pulsed doppler echocardiography (PDE) was used to evaluate mitral regurgitation (MR) non-invasively and quantitatively in 156 patients including 51 of rheumatic valvular disease, 57 of mitral valve prolapse (MVP) or chordal rupture of the mitral valve (RCT), and 48 of ischemic heart disease (IHD) or dilated cardiomyopathy (DCM). The severity of MR was estimated three-dimensionally by a MR scoring system as follows: As an index of direction and extent of regurgitation, nine sampling sites were selected in the left atrium at the level of the mitral annulus. These include the anterior, mid, and posterior parts of each portion of the postero-medial, middle, and antero-lateral sides. The depth of regurgitation was graded by three degrees in the long-axis projection of the left ventricle; grade 1; MR signals localized within the level of the mitral annulus, grade 2; MR detected beyond the mitral annulus but not reaching the aortic valve level; and grade 3; MR detected beyond the aortic valve level in the left atrium. The MR score was comprised of the products of numbers of points at which MR signals were detected and the grades of the maximum depth. The MR scores correlated well with the severity of MR as determined by the left ventriculogram (LVG); the MR score was 4.0 +/- 1.6 (mean +/- S.D.) points in grade 1; 9.6 +/- 2.6 points in grade 2; 18.0 +/- 3.2 points in grade 3; and 23.0 +/- 1.7 points in grade 4 by LVG. Doppler mapping of the left atrium at the level of the mitral annulus suggested that the directions of MR varied with each disease and valvular lesion. Thus, these observations were helpful in the investigation of MR by PDE. We concluded that the above-mentioned MR scoring system proves a very useful method for quantitatively evaluating MR non-invasively.

Adolescent↗
PubMed1983

Elevation of cytoplasmic free calcium concentration by stable thromboxane A2 analogue in human platelets.

9, 11-Epithio-11, 12-methano-thromboxane A2 (STA2), a stable analogue of thromboxane A2, caused a rapid rise in cytoplasmic free Ca2+ concentration ([Ca2+]i) in human platelets as measured with the fluorescent Ca2+ indicator quin2. Concomitantly, this compound induced phosphorylation of myosin light chain which is catalyzed by Ca2+, calmodulin-dependent protein kinase. These reactions were fast enough to trigger serotonin release. 13-Azaprostanoic acid, a receptor level antagonist of thromboxane A2 inhibited STA2-induced elevation of [Ca2+]i, phosphorylation of myosin light chain and serotonin release. These results provide evidence that STA2 interacts with a thromboxane A2 receptor which leads to elevation of [Ca2+]i.

Blood Platelets↗
PubMed1983

Effect of cyclic AMP on cytoplasmic free calcium in human platelets stimulated by thrombin: direct measurement with quin2.

With the fluorescent Ca2+ indicator quin2, we measured directly cytoplasmic free Ca2+ [( Ca2+]i) in washed human platelets stimulated by thrombin and examined the effect of cyclic AMP on [Ca2+]i levels and 14C-serotonin release. Thrombin (0.2 U/ml) evoked a rise in [Ca2+]i from the basal level of about 100 nM to integral of 3 microM which was fast enough to trigger serotonin release. This rise was inhibited in a dose-dependent manner by preincubation with prostaglandin E1 (PGE1) (0.1-10 microM) or dibutyryl cyclic AMP (0.01 -1 mM). Parallel to this, serotonin release was also inhibited by these drugs. When added to platelets after stimulation by thrombin, PGE1 caused the rapid decrease of elevated [Ca2+]i. These results provide direct evidence that [Ca2+]i levels in platelets are regulated by cyclic AMP.

Aminoquinolines↗
PubMed1983

Protein phosphorylation and diglyceride production during serotonin release induced by epinephrine plus ADP in human platelets.

Epinephrine (1 microM) plus ADP (5 microM) induced serotonin release from human platelets although neither epinephrine nor ADP alone brought about such a release. During this release reaction, the phosphorylation of 40K-dalton protein was induced to an extent similar to that induced by 0.5 unit/ml thrombin. The amount of diglyceride (DG) produced by epinephrine plus ADP, however, was much smaller than that produced by thrombin. The reaction velocities of these reactions induced by epinephrine plus ADP were slower than those induced by thrombin. Epinephrine or ADP alone hardly produced any DG and induced 40K-dalton protein phosphorylation only slightly. Indomethacin (1 microgram/ml), a cyclooxygenase inhibitor, remarkably inhibited epinephrine plus ADP induced serotonin release, 40K-dalton protein phosphorylation and DG production although this agent had little effect on the same reactions induced by thrombin. These results suggest that prostaglandin endoperoxides or thromboxane A2 may be involved in serotonin release, 40K-dalton protein phosphorylation and DG production induced by epinephrine plus ADP.

Adenosine Diphosphate↗
PubMed1983

The effect of oxygen on the development of atherosclerosis in WHHL rabbits.

The effect of hyperoxic or hypoxic inhalation on blood lipid levels and on the development of atherosclerosis was studied in young male WHHL rabbits. They were exposed to ordinary room air containing different concentrations of oxygen: 6 animals were exposed to 40% oxygen (hyperoxia group) or 5-10% oxygen (hypoxia group) for 5 h a day, 5 days a week for 8 weeks. Four control rabbits inhaled ordinary room air. The following results were obtained. (1) The severity of aortic lesions significantly decreased in the hyperoxia group and increased in the hypoxia group, when these two groups were compared. However, both hypoxic and hyperoxic groups did not statistically differ from the control. (2) Plasma cholesterol levels were not changed either by hyperoxic or hypoxic inhalation. (3) Plasma triglyceride levels were elevated only in the hypoxia group, with significant differences from the values in both control and hyperoxia groups. (4) There was no significant correlation between mean plasma lipid level and severity of aortic lesions. From these results, we conclude that hyperoxic or hypoxic inhalation respectively regresses or aggravates the development of atherosclerotic lesions, not by an indirect action on blood lipid concentrations but by a direct action on the vascular wall.

Animals↗
PubMed1983

Platelet reactivity and its dependence on alpha-adrenergic receptor function in patients with ischaemic heart disease.

We studied 57 patients admitted to hospital with ischaemic heart disease, including nine patients with variant angina, to evaluate platelet reactivity and its dependence on alpha-adrenergic receptor function. The threshold concentration for biphasic platelet aggregation in response to adrenaline and adenosine diphosphate was measured in fresh platelet rich plasma. There were age related alterations in platelet responsiveness to adrenaline. In 27 age matched control subjects platelets showed adrenaline induced aggregation at a concentration higher than 0.1 mumol. The threshold concentrations for adrenaline and adenosine diphosphate were 0.91 mumol and 4.68 mumol. In 16 patients with acute infarction, 14 with old infarction, nine with effort angina, and nine with rest angina, mean values of platelet aggregation threshold for both adrenaline and adenosine diphosphate were not altered significantly when compared with control subjects. In contrast, the values for adrenaline and adenosine diphosphate in nine patients with variant angina were 0.012 mumol and 2.24 mumol and seven of them showed obvious platelet hyperactivity to adrenaline at a concentration lower than 0.1 mumol. The threshold concentration for adrenaline induced aggregation did not correlate with serum cholesterol and triglyceride levels.

Adenosine Diphosphate↗
PubMed1983

Hyperreactivity of coronary arterial smooth muscles in response to ergonovine from rabbits with hereditary hyperlipidemia.

This study was undertaken to examine the response to ergonovine, an agent used to provoke spastic constriction of large epicardial coronary arteries, to elucidate the responsible underlying mechanism, and to determine the impact of endogenous hyperlipidemia on contractile properties of isolated vessels from different beds. The isolated arteries from both control and Watanabe hereditary hyperlipidemic rabbits (WHHL rabbits) were suspended for recording isometric force in oxygenated Krebs buffer and exposed to agonists and antagonists. In atherosclerotic aortas from WHHL rabbits, the concentration-response relations for ergonovine and serotonin exhibited a marked leftward shift with significantly depressed constrictor threshold concentration and lowered one-half maximally effective concentration values. In coronary arteries with no atherosclerotic lesions detectable macroscopically from WHHL rabbits, the concentration-response relations showed a leftward shift for ergonovine but not serotonin. Coronary contraction evoked by ergonovine was remarkably inhibited by 0.1 microM cyproheptadine and 0.3 microM methysergide, serotonergic antagonists, in both groups. alpha-Adrenergic blockade with 0.1 microM prazosin was effective in inhibiting ergonovine-induced contraction of aortas from control rabbits, but not that of atherosclerotic ones. The constrictor response to ergonovine of atherosclerotic aortas was inhibited by cyproheptadine. The responsiveness to ergonovine of both carotid and femoral arteries from WHHL rabbits with no sclerotic lesions, which was suppressed by prazosin was not different from that of control rabbits. In contrast, the concentration-response relations for phenylephrine in the four different types of arteries did not differ appreciably between the two groups, and the constrictor responses to 20 mM KCl were virtually identical. Thus, aortas and coronary arteries exposed to endogenous hyperlipidemia appear to be hyperreactive to ergonovine mediated by a serotonergic mechanism.

Animals↗