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S Hosoda

Publications and source records attributed to S Hosoda.

At least 37 records · Page 2Linked to original sources

Idiopathic ventricular fibrillation induced with vagal activity in patients without obvious heart disease.

BACKGROUND: Recently, idiopathic ventricular fibrillation (VF) has gained much attention. Although several subgroups have been described, its pathogenesis, mechanism, treatment, and prognosis remain unknown. METHODS AND RESULTS: We studied six cases of idiopathic VF with transient late r' waves and ST elevation (late r'/ST elevation) in leads V1 through V3. Late r'/ST elevation was augmented before and after VF episodes. Signal-averaged ECGs showed late potentials even when no late r'/ST elevation occurred. During late r', a conduction delay was observed by use of body-surface maps at the anterior wall and outflow tract of the right ventricle without inhomogeneity of the repolarization phase. There was a decrease or total disappearance of late r'/ST elevation with isoproterenol, atropine, and exercise stress testing and induction or exacerbation with propranolol, edrophonium, and hyperventilation. VF was induced by programmed electrical stimulation in all cases but two, in which it was induced only after edrophonium injection. In two cases, VF was exacerbated by propranolol, and in all cases, it was uninducible with isoproterenol. Heart rate spectral analysis just before VF episodes showed a sudden rise in vagal activity in two cases. As the VF mechanism, a conduction delay exists at the anterior wall and outflow tract of the right ventricle that is possibly exacerbated by an abrupt rise in vagal activity, inducing random reentry that results in VF. Class I antiarrhythmic agents and beta-blockers were ineffective for this VF. All subjects required implantable cardioverter-defibrillators. CONCLUSIONS: We propose this VF associated with late r'/ST elevation in the precordial leads and influenced by vagal activity as a new possible mechanism of idiopathic VF.

Adult↗

ATP-activated cationic current in rabbit sino-atrial node cells.

The electrophysiological effect of extracellular ATP was investigated in voltage-clamped single cells from the rabbit sino-atrial node. External 0.5 mM ATP consistently activated a time-independent, weakly inwardly rectifying current (2.26 +/- 0.14 pA/pF at -100 mV, n = 23). This external ATP-activated current increased in a dose-dependent manner over the concentration range 0.01 to 1 mM ATP. However, non-hydrolysable ATP analogs (a, beta-methylene ATP and beta,r-methylene ATP) failed to activate this current. Moreover, adenosine, adenosine monophosphate and adenosine diphosphate were all ineffective in eliciting the ATP-activated current over the concentration range 0.5 to 1 mM, suggesting that it is regulated via the P2-purinoreceptor. The permeability sequence for the ATP-activated current among different cations (determined from reversal potential measurements) was 1.09: 1: 1: 0.24: 0.22 for K+, Na+, Cs+, Tris and N-methyl-D-glucamine. The current component was not affected by substitution of external Cl- by aspartate or by the application of a stilbene-derivative Cl- channel blocker. Thus, the ATP-activated current in rabbit sino-atrial node cells was non-selective for monovalent cations, and could be carried by large molecular ions, such as N-methyl-D-glucamine or Tris. We suggest that it might make some contribution to the chronotropic effects seen on release of transmitters from autonomic nerve endings in the heart.

Adenosine↗

Increased cardiac sympathetic activity in patients with hypothyroidism as determined by iodine-123 metaiodobenzylguanidine scintigraphy.

Clinical manifestations of hypothyroidism, such as bradycardia, suggest decreased sympathetic tone. However, previous studies in patients with hypothyroidism have suggested that increased plasma noradrenaline (NA) levels represent enhanced general sympathetic activity. As yet, cardiac sympathetic activity (CSA) in hypothyroidism has not been clarified. To evaluate CSA in patients with hypothyroidism, iodine-123 metaiodobenzylguanidine (MIBG) scintigraphy was performed in eight patients with hypothyroidism before therapy and in ten normal control patients. Planar images were obtained at 15 min and 4 h after injection of MIBG. The ratio of early myocardial uptake to the total injected dose (MU) and myocardial clearance of MIBG within 4 h p.i. (MC) were calculated. Plasma NA was also measured, and echocardiography was performed in all patients. Those patients with hypothyroidism in the euthyroid state after medical therapy were also evaluated in a similar manner. Left ventricular ejection fraction, measured by echocardiography, did not differ significantly between the groups. NA, MU and MC were significantly higher in patients with hypothyroidism than in controls, and all parameters were decreased after therapy. MC was well correlated with NA in hypothyroidism (r=0.86) before therapy. We conclude that CSA is increased in patients with hypothyroidism, in parallel with the enhanced general sympathetic activity.

3-Iodobenzylguanidine↗

Functional activity of the CFTR Cl- channel in human myocardium.

The cyclic AMP (cAMP)-dependent chloride channel in the heart has been identified in various species as the cystic fibrosis transmembrane conductance regulator (CFTR). Although functional expression of the channel in the human atrium has been reported, we could not induce any cAMP-dependent chloride conductance in the atrial cells even with maximal cAMP stimulation, whereas the conductance could be induced in rabbit ventricular cells. To clarify the discrepancy between the results, we examined the level of CFTR mRNA expression in both conductance-positive (human colonic epithelium and rabbit ventricle) and -negative (human atrium) tissues. Total RNA samples prepared from these tissues were subjected to the reverse transcription-polymerase chain reaction (RT-PCR). While CFTR transcripts were amplified from the conductance-positive samples, no amplified products could be detected from the conductance-negative sample. A nested PCR performed on the RT-PCR products of the conductance-negative sample resulted in successful amplification of the transcripts, indicating that the level of the CFTR mRNA expression in human atrium is extremely low compared with that in colonic epithelium and rabbit ventricle. The same molecular results were observed in human ventricular tissues. A nucleotide sequencing of the amplified transcripts showed that exon 5 of the CFTR gene was not alternatively spliced in human atrium and ventricle, and both the exon 5 spliced and unspliced isoforms were expressed in rabbit ventricle, unlike the findings of previous reports. Our data suggest that the amount of CFTR expressed in human myocardium might be physiologically insufficient to activate detectable cAMP-dependent chloride conductance.

Adolescent↗

Disopyramide improves the balance between myocardial oxygen supply and demand in patients with hypertrophic obstructive cardiomyopathy.

We evaluated the effects of disopyramide in terms of the balance between myocardial oxygen supply and demand in patients with hypertrophic obstructive cardiomyopathy (HOCM). The myocardial oxygen supply was evaluated by measuring coronary flow velocity and the myocardial oxygen demand was assessed by the pressure-volume area (PVA). The time velocity integral of coronary flow did not change significantly (20 +/- 6 to 21 +/- 8 cm), but the peak left ventricular pressure and left ventricular external work decreased significantly (206 +/- 44 to 157 +/- 37 mmHg, P < 0.001; 1.09 +/- 0.33 to 0.80 +/- 0.23 J/beat, P < 0.001) after disopyramide administration. From theoretical analysis using these data, we concluded that disopyramide improves the myocardial oxygen supply-demand balance in patients with HOCM.

Adult↗

Cardiac memory in patients with intermittent Wolff-Parkinson-White syndrome.

This study used body surface mapping to evaluate the ventricular repolarization process in the absence of delta waves in 13 patients with the intermittent Wolff-Parkinson-White (WPW) syndrome. The findings were compared with data from 30 normal individuals and 50 patients with the overt WPW syndrome. The QRST isointegral maps of patients with the overt WPW syndrome exhibited abnormal areas and the QRST departure maps showed a peculiar distribution to each accessory pathway site. The QRST isointegral map exhibited abnormal areas in 11 of the 13 cases (85%) of the intermittent WPW syndrome in the absence of delta waves. In 8 of these 11 cases (73%), the distribution of the departure map resembled that in the overt WPW syndrome. These findings suggest that abnormal ventricular repolarization due to cardiac memory is present in patients with the intermittent WPW syndrome even in the absence of delta waves.

Adolescent↗

A prospective, randomized, double-blind multicenter trial of a single bolus injection of the novel modified t-PA E6010 in the treatment of acute myocardial infarction: comparison with native t-PA. E6010 Study Group.

OBJECTIVES: This prospective, randomized, double-blind multicenter trial evaluated the efficacy and safety of a single bolus injection of the novel modified tissue-type plasminogen activator (t-PA) E6010 in the treatment of acute myocardial infarction compared with that of native t-PA. BACKGROUND: E6010 is a novel modified t-PA with a prolonged half-life (t1/2 alpha > or = 23 min) compared with native t-PA (t1/2 alpha = 4 min). E6010 can be administered in patients as a single intravenous bolus injection, and early recanalization can be expected. METHODS: The efficacy of E6010 was compared with that of native t-PA in 199 patients with acute myocardial infarction who were treated within 6 h of onset in a prospective, randomized, double-blind multicenter trial. Patients were given either 0.22 mg/kg body weight of E6010 intravenously over 2 min or native t-PA (tisokinase) 28.8 mg or 14.4 million IU (10% of the total dose over 1 to 2 min, the remainder infused over 60 min). RESULTS: The primary end point was the recanalization rate of the infarct-related coronary artery at 60 min after the start of treatment. Time to reperfusion was shorter in the E6010 group than in the native t-PA group. Thrombolysis in Myocardial Infarction flow grade 2 or 3 recanalization at 15, 30, 45 and 60 min after administration was observed in 37%, 62%, 74% and 79% (95% confidence interval [CI] 70% to 87%) of the E6010-treated patients and in 14%, 32%, 50% and 65% (95% CI 55% to 74%) of native t-PA-treated patients, respectively (p = 0.032 at 60 min). CONCLUSIONS: The present study indicates that, compared with native t-PA, a single bolus injection of E6010 over 2 min produces a higher rate of early recanalization of the infarct-related coronary artery without fatal bleeding complications.

Aged↗

Contribution of phosphodiesterase isozymes to the regulation of the L-type calcium current in human cardiac myocytes.

1. To determine the contribution of the various phosphodiesterase (PDE) isozymes to the regulation of the L-type calcium current (ICa(L)) in the human myocardium, we investigated the effect of selective and non-selective PDE inhibitors on ICa(L) in single human atrial cells by use of the whole-cell patch-clamp method. We repeated some experiments in rabbit atrial myocytes, to make a species comparison. 2. In human atrial cells, 100 microM pimobendan increased ICa(L) (evoked by depolarization to +10 mV from a holding potential of -40 mV) by 250.4 +/- 45.0% (n = 15), with the concentration for half-maximal stimulation (EC50) being 1.13 microM. ICa(L) was increased by 100 microM UD-CG 212 by 174.5 +/- 30.2% (n = 10) with an EC50 value of 1.78 microM in human atrial cells. These two agents inhibit PDE III selectively. 3. A selective PDE IV inhibitor, rolipram (1-100 microM), did not itself affect ICa(L) in human atrial cells. However, 100 microM rolipram significantly enhanced the effect of 100 microM UD-CG 212 on ICa(L) (increase with UD-CG 212 alone, 167.9 +/- 33.9, n = 5; increase with the two agents together, 270.0 +/- 52.2%; n = 5, P < 0.05). Rolipram also enhanced isoprenaline (5 nM)-stimulated ICa(L) by 52.9 +/- 9.3% (n = 5) in human atrial cells. 4. In rabbit atrial cells, ICa(L) at +10 mV was increased by 22.1 +/- 9.0% by UD-CG 212 (n = 10) and by 67.4 +/- 12.0% (n = 10) by pimobendan (each at 100 microM). These values were significantly lower than those obtained in human atrial cells (P < 0.0001). Rolipram (1-100 microM) did not itself affect ICa(L) in rabbit atrial cells. However, ICa(L) was increased by 215.7 +/- 65.2% (n = 10) by the combination of 100 microM UD-CG 212 and 100 microM rolipram. This value was almost 10 times larger than that obtained for the effect of 100 microM UD-CG 212 alone. 5. These results imply a species difference: in the human atrium, the PDE III isoform seems dominant, whereas PDE IV may be more important in the rabbit atrium for regulating ICa(L). However, PDE IV might contribute significantly to the regulation of intracellular cyclic AMP in human myocardium when PDE III is already inhibited or when the myocardium is under beta-adrenoceptor-mediated stimulation.

1-Methyl-3-isobutylxanthine↗

Influence of early coronary reperfusion on QT interval dispersion after acute myocardial infarction.

We studied the influence of early coronary reperfusion on QT interval dispersion in patients with acute myocardial infarction (MI). There were 54 males and 18 females with a mean age of 60 +/- 10 years. Of the 51 patients with recanalization of the infarct related vessel in the recovery phase, 28 (group A) had early coronary reperfusion (5.5 +/- 2.7 hours), 23 other patients (group B) were not confirmed with early coronary reperfusion. Twenty-one patients (group C) did not undergo recanalization of the infarct related vessel in the recovery phase. Corrected QT (QTc) maximum, QTc minimum, and QTc dispersion calculated as the difference between the maximum and minimum QTc intervals, were compared among these three groups at both acute and recovery phase. At the acute phase after MI, there were no significant differences in the QTc maximum, QTc minimum, QT dispersion, and QTc dispersion among these three groups. At the recovery phase after MI, there were also no significant differences in the QTc maximum and QTc minimum. However, there were significant differences in the QT dispersion (0.035 +/- 0.010 in group A, 0.049 +/- 0.015 in group B, and 0.061 +/- 0.031 s in group C, respectively; P = 0.0001), and QTc dispersion (0.038 +/- 0.012 in group A, 0.050 +/- 0.015 in group B, and 0.063 +/- 0.032 s in group C, respectively; P = 0.0003) among the three groups. Comparison of QTc dispersion between acute and recovery phase revealed significant reduction from acute to recovery phase in group A. The number of premature ventricular contraction was lower in group A and B than group C. In summary, early coronary reperfusion may reduce electrophysiological instability by reducing QT dispersion in the recovery phase after acute MI.

Cardiac Catheterization↗

An index predicting coronary heart disease: LDL/HDL x 5.

Atherosclerotic changes in the coronary artery are exacerbated by the balance between LDL, which carries cholesterol into the arterial wall, and HDL, which carries it out from the wall. The molecular weight of LDL is about 2 x 10(6) and that of HDL is about 4 x 10(5), which is almost 1/5 of the molecular weight of LDL. For this reason, LDL/HDL x 5 should be a good indicator of coronary heart disease. We evaluated this index in two subject groups. At first, we determined whether it could predict the incidence of effort angina in participants of a medical examination system. Most of the subjects were healthy and good candidates for primary prevention. LDL/HDL x 5 was a more sensitive index predicting effort angina than total cholesterol, LDL or HDL. The concentrations of HDL were significantly lower in myocardial infarction patients at all ages in both sexes. The average serum concentration of HDL was 56.6 +/- 15.0 mg/dl in the medical examination group and 38.9 +/- 12.2 mg/dl in the AMI group. We tested whether our new index, LDL/HDL x 5, could predict the incidence of re-infarction in patients with myocardial infarction who were candidates for secondary prevention. LDL/HDL x 5 was a more sensitive index predicting re-infarction than total cholesterol, LDL or HDL.

Aged↗

[Transesophageal echocardiographic findings in patients after heart transplantation].

The diagnostic value of transesophageal echocardiography was investigated in heart transplant recipients, i.e., four patients who received orthotopic heart transplantation and one patient who received total heart transplantation. Donor-recipient atrial anastomosis was identified in the four patients with orthotopic heart transplantation, but not in the patient with total heart transplantation. Transthoracic and transesophageal echocardiography detected no thrombus or spontaneous echo contrast in any of the patients. Color Doppler transesophageal echocardiography showed trivial mitral regurgitation in all patients. Total heart transplantation resulted in no protruding suture line and normal atrial cavity size. The patient with total heart transplantation showed some difference in the peak flow velocity of the right and left pulmonary veins (left superior pulmonary vein: 48 cm/sec; right superior pulmonary vein: 86 cm/sec), possibly due to stenosis at the suture line between the left atrium and right superior pulmonary vein, or compression of the right superior pulmonary vein by the anastomosis between the superior vena cava and right atrium. Transesophageal echocardiography was helpful for detecting thrombus in the left atrium and left atrial appendage after heart transplantation, and allowed evaluation of the flow pattern in the pulmonary veins and left atrial appendage as well as abnormal flow in the atrium. In conclusion, transesophageal echocardiography is useful in the follow-up of heart transplant recipients.

Adult↗

[Reproducibility of spasm in patients with long-term remission of vasospastic angina by medical treatment].

The reproducibility of coronary vasospasm was assessed in nine patients with complete remission of vasospastic angina by medical treatment by reexamination at intervals of mean [+/-SD] 5.7 +/- 0.9 years. Twenty-one segments were defined as spastic, demonstrating more than 90% narrowing after acetylcholine injection at the initial angiography. The degree of spasticity, type of spasm (diffuse or focal) and coronary artery diameter in these segments at the initial and follow-up studies were compared. Of the 21 segments, 17 (81%) still had some spasticity (> 25%) at the follow-up study and 8 (38%) of these 17 showed spasticity with greater than 90% narrowing. On the other hand, spasm was not reprovoked in 4 (19%) segments. Luminal diameter of the spastic segments decreased significantly at the follow-up study (2.52 +/- 0.83 vs 2.26 +/- 0.62 mm, p = 0.01), but percentage stenosis was not different between the initial and follow-up studies (9.1 +/- 7.2 vs 10.3 +/- 8.0%, NS). The reproducibility of the type of spasm provoked was 83%. Coronary vasospasticity persists to some extent in spite of complete remission of angina by medical treatment, and the type of spasm provoked has high reproducibility. Therefore, the cessation of drug treatment should be done carefully.

Acetylcholine↗

[Right atrial thrombus recognized 18 years after tricuspid valve replacement: a case report].

A 53-year-old man, who had undergone tricuspid valve replacement with Hancock valve and direct closure of a ventricular septal defect when aged 34 years, was admitted with signs of right heart failure. Two-dimensional echocardiography showed bioprosthetic tricuspid valve malfunction with right atrial thrombus. He was treated by tricuspid valve replacement using a Hancock II valve and removal of the right atrial thrombus with remarkable improvement. Transesophageal echocardiography was the most useful method for recognizing the presence of right atrial thrombus and assessing its actual or potential hemodynamic effects.

Echocardiography↗

Experience of patients with end-stage heart failure who underwent heart transplant at UCLA.

From 1993 to 1997, nine Japanese heart transplant candidates were accepted by the University of California at Los Angeles (UCLA) Medical Center, because no donor heart was available in Japan from a brain-dead patient. In all nine heart transplant patients described in this investigation, the preoperative diagnosis was dilated cardiomyopathy. One patient underwent implantation with a Novacor left ventricular assist device (Baxter Japan, Tokyo, Japan) as a bridge to heart transplant. All patients survived surgery and for a long-term period. The actuarial 1-year and 3-year survival curves of these patients were both 100%. The postoperative functional status was New York Heart Association Class 1 in all patients (100%). Immunosuppressive triple drug therapy (azathioprine, steroids, and cyclosporine) was given in seven patients; in two patients, cyclosporine was withdrawn and replaced by FK506 due to refractory rejection. The incidence of acute rejection per patient of more than grade 3 according to the International Society for Heart and Lung Transplantation was 6% within 3 months and 4.5% in 3-6 months; there was no rejection episode more than 6 months after transplantation. Post-transplant coronary artery disease was seen in two patients. However, no disease progression was seen after diltiazem therapy. These results may encourage heart transplantation in Japan.

Adult↗

The role of cadherin-catenin-cytoskeleton complex in angiogenesis: antisense oligonucleotide of plakoglobin promotes angiogenesis in vitro, and protein kinase C (PKC) enhances angiogenesis through the plakoglobin signaling pathway.

Angiogenesis plays an important role in various diseases and conditions such as malignant tumor, wound healing, and atherosclerosis. Since cell-to-cell adhesion may play a key role in angiogenesis, we investigated the effect of the cadherin-catenin-cytoskeleton complex on angiogenesis in human umbilical vein endothelial cells (HUVECs). Immunofluorescence staining revealed that alpha-catenin, beta-catenin, and plakoglobin were concentrated at cell-cell contacts in HUVECs. Antisense oligonucleotide (AS-oligo), complementary to the region of human plakoglobin was dissolved in saline and applied to the media at 1 mM every 12 h for 4 days, and sense oligonucleotide (S-oligo) was used as control. HUVEC migration from an injury line was enhanced by AS-oligo. Interestingly, HUVECs migrated in line with S-oligo, and in a scattered fashion with AS-oligo. Tube formation on Matrigel occurred earlier with AS-oligo than with S-oligo. These findings indicate that plakoglobin inhibited HUVEC migration and tube formation (angiogenesis) by regulating cell-cell adhesion.

Cadherins↗

Role of QT interval prolongation in the creation of spiral wave type reentry.

The inducibility of reentry was compared for four QT patterns in a heart conduction simulation model. Local (L) and gradual (G) QT prolongation models are more susceptible to reentry induction than the no (N) QT prolongation model (reentry induced episodes for N, L, and G numbered 90, 120, and 122, respectively). This increased vulnerability was diminished when the QT interval was prolonged at all simulation sites (reentry induced episodes for the diffuse QT prolongation model, D model, numbered 82). Decreased QT dispersion might be important for the prevention of reentry induction regardless of whether the QT interval is increased.

Action Potentials↗

Measurement of plasma annexin V by ELISA in the early detection of acute myocardial infarction.

Annexin V is a calcium binding protein which is widely present in various cells and tissues. Using annexin V which we isolated and purified from human cardiac muscle, we prepared an anti-human cardiac annexin V monoclonal antibody. Identification of annexin V was made by means of partial amino acid sequences. An enzyme-linked immunosorbent assay (ELISA) was developed using this monoclonal antibody and anti-canine cardiac annexin V polyclonal antibody. With this ELISA, plasma annexin V concentration was measured in 196 normal healthy individuals, 23 acute myocardial infarction (AMI) patients who were hospitalized within 6 h after the onset of chest pain, and 130 patients with other diseases, including lung, liver and kidney disease. The plasma annexin V concentration in normal healthy individuals was 1.7 +/- 0.6 ng/ml (mean +/- S.D.), while that in AMI patients was elevated to 13.2 +/- 6.8 ng/ml (P < 0.0001) at the time of initial blood drawing, 3.2 +/- 1.5 h after onset of pain, and these values were higher than normal in 21 out of 23 cases (91.3%) of AMI. In all cases excepting 3, annexin V concentration immediately decreased after the onset of pain. The annexin V concentration in patients with old myocardial infarction, chest pain syndrome, valvular heart disease, lung disease and kidney disease was 1.8 +/- 0.8, 2.0 +/- 0.7, 1.7 +/- 1.1, 2.3 +/- 1.4 and 2.1 +/- 1.2 ng/ml, respectively, being within normal limits. The values in liver disease patients and trauma patients were 3.7 +/- 2.7 (P < 0.05) and 3.3 +/- 2.4 (P < 0.05) ng/ml, respectively, being slightly higher than that in normal healthy individuals.

Adult↗