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Biomedical subjects

Seibu Mochizuki

Publications and source records attributed to Seibu Mochizuki.

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

Post-transcriptional downregulation of sarcolipin mRNA by triiodothyronine in the atrial myocardium.

Thyroid hormone-mediated positive cardiotropic effects are differently regulated between the atria and ventricles. This regulation is, at least in part, dependent on sarcoplasmic reticulum (SR) proteins. Sarcolipin, a homologue of phospholamban, has been recently identified as an atrium-specific SR protein. The expression of sarcolipin mRNA was significantly decreased in the atria of mice with hyperthyroidism and in 3,5,3'-triiodo-l-thyronine-treated neonatal rat atrial myocytes. Promoter activity and mRNA stability analyses revealed that thyroid hormone post-transcriptionally down regulated the expression of sarcolipin mRNA. The atrium-specific effect of thyroid hormone may occur in part through the regulation of atrial sarcolipin gene expression.

Animals↗
PubMed2006

Pravastatin prevents myocardium from ischemia-induced fibrosis by protecting vascular endothelial cells exposed to oxidative stress.

HYPOTHESIS: Statins potently prevents cardiac myocytes from acute ischemia besides chronic inhibition of cholesterol synthesis. We investigated how pravastatin preserves the cardiac function after myocardial infarction (MI). METHODS: Echocardiographically comparing rats with myocardial ischemia (MI group) with those treated with pravastatin (MI/statin group), we found that cardiac contractility was statistically preserved in the MI/statin whereas it was deteriorated in MI group. RESULTS: Histochemical analysis suggested that ischemia-induced cardiac fibrosis was prevented by pravastatin. Because there was no significant myocyte apoptosis reflecting myocytes loss between two groups, ischemia-induced interstitial fibrosis might affect the contractility. CONCLUSION: We hypothesized that statin may directly affect vascular endothelial cells regulating blood supply to the myocardium rather than affecting myocytes. Pravastatin perturbed H2O2-induced endothelial NOS reduction and inhibited H2O2-increased caspase-3 activation in cultured vascular endothelial cells. These data suggested that pravastatin prevent cardiac dysfunction by acting on vascular endothelial cells. Furthermore, early administration of pravastatin to the patients during acute onset of myocardial infarction may be beneficial to prevent myocardial damage caused by fibrosis associated with ischemia.

Animals↗
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

Documented subacute stent thrombosis within thirty days after stenting with sirolimus-eluting stent (Cypher) for acute myocardial infarction: a Japanese single center retrospective non-randomized study.

BACKGROUND: The incidence of subacute stent thrombosis (SAT) within 30 days after stenting with a sirolimus-eluting stent (Cypher) for acute myocardial infarction (AMI) was retrospectively compared to that with bare-metal stents (BMS). METHODS AND RESULTS: Among 559 lesions in 558 consecutive AMI from April 2003 to February 2006, the incidence of documented SAT after Cypher implantation (2/276 lesions, 0.72%) was almost the same as for BMS (2 cases, 0.71%). Aspirin (81-100 mg/day) plus ticlopidine (200 mg/day) were administered continuously after admission in all 4 cases. CONCLUSION: Documented SAT did not increase after stenting with Cypher for AMI under aspirin plus ticlopidine.

Aged↗
PubMed2006

Cross-bridge-dependent change in Ca2+ sensitivity is involved in the negative inotropic effect of nifedipine in aequorin-injected ferret ventricular muscles.

BACKGROUND: We hypothesized that the negative inotropic effect of nifedipine (Nif) on cardiac ventricular muscle is partly due to the cross-bridge-dependent decrease of Ca2+ sensitivity of the myofilaments as well as the decrease in Ca2+ influx. METHOD AND RESULTS: We used aequorin-injected ferret papillary muscles and measured the slope of the extra-Ca(2+)-tension relation which expresses the change in the Ca2+ sensitivity through the feedback from the cross-bridges. Twitch tension was decreased significantly by 0.5 micromol/L Nif accompanying a significant reduction of the Ca2+ transient peak. When Nif (0.2-0.5 micromol/L) was added to the solution with 8 mmol/L Ca2+, the slope of the extra-Ca2+-tension relation became steeper in a concentration-dependent manner, which was similar to the change in the slope when the concentration of Ca2+ was decreased from 8 to 1 mmol/L in the absence of Nif. BAY-K 8644 (0.3 micromol/L), a dihydropyridine receptor agonist, showed the opposite effect on the slope of the extra-Ca2+-tension relation to that observed in Nif. However, 2,3-butanedione monoxime (3 mmol/L), an inhibitor of the active cross-bridges, antagonized the effect of BAY-K 8644. CONCLUSION: Nif exerts its negative inotropic effect on cardiac muscle by suppressing Ca2+ binding to troponin C via the inhibition of the L-type Ca2+ channel, and by the cross-bridge-dependent decrease in the Ca2+ sensitivity, as in low extracellular Ca2+ concentration.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2006

Cross-bridge-dependent change of the Ca2+ sensitivity during relaxation in aequorin-injected tetanized ferret papillary muscles.

UNLABELLED: BACKGROUND The aim of the present study was to indicate the cross-bridge-dependent change in the Ca2+ affinity of troponin-C (TnC) during relaxation in an intact preparation, because the intracellular mechanism of relaxation is not fully understood, although several methods of evaluating global diastolic function have been reported. METHODS AND RESULTS: The aequorin method was used with intact ferret papillary muscles and a tetanic contraction was induced by a repetitive electrical stimulation in the presence of ryanodine. The extra-Ca2+, the transient increase in the intracellular Ca2+ concentration in response to a rapid reduction in muscle length, which reflects the change in the Ca2+ affinity of TnC because of cross-bridge detachment, was measured, and the cross-bridge-dependent change in the Ca2+ affinity of TnC was estimated by observing the change in the slope of the extra-Ca2+ -tension relation. The extra-Ca2+ -tension relation measured during relaxation became steeper than that during contraction in all cases. The extra-Ca2+ -tension relation became steeper in the presence of 20 mmol/L caffeine during contraction in all cases. CONCLUSION: During relaxation, the downstream-dependent change in the Ca2+ affinity of TnC was enhanced, compared with that during contraction, because of a decrease in the number of attached cross-bridges.

Aequorin↗
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↗
PubMed2006

Effects of eplerenone and salt intake on left ventricular remodeling after myocardial infarction in rats.

Eplerenone, a selective aldosterone blocker, has been shown to attenuate cardiac fibrosis and decrease cardiovascular events in both experimental and clinical studies. We examined the cardioprotective effect of eplerenone in myocardial infarction (MI) rats receiving different levels of salt in their diet. The MI rats were randomly divided into five groups: Group CL, animals received a low-salt diet (0.015%); Group EpL, a low-salt diet with eplerenone (100 mg/kg/day in food); Group CH, a high-salt diet (0.9%); Group EpH, a high-salt diet with eplerenone; and Group C, a normal salt diet (0.3%). These diets were continued for 4 weeks. Echocardiographic and histomorphological examinations revealed that the administration of eplerenone significantly improved the cardiac function, significantly suppressed compensatory cardiac hypertrophy and significantly reduced cardiac fibrosis in both the interstitial and the perivascular areas in the high-salt diet group (Group EpH). However, eplerenone had no observable effects in the low-salt diet group (Group EpL). Also, these examinations demonstrated that the left ventricular remodeling after MI was suppressed and the cardiac function was improved in the group receiving a low-salt diet without eplerenone (Group CL), even though there was a significant increase of aldosterone level in blood, in comparison to the group receiving a high-salt diet without eplerenone (Group CH). These results indicate that the cardioprotective effect of eplerenone varies depending on the salt intake.

Aldosterone↗
PubMed2006

Facilitation of rotablator-stenting by measuring angiographic lesion length with the navicath (type-MUTO), a new measuring microcatheter.

In the present study, the usefulness and feasibility of a new measuring microcatheter, the Navicath (Type-MUTO) microcatheter, for facilitating the stenting procedure subsequent to ablation using a rotablator (rota-stenting) is described. A method for measuring the length of the targeted lesion (lesion length) angiographically with the Navicath when exchanging the guide wires is presented using 2 representative cases of rota-stenting. In addition, the validity of the selected stent according to the measurement of lesion length with the Navicath was evaluated by comparing the length of the selected stent with lesion length before PCI measured by quantitative coronary angiography. Based on the results obtained, we believe the Navicath is useful for facilitating rota-stenting, and may even be applicable to PCI in general.

Aged↗
PubMed2006

Myocyte morphological characteristics differ between the phases of pulmonary hypertension-induced ventricular hypertrophy and failure.

Pulmonary hypertensive model rats were prepared by treating them with monochrotaline (MCT). Using these model rats, we examined myocyte remodeling in the right ventricle in response to increased right ventricular pressure. Male Sprague-Dawley rats were divided into 2 groups. Group M received MCT and group C received physiological saline. The 2 groups were examined at weeks 2, 5, and 7 after MCT or saline injection, respectively. At week 2, a significant difference in cell form was not observed in either group. At week 5, cell volume and myocyte cross-sectional area (CSA) of the right ventricle in group M were significantly greater than those in group C. At week 7, cell volume, CSA, and cell length of the right ventricle in group M were all significantly greater than those in group C. These results suggest that pulmonary hypertension causes hypertrophy, accompanying the enlargement of CSA in the right ventricle, and that cells lengthen in the phase of right ventricular failure. These results are similar to the changes observed in left ventricular myocytes due to overload pressure. Both right and left ventricular myocytes may share a common mechanism for myocyte remodeling as an adaptive and maladaptive response to increased ventricular pressure.

Animals↗
PubMed2006

Effectiveness of a sirolimus-eluting stent (Cypher) for diffuse in-stent restenosis inside a bare metal stent.

We estimated the benefit of a sirolimus-eluting stent (SES, Cypher) for diffuse (> 10 mm) in-stent restenosis (ISR) inside bare metal stents (BMS) because the feasibility of the SES was not confirmed after its recent approval in Japan. Clinical and angiographic outcomes after SES implantation to 93 diffuse ISR were compared with those of 3 groups treated by plain old balloon angioplasty (POBA, (n = 54)), cutting balloon angioplasty (CB, (n = 24)), and BMS (n = 41) in a series of 153 patients whose follow-up quantitative coronary angiography (QCA) evaluated 3-9 months after the treatments was obtained from January 2003 through December 2005. For 33 lesions in the SES group, 12-month follow-up QCA results were obtained and compared with those at 6 months. Ticlopidine (200 mg/day) was prescribed for at least 12 weeks after SES implantation and for 2 weeks after BMS in addition to aspirin (81-100 mg/day). Patient characteristics and the characteristics of previous implanted BMS in the SES group were not significantly different from those in the other groups. Death from cardiac causes and nonfatal myocardial infarction did not occur in any group. Stent thrombosis was not observed in the BMS and SES groups. The incidence of repeat target lesion revascularization (re-TLR) in the SES group (3.23%) was significantly lower compared with that of the POBA (37.0%), CB (25.0%), and BMS (29.3%) groups (P < 0.001, respectively). Late loss in the SES group (0.44 +/- 0.41 mm) was significantly smaller than that in the BMS group (1.34 +/- 0.74 mm) (P < 0.05). The rate of recurrent ISR (re-ISR) in SES (5.38%) was significantly lower than that in POBA (46.3%), CB (41.7%), and BMS (46.3%) (P < 0.001, respectively). The QCA variables at 6 months in the SES group were not significantly different from those at 12 months. Thus, SES implantation for diffuse ISR was far superior since it markedly reduced the incidence of re-TLR with re-ISR at up to 6-months follow-up. In addition, this angiographic patency after SES implantation continued until 12 months.

Angioplasty, Balloon, Coronary↗
PubMed2006

Combined treatment with valsartan and spironolactone prevents cardiovascular remodeling in renovascular hypertensive rats.

Treatment with an angiotensin blocker (ARB) and an aldosterone blocker has been shown to have beneficial effects on cardiac remodeling in several cardiac diseases. It is still not clear whether the combination of these drugs is more effective against cardiac remodeling than the use of either agent alone. We examined the effects of combined treatment with valsartan, an ARB, and spironolactone, an aldosterone blocker, on cardiac remodeling in the renovascular hypertensive (RHT) rat. The RHT rats were divided into 4 groups administered valsartan (3 mg/kg/day, ARB group), spironolactone (4 mg/kg/day, SPRL group), both drugs at these doses (combined group), or neither drug (untreated RHT group). After 5 weeks, systolic blood pressure was significantly reduced in the 3 treatment groups, however, there were no significant differences in the extent of blood pressure reduction among the 3 treatment groups. The heart weight/body weight ratio in each of the 3 treatment groups was significantly lower than that in the untreated RHT group. The degree of cardiac and perivascular fibrosis in the SPRL group and the combined group were significantly lower than that in the untreated RHT group. Myocyte remodeling in the ARB group and in the combined group was significantly smaller than that in the untreated RHT group. These results suggest that SPRL treatment prevents cardiac and perivascular fibrosis and ARB treatment suppresses the cellular hypertrophy of myocytes, and that, therefore, combined treatment with both drugs prevents cardiac remodeling by acting against both myocyte hypertrophy and cardiac fibrosis in RHT rats.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

[Peripartum cardiomyopathy with antiphospholipid antibody: a case report].

A 32-year-old woman tested positive for lupus anticoagulant when she had fever of unknown origin at 18 weeks of pregnancy. Sixteen days after a normal delivery at 35 weeks, she developed dyspnea and was hospitalized with heart failure. Chest radiography showed severe pulmonary edema. Echocardiography showed dilation and diffuse hypokinesis of the left ventricle. The diagnosis was peripartum cardiomyopathy. The patient responded to diuretic and vasodilator therapy. Endomyocardial biopsy revealed mild myocardial degeneration and interstitial fibrosis. Heart failure due to coronary microthrombosis has been indicated in patients with antiphospholipid antibodies, suggesting such a relationship in this case.

Adult↗