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Biomedical subjects

Taro Date

Publications and source records attributed to Taro Date.

At least 19 recordsLinked to original sources
PubMed2006

Dual mechanisms underlying pulmonary vein tachycardias in a patient with paroxysmal atrial fibrillation.

We report a case of a 46-year-old man with paroxysmal atrial fibrillation who underwent pulmonary vein isolation. After a complete isolation of each pulmonary vein was performed, two different types of pulmonary vein tachycardia appeared: a regular tachycardia in the left inferior pulmonary vein with a supposed reentrant mechanism, and an irregular tachycardia in the right superior PV showing a nonreentrant character.

Atrial Fibrillation↗
PubMed2006

Elevated plasma brain natriuretic peptide level in cardiac sarcoidosis patients with preserved ejection fraction.

We sought to examine whether the plasma brain natriuretic peptide (BNP) levels are elevated in the cardiac sarcoidosis patients even with a preserved ejection fraction. The data from the patients with either pulmonary sarcoidosis without any evidence of cardiac involvement (n = 13) or cardiac sarcoidosis (n = 8) with a preserved ejection fraction (>55%) on echocardiography were analyzed. The median plasma BNP levels were significantly higher in the patients with cardiac sarcoidosis than in those with pulmonary sarcoidosis (101.5 +/- 65.1 vs. 15.6 +/- 10.5 pg/ml, p < 0.001), although there was no significant difference in left ventricular ejection fraction between the two populations. The plasma BNP level is thus considered to be a useful non-invasive biomarker for identifying a possible cardiac involvement in the sarcoidosis patients with a preserved ejection fraction.

Adult↗
PubMed2006

Behavior of atrial ectopic beats before and after pulmonary vein isolation in patients with atrial fibrillation: a reduction in the number and arrhythmogenicity of ectopic firings.

BACKGROUND: No studies evaluating in a quantitative manner the effect of pulmonary vein (PV) isolation on the behavior of atrial premature beats have been reported. OBJECTIVES: The purpose of this study was to reveal the behavior of atrial premature beats before and after PV isolation in patients with paroxysmal atrial fibrillation (AF). METHODS: In 108 patients free from AF following PV isolation, both the number of atrial premature beats and their coupling intervals before and following PV isolation were evaluated with periodic 24-hour ambulatory monitoring. RESULTS: After a successful PV isolation procedure (group 1, n = 78), the number of atrial premature beats significantly decreased with two distinct time courses: an acute reduction on the following day and a subsequent gradual decrease throughout the whole observation period. The mean atrial premature beat coupling interval at baseline was 420 +/- 30 ms, which was significantly prolonged to 560 +/- 100 ms at 3 months after PV isolation (P <.01). Although patients with AF recurrence after PV isolation (group 2, n = 30) had transiently depressed atrial premature beats shortly after the procedure, they recovered to the former level 3 months after PV isolation. Repeat PV isolation targeting the reconnected PVs successfully suppressed these residual atrial premature beats both in their number and the coupling interval in a manner similar to those in group 1. CONCLUSION: Successful PV isolation reduced the number of atrial premature beats with both rapid and gradual time courses. The residual atrial premature beats appeared less arrhythmogenic, with longer coupling intervals than those at baseline. AF recurrences after PV isolation were associated with increased atrial premature beat number and shortened coupling interval, which were depressed by reisolation of reconnected PVs.

Atrial Fibrillation↗
PubMed2006

Pseudosinus tachycardias originating from left pulmonary veins.

The case of a 55-year-old man with LV dysfunction in whom the baseline cardiac rhythm falsely mimicked a sinus rhythm (SR) but actually originated from the left superior and inferior pulmonary vein (PV) is reported. The P waves before ablation were flat in leads I and V1, negative in lead aVL, and positive in leads II, III, aVF. After the left superior PV was isolated from the left atrium, another ectopic rhythm newly appeared from the left inferior PV. Interestingly, the LV systolic function improved after the resumption of the SR, thus suggesting that tachycardia-induced cardiomyopathy might be involved in the mechanism of LV systolic disturbance.

Atrial Premature Complexes↗
PubMed2006

Effects of spironolactone during an angiotensin II receptor blocker treatment on the left ventricular mass reduction in hypertensive patients with concentric left ventricular hypertrophy.

BACKGROUND: Angiotensin II receptor blockers (ARB) are now commonly used to treat hypertension because of their beneficial effects on cardiovascular remodeling. However, ARB treatment can not inhibit the left ventricular (LV) remodeling sufficiently, which may be related with aldosterone secretion. To inhibit the action of aldosterone during ARB treatment, the additional effects of an aldosterone blocker and spironolactone (SPRL) on LV hypertrophy in patients with essential hypertension was studied. METHODS AND RESULTS: The patients with essential hypertension were randomly divided into 2 groups; 1 group was treated with an ARB, candesartan (8 mg/day), for 1 year (ARB group) and other group was treated with the ARB for the first 6 months and with the ARB plus SPRL (25 mg/day) for the next 6 months (combination group). Seventy patients who underwent echocardiography every 6 months were analyzed and were also classified into 4 subgroups of LV geometric pattern according to the LV mass index (LVMI) and the relative wall thickness (RWT). The ARB treatment and the addition of SPRL significantly reduced the blood pressure, however, both treatments did not affect the LV geometry in both groups. The ARB treatment in the subgroups of concentric LV remodeling (RWT>or=0.45 and LVMI<125) and concentric LV hypertrophy (RWT>or=0.45 and LVMI>or=125) significantly reduced RWT. However, ARB treatment in all subgroups did not affect LVMI. The addition of SPRL only in the concentric LV hypertrophy subgroup significantly reduced the LVMI, despite similar changes in blood pressure. CONCLUSIONS: These results indicated that the addition of SPRL treatment during the ARB treatment and conventional treatments is clinically useful to reduce the LVMI in hypertensive patients with concentric LV hypertrophy; however, does not improve the eccentric LV hypertrophy.

Aged↗
PubMed2005

Adenovirus-mediated expression of beta-adrenergic receptor kinase C-terminus reduces intimal hyperplasia and luminal stenosis of arteriovenous polytetrafluoroethylene grafts in pigs.

BACKGROUND: Hemodialysis vascular access dysfunction is the single most important cause of morbidity in kidney hemodialysis patients. Failure of an arteriovenous polytetrafluoroethylene (PTFE) graft, the most common form of hemodialysis access, is primarily due to intimal hyperplasia and thrombosis at the venous anastomosis. METHODS AND RESULTS: This study was aimed at evaluating the efficacy and safety of an adenoviral vector (Ad2/betaARKct) encoding the carboxyl terminus of beta-adrenergic receptor kinase (betaARKct) in a pig model of arteriovenous PTFE graft failure. Transduction of the external jugular vein with Ad2/betaARKct (5E9, 5E10, or 5E11 particles per vein) did not result in systemic toxicity, as measured by clinical and pathological assessments. Ad2/betaARKct significantly reduced neointimal hyperplasia in the graft/vein anastomosis. It also improved the graft patency rate and angiographic score, as measured histologically and angiographically, compared with vehicle or empty viral vector controls. CONCLUSIONS: Our results suggest that local administration of adenoviral vectors encoding betaARKct into the jugular vein represents a viable strategy to treat AV graft hemodialysis vascular access failure.

Adenoviridae↗
PubMed2005

Nicorandil inhibits serum starvation-induced apoptosis in vascular endothelial cells.

The Impact Of Nicorandil in Angina (IONA) randomized trial showed a significant reduction in coronary events, in patients with stable angina treated with a KATP channel opener, nicorandil. However, the impact of nicorandil on endothelial apoptosis remains to be examined. We tested the hypothesis that nicorandil has anti-apoptotic effects in endothelial cells (ECs). Apoptosis was induced by serum starvation in the culture media in human umbilical vein endothelial cells. We examined the effects of nicorandil on endothelial cell apoptosis. Cell viability after serum starvation was significantly higher in the nicorandil-treated group compared with the control group (81 +/- 8% vs. 63 +/- 3%, P < 0.01). Apoptosis, as detected by caspase 3 activation and Hoechst 33258 assay, induced by serum starvation was also effectively abrogated by the treatment of nicorandil (100 muM). The protective effects of nicorandil on endothelial survival were significantly inhibited by a specific mitochondrial KATP channel blocker, 5-Hydroxydecanoic acid. A mitochondrial permeability transition pore activator significantly abolished the anti-apoptotic effect of nicorandil in endothelial cells, indicating that the mechanism of protective effect of nicorandil is involved in the mitochondrial apoptotic pathway although it affects neither Bcl-2 nor Bax protein expression levels. In conclusion, nicorandil inhibits serum starvation-induced endothelial cell apoptosis possibly through mitochondrial KATP channels.

Angina Pectoris↗
PubMed2005

Focal source of atrial fibrillation arising from the ostium of the inferior vena cava.

A patient presented with paroxysmal atrial fibrillation (AF) caused by focal rapid discharges arising from the ostium of the inferior vena cava (IVC). Surface ECG showed typical features of AF and flutter when rapid activation at the IVC ostium was conducted to the right atrium in a 1-to-1 and 2-to-1 fashion, respectively. Discrete radiofrequency energy applications at the medial ostium of the IVC completely eliminated the atrial tachyarrhythmias.

Atrial Fibrillation↗
PubMed2005

Atrial septal pacing to resynchronize atrial contraction and improve atrial transport function.

OBJECTIVES: Atrial septal pacing via a trans-septal breakthrough site within the right atrial septum can shorten global atrial activation time, resulting in significant reduction of recurrence of atrial fibrillation events. This study examined whether this pacing method will lead to resynchronization of atrial contraction and its benefit on hemodynamic function can be maintained for 24 months. METHODS: Thirty patients with atrial fibrillation and delayed atrial conduction were enrolled (17 males, 13 females, mean age 73 +/- 7 years). Trans-septal breakthrough site within the right atrial septum was identified through pacing from the dorsal left atrium. Continuous atrial septal pacing at the trans-septal breakthrough site was performed for 24 months. Time difference (TD) between right and left atrial contractions was measured during atrial septal pacing and sinus rhythm by pulse Doppler echocardiography of the trans-tricuspid (P-At) and mitral (P-Am) blood flows (TD = P-Am - P-At). RESULTS: The atrial lead was screwed near the fossa ovalis in 29 of 30 patients. Atrial septal pacing yielded significantly shorter P wave duration (101.9 +/- 10.4 vs 139.6 +/- 14.7 msec, p < 0.001), leading to significant reduction of TD in atrial contraction (-8.8 +/- 10.0 vs 29.8 +/- 13.6 msec, p < 0.001)as compared to sinus rhythm. Both shorter P wave duration and reduced TD during atrial septal pacing remained statistically significant during the follow-up period as compared to sinus rhythm. Both left atrial diameter and A to E ratio of filling waves at mitral valve were significantly decreased at 12 months and remained decreased at 24 months. CONCLUSIONS: Atrial septal pacing at the trans-septal breakthrough site can resynchronize atrial contraction and results in improved hemodynamic effects during 24 months of follow-up.

Aged↗
PubMed2004

Expression of constitutively stable hybrid hypoxia-inducible factor-1alpha protects cultured rat cardiomyocytes against simulated ischemia-reperfusion injury.

Preconditioning in cultured cardiomyocytes elevates the expression of several protective genes including Glut-4 and heat shock protein (HSP)70. Hypoxia-inducible factor-1 (HIF-1) is known to mediate the transcriptional activation of hypoxia-responsive genes. In this study, we examined the effect of adenovirus-mediated expression of constitutively stable hybrid forms of HIF-1alpha on cardiomyocyte viability and gene expression. Cultured neonatal rat cardiomyocytes were subjected to simulated ischemia-reperfusion with or without preinfection with recombinant adenoviral vectors [Ad2/HIF-1alpha/herpes simplex virus protein VP16 and Ad2/HIF-1alpha/nuclear factor-kappaB (NF-kappaB)]. Cellular viability and mRNA levels of several cardioprotective genes were measured. We demonstrated that infection with Ad2/HIF-1alpha/VP16 and Ad2/HIF-1alpha/NF-kappaB mimicked the upregulation of the mRNA levels of vascular endothelial growth factor (VEGF), Glut-1, Glut-4, HSP70, and inducible NO synthase (iNOS) and the protection of cultured neonatal rat cardiomyocytes by late-phase preconditioning against simulated ischemia-reperfusion. The same dose of a control viral vector expressing no transgene had no effect. Preconditioning also elevated HIF-1alpha protein levels. These results suggest that adenovirus-mediated expression of HIF-1alpha/VP16 or HIF-1alpha/NF-kappaB, a constitutively stable hybrid transcriptional factor, protected cultured neonatal cardiomyocytes against simulated ischemia-reperfusion injury by inducing multiple protective genes.

Adenoviridae↗
PubMed2004

Expression of angiopoietins in renal epithelial and clear cell carcinoma cells: regulation by hypoxia and participation in angiogenesis.

The hereditary von Hippel-Lindau (VHL) syndrome predisposes sufferers to highly vascularized tumors such as renal clear cell carcinoma (RCC) and central nervous system hemangioblastoma. In RCC4 and RCC786-0 VHL- cells with VHL mutations, the protein of hypoxia-inducible factor-1alpha (HIF-1alpha) is constitutively stabilized and the mRNA levels of HIF target genes, including vascular endothelial growth factor (VEGF), are elevated. However, the expression of angiopoietins in these cells and their involvement in angiogenesis are not well known. In this study, we compared the mRNA levels of angiopoietins in human kidney proximal tubule epithelial (RPTE) and RCC4 and RCC786-0 VHL- cells. In RPTE cells, angiopoietin-4 (Ang-4) expression was selectively induced by hypoxia or by expression of a hybrid form of HIF-1alpha. Under normoxic conditions, the mRNA levels of Ang-4 were higher in RCC4 and RCC786-0 VHL- than RPTE cells. Angiopoietin-1 expression was detectable in RCC4 and RCC786-0 VHL- cells but not RPTE cells. In RCC786-0 VHL+ cells, which were stably transfected with a wild-type copy of VHL, the mRNA levels of VEGF and Ang-4 were suppressed and the hypoxic response was restored. We also demonstrated that stimulation of endothelial tube formation by conditioned medium harvested from RCC4 cells was inhibited by a soluble Tie-2 receptor. These results suggest that the angiopoietin/Tie-2 system may participate in the angiogenic response to hypoxia in renal tissues and in tumor angiogenesis in renal carcinoma.

Adenocarcinoma, Clear Cell↗
PubMed2004

A focal source of atrial fibrillation in the superior vena cava: isolation and elimination by radiofrequency ablation with the guide of basket catheter mapping.

Although it has been reported that pulmonary veins sometimes act as a focal driver of atrial fibrillation (AF), little has been reported concerning the contribution of the superior vena cava (SVC) to the maintenance of AF. Here we report a patient with sustained AF due to focal discharges inside the SVC after pulmonary vein isolation procedure. Stepwise radiofrequency current applications with the guide of multielectrode basket catheter mapping first disconnected the arrhythmogenic SVC from the right atrium and then eliminated the tachycardia.

Atrial Fibrillation↗
PubMed2004

Effects of bradykinin on cardiovascular remodeling in renovascular hypertensive rats.

Angiotensin converting enzyme (ACE) inhibitors inhibit both the formation of angiotensin II and the catabolism of bradykinin (BK). They prevent not only hypertension but also cardiac hypertrophy and fibrosis. An increase in BK level stimulates the expression of nitric oxide (NO) synthase (NOS) and induces prostaglandins, both of which are powerful vasodilator factors. The direct effect of BK against cardiac hypertrophy is still unclear. This study was performed to examine the cardioprotective effects of BK in hypertrophic models. Renovascular hypertensive (RHT) rats were treated with BK (1,000 ng/kg/day), BK+D-arginyl-[Hyp(3), Thi(5), D-Tic(7), Oic(8)]-bradykinin (HOE140) (a BK B(2) receptor antagonist), and BK+N(omega)-nitro-L-arginine methyl ester (L-NAME) (a NOS inhibitor) for 3 weeks. Blood pressure was measured and echocardiographic analysis performed during the treatment. Histological data were analyzed to confirm the hypotrophic effect of BK. Treatment with BK improved cardiac remodeling, reducing both the heart weight/body weight ratio and the left ventricular wall thickness. However, co-treatment with HOE140 or L-NAME reversed the anti-hypertrophic action of BK. In particular, cardiac fibrosis or perivascular fibrosis, along with collagen accumulation, were inhibited by treatment with BK, while HOE140 and L-NAME counteracted these changes. In addition, expressions of atrial natriuretic peptides (ANP) and brain natriuretic peptides (BNP), which are markers of cardiac abnormalities, were down-regulated by treatment with BK. These effects were reversed by co-treatment with HOE140 and L-NAME. Together, these results indicate that BK directly inhibits the progression of cardiac hypertrophy and cardiac fibrosis due to NO release via the BK B(2) receptor. The BK-NO pathway may play an important role in the progression of cardiac remodeling.

Adrenergic beta-Antagonists↗
PubMed2003

Hypoxia-inducible factor-1 mediates activation of cultured vascular endothelial cells by inducing multiple angiogenic factors.

Hypoxia-inducible factor-1 (HIF-1) mediates transcriptional activation of vascular endothelial growth factor (VEGF) and other hypoxia-responsive genes. Transgenic expression of a constitutively stable HIF-1alpha mutant increases the number of vascular vessels without vascular leakage, tissue edema, or inflammation. This study aimed to investigate the molecular basis by which HIF-1 mediates the angiogenic response to hypoxia. In primary human endothelial cells, hypoxia, desferrioxamine, or infection with Ad2/HIF-1alpha/VP16, an adenoviral vector encoding a constitutively stable hybrid form of HIF-1alpha, increased the mRNA and protein levels of VEGF, angiopoietin-2 (Ang-2), and angiopoietin-4 (Ang-4). Infection with Ad2/CMVEV (a control vector expressing no transgene) had no effect. Angiopoietin-1 (Ang-1) expression was not detected in human endothelial cells. Ang-4 was also induced by hypoxia or Ad2/HIF-1alpha/VP16 in human cardiac cells, whereas Ang-1 expression remained unchanged. Recombinant Ang-4 protein protected endothelial cells against serum starvation-induced apoptosis and increased cultured endothelial cell migration and tube formation. Ad2/HIF-1alpha/VP16 stimulated endothelial cell proliferation and tube formation. Hypoxia- or Ad2/HIF-1alpha/VP16-induced tube formation was significantly reduced by a Tie-2 inhibitor. These results suggest that HIF-1 mediates the angiogenic response to hypoxia by upregulating the expression of multiple angiogenic factors. Ang-4 can function similarly as Ang-1 and substitute for Ang-1 to participate in hypoxia-induced angiogenesis. Activation of the angiopoietin/Tie-2 system may play a role in the ability of HIF-1 to induce hypervascularity without excessive permeability.

Angiogenesis Inducing Agents↗
PubMed2003

Myocardial expression of baculoviral p35 alleviates doxorubicin-induced cardiomyopathy in rats.

The clinical use of doxorubicin, one of the most effective antitumor drugs, is limited by its cardiotoxicity, which results in irreversible cardiomyopathy and congestive heart failure. This study aimed to evaluate a gene therapy approach using adenovirus-mediated expression of p35, a baculoviral antiapoptotic gene, for alleviating doxorubicin-induced cardiomyopathy. In cultured neonatal rat cardiomyocytes, transduction with a recombinant adenoviral vector expressing p35 (Ad2/CMVp35) but not a control adenoviral vector expressing no transgene (Ad2/CMVEV) significantly inhibited doxorubicin-induced increase in cellular reactive oxygen species (ROS), the activity of caspases 8 and 3, cytochrome c release, and apoptosis. Direct injection of Ad2/CMVp35 into the left ventricular wall inhibited myocardial caspase 3 activity and apoptosis and improved left ventricular performance in rats treated with doxorubicin, whereas the same dose of Ad2/CMV beta gal encoding beta-galactosidase had no effect. These results suggest that adenovirus-mediated expression of p35 protects cardiomyocytes against doxorubicin cardiotoxicity, possibly by inhibiting caspase activity and by reducing cellular ROS levels. Localized delivery of gene transfer vectors expressing an antiapoptotic protein such as p35 to the myocardium may represent a therapeutic approach to alleviate doxorubicin-induced cardiomyopathy.

Adenoviridae↗