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Biomedical subjects

H Fukuzaki

Publications and source records attributed to H Fukuzaki.

At least 73 records · Page 4Linked to original sources
PubMed1990

Value of the signal-averaged electrocardiogram as a predictor of sudden death in myocardial infarction and dilated cardiomyopathy.

To clarify the prognostic significance of signal averaged electrocardiogram (SAE), 100 patients with old myocardial infarction (OMI) and 54 patients with dilated cardiomyopathy (DCM) were studied. Late potentials (LPs) were detected in 31 patients with OMI and in 21 patients with DCM. During a mean follow up of 18 months (3 to 60) in OMI and 28 months (3 to 71) in DCM, 29 patients died. Fifteen patients died suddenly (8 in OMI, 7 in DCM). In OMI, the sensitivity (Se), specificity (Sp), predictive accuracy (PA) of LPs for sudden death were 75%, 72%, and 73%, respectively. The presence of either LPs or prolonged filtered QRS (f-QRS) predicted sudden death with a high Se, and the presence of both LPs and prolonged f-QRS predicted with high Sp and PA. In DCM, Se, Sp, and PA of LPs were lower than those in OMI (Se; 71%, Sp; 66%, PA; 67%). A life table analysis showed that the probability of remaining free from sudden death was significantly lower in patients with LPs than those without them in OMI, but no significant difference was observed between those with and without LPs in DCM. Patients with either LPs or prolonged f-QRS, however, had a significantly higher probability of sudden death in both diseases and no patient with normal SAE died suddenly. SAE was also useful in separating high risk patients in either normal or low cardiac index group in both diseases. Ventricular tachycardia (VT) and % fractional shortening in OMI and only VT in DCM were also useful predictors among other parameters. In conclusion, SAE provides useful information in a noninvasive method to identify patients at risk of sudden death, and patients with normal SAE have a low risk of sudden death in OMI and DCM.

Arrhythmias, Cardiac↗
PubMed1990

Characterization of slow conduction in the common type of atrial flutter--using transient entrainment.

To characterize slow conduction of the common type of atrial flutter (common AF), in which excitation wave propagated in a counterclockwise fashion, transient entrainment during the distal high lateral right atrium (HRAd) pacing and during the proximal coronary sinus (CSp) pacing was studied in 7 patients with common AF. In transient entrainment of common AF, conduction time from stimulus to CSp during HRAd pacing was always longer than that from stimulus to HRAd during CSp pacing. It was also longer than that from stimulus to CSp during HRAd pacing in 5 control patients without common AF in sinus rhythm. Return cycles at HRA and CS after cessation of rapid pacing during transient entrainment were studied. In HRAd pacing, return cycle at the proximal high lateral right atrium was almost equal to the pacing cycle length, or almost equal to or slightly shorter than the flutter cycle length (AFCL). Return cycle at CSp was almost equal to AFCL. In CSp pacing, return cycle at the distal coronary sinus was much longer than AFCL and increased at progressively shorter pacing cycle lengths. In conclusion, slow conduction was demonstrated in the lateral limb (from HRA laterally to CS) of the reentrant circuit in common AF, but it did not exhibit decremental conduction property. Return cycle at an endocardial recording site after transient entrainment in common AF does not always exhibit an uniform pattern, affected by the relative location of and the distance between the recording site, the pacing site, the reentrant circuit and the area of slow conduction.

Aged↗
PubMed1990

Regional wall motion abnormality and its relation to myocardial histopathological change and clinical prognosis in dilated cardiomyopathy--usefulness of dobutamine loading echocardiographic study.

Regional wall motion abnormality in 28 patients with dilated cardiomyopathy (DCM) was evaluated by M-mode and two-dimensional echocardiography (2DE) before and during dobutamine administration. In 6 autopsied hearts obtained from deceased cases during the follow up period, the relationship between regional myocardial fibrosis and wall motion abnormality was investigated. Left ventricular wall was divided into 11 segments by 2DE. The wall motion of each segment was evaluated and scored into 4 degrees (0: normokinesis, 1: hypokinesis, 2: severe hypokinesis, 3: akinesis or dyskinesis), and the total sum of wall motion abnormality scores in 11 segments (TWS) for each case was calculated. Wall motion abnormality was observed in 231 of the total 308 segments, and in 121 of the 231 segments, the severity of the wall motion abnormality was reduced by dobutamine administration. The rate of fibrosis was lower in segments with improved wall motion abnormality than in those without improvement. Sixteen deteriorated or deceased cases during the follow up period (D group) had larger TWS than 12 non-deteriorated cases (ND group), but percent fractional shortening (%FS) obtained by M-mode echocardiography was not significantly different between the 2 groups. The changes in %FS and TWS by dobutamine (delta%FS, %delta TWS) were significantly larger in ND group than in D group. The cases with %delta TWS greater than or equal to 45% were all in the ND group, and all deceased cases had the value of %delta TWS less than or equal to 36%. Thus, the observation of regional wall motion by dobutamine loading echocardiography was useful for evaluating regional histopathological findings and prognosis in patients with DCM.

Adult↗
PubMed1990

Analysis of ventricular arrhythmias in patients with dilated cardiomyopathy--relationship between the effects of antiarrhythmic agents and severity of myocardial lesions.

In order to investigate the usefulness of antiarrhythmic drugs in patients with dilated cardiomyopathy (DCM), 42 patients with DCM were studied using 24 h ambulatory ECG monitoring, echocardiography and right ventricular endomyocardial biopsy. All 42 patients had ventricular arrhythmias with a Lown's classification of grade II or greater (grade IVb, 25; IVa, 7; III, 7; II, 3). The patients with grade IV arrhythmias tended to have greater dilating of the left ventricle and more pronounced interstitial myocardial fibrosis than patients with lower grades. Following procainamide and/or disopyramide treatment the severity of the ventricular arrhythmias improved in 12 (29%) of the 42 patients, did not change in 27 patients (64%), and deteriorated in 3 patients (7%). Treatment with aprindine or mexiletine was effective in 7 (50%) of the 14 patients who did not respond to procainamide and/or disopyramide. Although there were no significant differences in left ventricular dimension and contractility between patients in each group who did and did not respond to antiarrhythmic treatment, those who did respond had less interstitial myocardial fibrosis. Thus, in the procainamide and/or disopyramide treated group the percent interstitial fibrosis in responding vs nonresponding patients was 10.3 +/- 4.1% vs 18.7 +/- 8.3% (p less than 0.05) respectively, while in the group treated with aprindine or mexiletine these figures were 13.0 +/- 3.2% vs 26.1 +/- 7.9% (p less than 0.02), respectively. In conclusion, the effect of antiarrhythmic drugs in DCM was dependent on the severity of the pathological changes in the myocardium, and antiarrhythmic drugs should be appropriately used for the management of ventricular arrhythmias in DCM.

Adult↗
PubMed1990

Left ventricular reserve of the hypertrophied heart in patients with systemic hypertension and hypertrophic cardiomyopathy--relation to age and left ventricular relative wall thickness.

To determine the effects of aging and concentric hypertrophy on the reserve of the left ventricle (LV), 36 patients with hypertension (HT), 22 with hypertrophic cardiomyopathy (HCM) and 25 age-matched normal subjects (N) were studied by isoproterenol (ISP) infusion echocardiography. The end-diastolic LV relative wall thickness (RWT), fractional shortening (FS), peak mitral flow velocity during the rapid filling phase (R) and atrial systole (A), and the A/R ratio were measured. At rest, the RWT and A/R were larger in groups HT and HCM than in group N. There were no significant differences in age, heart rate (HR), and FS among the groups. The A/R of all groups showed a good positive correlation with increasing age. The A/R of the HT group was also positively correlated with RWT. During ISP infusion, the HR, R, A, A/R and FS increased in all groups. The changes in R and FS were smaller in groups HT and HCM than in group N. The change in HR in groups N and HT, and the change in FS in all groups during ISP infusion were all inversely correlated with increasing age. The change in FS during ISP infusion was inversely correlated with RWT in the HT group, but not in HCM. Thus, it was suggested that the impairment of LV reserve in patients with HCM is not only caused by concentric hypertrophy and the aging process, but also by other myocardial factors.

Adolescent↗
PubMed1990

Afterload mismatch in patients with hypertrophic nonobstructive cardiomyopathy.

To investigate the cardiac reserve of hypertrophic nonobstructive cardiomyopathy (HNCM), an echocardiographic study was performed before and during angiotensin II loading in 22 HNCM patients without left ventricular (LV) systolic dysfunction at rest and 8 normal subjects. LV end-diastolic dimension (LVDd) and time velocity integral (Ie) at aortic annulus were obtained as parameters of preload and forward ejection respectively. Responses of these indices to afterload stress were compared with clinical findings and right ventricular biopsy findings. Based on the reserve of forward ejection characteristics to afterload stress, 22 HNCM patients were divided into 2 groups; Group I: 9 cases with more than 15% decrease of Ie which corresponded to the value of mean - 1SD in normal subjects, Group II: 13 cases with a decrease of Ie less than 15%. There were no significant differences in echocardiographic findings between Group I and II before angiotensin II loading. On the other hand, Group I had a smaller increase of LVDd (p less than 0.05) to afterload stress, a higher incidence of ventricular tachycardia on a Holter electrocardiogram (p less than 0.05), lower maximal oxygen consumption with treadmil exercise test (p less than 0.01), and a larger value of LV end-diastolic pressure (p less than 0.05) than those in Group II, respectively. Although no difference in myocyte diameter was found between the 2 groups, myocardial fibrosis was more severe (p less than 0.001) and the incidence of moderate or severe disarray was higher (p less than 0.05) in Group I than in Group II. Thus, some HNCM patients cannot maintain forward ejection to afterload stress because of impaired preload reserve attributable to a greater stiffness of the left ventricle with severe myocardial lesion.

Adolescent↗
PubMed1990

Clinical and exercise echocardiographic findings in patients with mitral valve prolapse.

To assess the relationship between left ventricular functional reserve and prognosis in patients with idiopathic mitral valve prolapse, ergometer exercise echocardiography was performed in 10 normal subjects and 30 patients with mitral valve prolapse having either mild, or no mitral regurgitation. These 30 patients with mitral prolapse were followed for 2 to 8 (mean 4.5) years. Increment of % fractional shortening during maximum exercise at the initial study in patients with mitral valve prolapse and normal subjects were 7 +/- 7 and 11 +/- 3%, respectively. Based on increment of % fractional shortening, patients with mitral valve prolapse were divided into 2 groups; Group I: 13 cases with delta% fractional shortening less than 5%, Group II: 17 cases with delta% fractional shortening greater than or equal to 5%. The incidence of cardiac symptoms was higher in Group I than in Group II (85 vs 41%, p less than 0.05). ST-T changes and life-threatening arrhythmias were more frequently observed in Group I. During the follow-up period, M-mode echocardiographic measurements did not vary in Group II, but left ventricular and left atrial dimensions increased significantly (p less than 0.05, p less than 0.01, respectively) and % fractional shortening decreased significantly (p less than 0.01) in Group I without any change in mitral regurgitation severity. Thus, some patients with mitral valve prolapse not having significant mitral regurgitation may develop progressive deterioration of the cardiac function, which may be predicted by exercise echocardiography.

Adult↗
PubMed1990

Bronchial hyperreactivity in patients with mitral valve disease.

To elicit the mechanism of bronchial hyperreactivity (BHR) in chronic heart failure (CHF), a methacholine inhalation test, pulmonary function test, and cardiac catheterization were performed in 19 patients with mitral valve disease (MVD), and the change of severity of BHR before and after mitral valve replacement (MVR) was also examined in seven of 19 patients with MVD. Sixteen of 19 patients with MVD showed significant increase in respiratory resistance in methacholine inhalation test, while all normal subjects did not. The maximal expiratory flow at 25 percent of vital capacity (Vmax25), a parameter of small airway disease, correlated significantly with log cumulative dose producing a 35 percent decrease in respiratory conductance (PD35Grs) (r = 0.536) and the duration of symptoms (r = -0.682). There was a significant correlation between log PD35Grs and mean pulmonary artery wedge pressure (r = -0.466). After MVR, log PD35Grs was significantly improved in all seven operated-on patients, although six patients retained BHR. We conclude that patients with long-term MVD have marked BHR and that BHR in long-term MVD is related to peripheral airway narrowing with organic remodeling, which was not ameliorated with MVR procedure, in addition to pulmonary congestion.

Bronchial Provocation Tests↗
PubMed1990

[Mitral valve prolapse as an initial clinical feature of dilated cardiomyopathy: report of two cases].

Two cases with mitral valve prolapse (MVP), without any other cardiac abnormalities at the initial evaluation, developed the clinical features mimic to dilated cardiomyopathy (DCM) during follow-up period. Case 1. A 40-year-old man visited our hospital in May 1982 to evaluate a heart murmur. A standard 12-lead electrocardiogram (ECG) showed an abnormal Q wave in lead III. Echocardiography revealed MVP, but neither dilatation nor wall motion abnormality of the left ventricle (LV) were observed. Thallium-201 scintigraphy revealed an abnormal thallium uptake at the apex and inferior wall. He had no episode of acute myocardial infarction or myocarditis, but complete right bundle branch block developed, thus, he was hospitalized in October 1984. He had no coronary artery lesions, and had only mild mitral regurgitation on left ventriculography. The motion of the interventricular septum and apex was reduced on echocardiogram and a persistent perfusion defect was observed at the inferior wall and the interventricular septum on Tl-201 scintigrams. In December 1985, he experienced an Adams-Stokes attack due to complete atrioventricular block. Echocardiographically, the left ventricle enlarged, and the wall motion abnormalities and a perfusion defect on Tl-201 scintigrams were relatively severe. Case 2. A 46-year-old woman occasionally experienced palpitation of short duration and chest oppression since 1977. She was admitted to our hospital because of cardiac symptoms in 1982. A heart murmur of Levine II was heard and a standard 12-lead ECG showed single supraventricular extrasystole and T wave inversion in lead III and aVF. Echocardiography revealed MVP and mild mitral regurgitation, but neither dilatation nor wall motion abnormality of the LV was observed. During 6-year follow-up period, permanent atrial fibrillation developed and LV developed dilatation and wall motion abnormalities progressed. Thus, during follow-up periods, DCM-like features developed in two cases who had had MVP as a sole echocardiographic abnormality with systolic murmur and non-specific ECG changes. We consider that these two may be important cases who may show a relation between cardiomyopathic process and MVP.

Adult↗
PubMed1989

Alpha 2-adrenoceptors and platelet function in patients with variant angina.

We have previously reported that platelets of patients with variant angina exhibited pronounced hyperactivity to epinephrine, as assessed by aggregation study. To determine whether this is associated with a change in surface alpha-adrenoceptor status, we investigated the capacity and affinity of binding sites for [3H]dihydroergocryptine, a potent alpha-antagonist, of platelet lysates prepared from 22 patients with ischemic heart disease and 13 control subjects of similar age. [3H]DHE binding capacity to platelets from control subjects, 6 patients with acute myocardial infarction, 9 with effort angina and 7 with variant angina were 233 +/- 44 (SD), 226 +/- 53, 252 +/- 58 and 348 +/- 48 fmol/mg protein and its affinity were 2.05 +/- 1.40, 0.98 +/- 0.46, 1.59 +/- 0.37 and 1.49 +/- 0.66 nM, respectively. The patients with variant angina had significantly higher capacity of platelet alpha-adrenoceptor than controls (49% increase) or patients with other types of ischemic heart disease. In contrast, the affinity for [3H]DHE was not significantly different as compared with other three groups. Similar increments in the binding capacity for [3H]-rauwolscine, alpha 2 antagonist, were found in platelet lysates prepared from 6 patients with variant angina. These results suggest that increased capacity of platelet alpha-adrenoceptor may explain enhanced reactivity to epinephrine in patients with variant angina.

Adrenergic alpha-Agonists↗
PubMed1989

Identification of a major GTP-binding protein in bovine aortic smooth muscle membranes as smg p21, a GTP-binding protein having the same effector domain as ras p21s.

At least two GTP-binding proteins (G proteins) with Mr values of about 20,000 were extracted from bovine aortic smooth muscle membranes by sodium cholate. The most abundant G protein (22K G) was purified to near homogeneity by successive column chromatographies of Ultrogel AcA-44, phenyl-Sepharose CL-4B, hydroxyapatite and Mono Q HR5/5. 22K G showed kinetic and physical properties very similar to those of smg p21, a G protein recently isolated from bovine brain and human platelet membranes, having the same effector domain as ras p21s. Moreover, 22K G was recognized specifically by the anti-smg p21 antibody. These results indicate that the major G protein in bovine aortic smooth muscle membranes is smg p21.

Animals↗
PubMed1989

The structures of the asparagine-linked sugar chains of human apolipoprotein B-100.

The asparagine-linked sugar chains of human apolipoprotein B-100 were liberated from the polypeptide portion by hydrazinolysis followed by N-acetylation and NaB3H4 reduction. Their structures were elucidated by sequential exoglycosidase digestion in combination with methylation analysis after fractionation by paper electrophoresis and gel permeation chromatography. One neutral and two acidic fractions were obtained by paper electrophoresis in a molar ratio of 7:8:5. The neutral fraction contained high-mannose type oligosaccharides consisting of Man5GlcNAc2 to Man9GlcNAc2. The acidic fractions contained monosialylated and disialylated biantennary complex type oligosaccharides. As minor components in the monosialylated fraction, biantennary complex-type oligosaccharides which were absent one terminal galactose residue, monoantennary complex type, and hybrid type oligosaccharides were detected. Apolipoprotein B-100 was calculated to contain 5-6 mol of high-mannose type and 8-10 mol of complex type oligosaccharides per mole protein.

Apolipoprotein B-100↗
PubMed1989

Two types of protein kinase C with different functions in cultured rabbit aortic smooth muscle cells.

Incubation of cultured rabbit aortic smooth muscle cells (SMC) with phorbol-12, 13-dibutyrate (PDBu) for 48 h caused the down-regulation of protein kinase C (PKC) to the level of 30-40% of that in the control cells. The proliferative and antiproliferative actions of PKC were abolished in parallel with the loss of the down-regulation-sensitive component of PKC, but the inhibitory actions in the whole blood serum (WBS)-induced phospholipase C (PLC) reactions and intracellular Ca2+ mobilization were not affected. Immunoblot analysis with specific monoclonal antibodies against three PKC isozymes (type I, II and III) revealed that only the type III isozyme was detected in rabbit aortic SMC and that this isozyme completely disappeared after the incubation with PDBu. These results indicate that the type III isozyme is responsible for the proliferative and antiproliferative actions and suggest that the unidentified isozyme(s) is involved in the inhibitory actions in the WBS-induced PLC reactions and intracellular Ca2+ mobilization in rabbit aortic SMC.

Animals↗
PubMed1989

Endothelin-induced biphasic formation of 1,2-diacylglycerol in cultured rabbit vascular smooth muscle cells--mass analysis with a radioenzymatic assay.

Mass analysis of 1,2-diacylglycerol (DG) with a radioenzymatic assay revealed that endothelin induced a biphasic formation of DG with an early transient phase peaking at 30 sec and a late sustained phase peaking at 5 min in cultured rabbit vascular smooth muscle cells (VSMCs). The amounts of DG after the 30-sec and 5-min incubation with endothelin were 0.74 +/- 0.08 (mean +/- SE) nmol and 0.87 +/- 0.10 nmol/100 nmol of lipid phosphorus, representing 2.6- and 3.1-fold increases of the resting level, respectively. The EC50 values of endothelin for the early and late phases of DG formation were about 1 nM and 40 nM, respectively. In the [3H] inositol-labeled VSMCs, endothelin induced a rapid transient formation of inositol tris- and bisphosphates which peaked at 30 sec and a sustained formation of inositol monophosphate which peaked at 5 min. The EC50 values for the formation of these inositol phosphates were the same and about 1 nM. These results suggest that the early transient phase of DG is derived from the hydrolysis of polyphosphoinositides, while a large part of the late sustained phase of DG is from the reaction(s) other than the hydrolysis of phosphoinositides but its sources remain to be clarified.

Animals↗
PubMed1989

Stimulation of phospholipase C-mediated hydrolysis of phosphoinositides by endothelin in cultured rabbit aortic smooth muscle cells.

Incubation of the [3H] inositol-labeled cultured rabbit vascular smooth muscle cells (VSMCs) with either endothelin or angiotensin II caused a rapid formation of inositol mono-, bis- and trisphosphates (IP1, IP2 and IP3, respectively). Time courses of the endothelin- and angiotensin II-induced formation of these inositol phosphates were similar. The maximal levels of IP1, IP2 and IP3 formation induced by endothelin were about 50%, 25% and 40%, respectively, of those induced by angiotensin II. The doses of endothelin necessary for the half maximal and maximal extents of the formation of IP1 were about 1 nM and 100 nM, respectively. Protein kinase C-activating 12-Q-tetradecanoylphorbol-13-acetate (TPA) inhibited the endothelin-induced formation of IP1 with the half maximal extent of inhibition seen at 3 nM. The inhibitory action of TPA was mimicked by another protein kinase C-activating phorbol ester, phorbol-12,13-dibutyrate, but not by 4 alpha-phorbol-12,13-didecanoate, known to be inactive for this enzyme. These results indicate that endothelin causes the phospholipase C-mediated hydrolysis of phosphoinositides, though to a lesser extent than angiotensin II, in cultured VSMCs and suggest that protein kinase C modulates the signaling mechanism of endothelin to the phospholipase C.

Angiotensin II↗
PubMed1989

Phosphatidylinositol turnover in human monocyte-derived macrophages by native and acetyl LDL.

Monocyte-derived macrophages play a key role in pathogenesis of atherosclerosis. However, the mechanism of activating macrophages in atheromatous lesions has not been fully investigated. This report describes the contribution of phosphatidylinositol turnover to the uptake of low density lipoproteins (LDL) by macrophages. Both native and acetyl LDL stimulated inositol 1,4,5-triphosphate (IP3) formation in a dose-dependent manner at concentrations of 0-70 micrograms/ml. The potency of IP3 formation by acetyl LDL (0.44 nmol/mg protein) was 2-fold higher than that by native LDL (0.21 nmol/mg protein). Time course studies showed that a maximal effect of IP3 formation by acetyl LDL at concentrations of 30 micrograms/ml was observed at 3 min. Longer incubation diminished IP3 formation. Oxidized LDL also stimulated IP3 formation with a similar efficiency to acetyl LDL. It was indicated that chemically modified LDL which were taken up through the scavenger receptor pathway activated the macrophages by mediating the phosphatidylinositol hydrolysis and IP3 formation.

Cells, Cultured↗
PubMed1989

Antiproliferative action of cyclic GMP-elevating vasodilators in cultured rabbit aortic smooth muscle cells.

In cultured rabbit aortic smooth muscle cells (SMCs), sodium nitroprusside (SNP) (10(-7) to 10(-4) M), atrial natriuretic peptide (ANP) (10(-9) to 10(-6) M) and 8-bromo-cyclic GMP (10(-6) to 10(-3) M) inhibited the whole blood serum (WBS)-induced DNA synthesis by about 30%. The doses of SNP and ANP necessary for the inhibition of the WBS-induced DNA synthesis were similar to those necessary for the formation of cellular cyclic GMP (cGMP). These agents were effective even when added 6 h after stimulation of the cells with WBS. These results suggest that cGMP inhibits the proliferation of rabbit aortic SMCs by inhibiting the progression from the G1 into S phase of the cell cycle and raise the possibility that cGMP-elevating vasodilators may suppress the atherogenic process by inhibiting vascular SMC proliferation.

Animals↗