Language：English   Publishing type：Research paper (scientific journal)  

BACKGROUND: Fractional flow reserve (FFR) is widely used for the assessment of myocardial ischemia. Intravascular ultrasound (IVUS) is an intracoronary imaging method that provides information about lumen and vessel morphology. Previous studies on the expanded use of IVUS to identify functional ischemia have noted an association between anatomy and physiology, but IVUS-derived minimum lumen area (MLA) has a weak-moderate correlation with myocardial ischemia compared with FFR. We developed a method to calculate FFR using IVUS-derived anatomical information for the assessment of myocardial ischemia. The aims of this study were to investigate the relationship between wire-based FFR and IVUS-derived FFR (IVUS-FFR) and to compare the usefulness of IVUS-FFR and IVUS-derived MLA for functional assessment.Methods and Results:We retrospectively analyzed 50 lesions in 48 patients with coronary stenosis who underwent IVUS and FFR simultaneously. IVUS-FFR was calculated using our original algorithm and fluid dynamics. Mean percent diameter stenosis determined on quantitative coronary angiography and on FFR was 56.4±10.7 and 0.69±0.08, respectively. IVUS-FFR had a stronger linear correlation with FFR (R=0.78, P<0.001; root mean square error, 0.057 FFR units) than with IVUS-derived MLA (R=0.43, P=0.002). CONCLUSIONS: IVUS-FFR may be a more valuable method to identify myocardial ischemia, compared with IVUS-derived MLA.

DOI： 10.1253/circj.CJ-17-1042

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC  

Fractional flow reserve (FFR) is widely used for the assessment of myocardial ischemia. Optical coherence tomography (OCT) provides accurate visualization of coronary artery morphology. The aim of this study was to investigate the relation between FFR and OCT-derived FFR. We retrospectively analyzed 31 lesions (25 left anterior descending arteries, 2 left circumflex arteries, and 4 right coronary arteries) in 31 patients with moderate-to severe coronary stenosis, who underwent OCT and FFR measurements simultaneously. OCT-derived FFR was calculated by the original algorithm, which was calculated using the following equation based on fluid dynamics: Delta P = FV + SV2, where V is the flow velocity, F is the coefficient of pressure loss because of viscous friction (Poiseuille resistance), and S is the coefficient of local pressure loss because of abrupt enhancement (flow separation). Mean values of % diameter stenosis by quantitative coronary angiography and FFR were 55.2 +/- 14.0% and 0.70 +/- 0.14, respectively. OCT-derived FFR showed a stronger linear correlation with FFR measurements (r = 0.89, p &lt;0.001; root mean square error = 0.062 FFR units) than quantitative coronary angiography % diameter stenosis (r = 0.65, p &lt;0.001), OCT measurements of minimum lumen area (r = 0.68, p &lt;0.001), and % area stenosis (r = 0.70, p &lt;0.001). OCT-derived FFR has the potential to become an alternative method for the assessment of functional myocardial ischemia, and may elucidate the relation between coronary morphology and FFR. (C) 2017 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.amjcard.2017.07.083

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Perivascular adipose tissue exhibits characteristics of active local inflammation, which contributes to the development of atherosclerotic disease as a complication of obesity/metabolic syndrome. However, the precise role of perivascular adipose tissue in the progression of abdominal aortic aneurysm remains unclear. To test the hypothesis that genetic deletion of angiotensin II type 1a (AT(1a)) receptor in perivascular visceral adipose tissue (VAT) can attenuate aortic aneurysm formation in apolipoprotein E-deficient (ApoE(-/-)) mice, we performed adipose tissue transplantation experiments by using an angiotensin II-induced aneurysm murine model, in which we transplanted VAT from ApoE(-/-) or ApoE(-/-) AT(1a)(-/-) donor mice onto the abdominal aorta of ApoE(-/-) recipient mice. Compared with ApoE-/VAT transplantation, ApoE(-/-)AT(1a)(-/-) VAT transplantation markedly attenuated aortic aneurysm formation, macrophage infiltration, and gelatinolytic activity in the abdominal aorta. AT(1a) receptor activation led to the polarization of macrophages in perivascular VAT toward the proinflammatory phenotype. Moreover, osteopontin expression and gelatinolytic activity were considerably lower in ApoE(-/-)AT(1a)(-/-) perivascular VAT than in ApoE(-/-) perivascular VAT, and angiotensin II-induced osteopontin secretion from adipocytes was eliminated after deletion of AT(1a) receptor in adipocytes. Notably, induction of macrophage migration by conditioned medium from angiotensin II-stimulated wild-type adipocytes was suppressed by treatment with an osteopontin-neutralizing antibody, and ApoE(-/-) OPN-/- VAT transplantation more potently attenuated aortic aneurysm formation than ApoE(-/-) VAT transplantation. Our findings indicate a previously unrecognized effect of AT(1a) receptor in perivascular VAT on the pathogenesis of abdominal aortic aneurysm.

DOI： 10.1161/HYPERTENSIONAHA.117.09512

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER  

AHI measured using type-3 PM is a useful predictor of outcome following initial PVI in patients with paroxysmal AF.

DOI： 10.1007/s10840-016-0148-z

Web of Science

PubMed

researchmap

Language：English   Publisher：ELSEVIER IRELAND LTD  

DOI： 10.1016/j.ijcard.2016.08.248

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE INC  

We previously reported interferon regulatory factor (IRF) 1 plays physiological roles in "growth"-regulated angiotensin II type 2 (AT(2)) receptor expression in fibroblasts. Here, we investigated whether IRF-1 is involved in attenuation of vascular remodeling in association with AT(2) receptor upregulation. Neointimal area in injured artery after 14 days of cuff placement was significantly increased in IRF-1 knockout mice (IRF-1KO) and AT(2) receptor knockout mice (AT(2)KO) compared with wild-type mice (WT: C57BL/6J). Treatment with compound 21 attenuated neointima formation in both WT and IRF-1KO. AT(2) receptor mRNA expression after 7 days of cuff placement was significantly decreased in IRF-1KO compared with WT; however, IRF-1 expression did not differ between AT(2)KO and WT. Apoptotic changes in injured artery after 14 days of cuff placement were significantly attenuated in IRF-1KO, with a decrease in interleukin-1 beta-converting enzyme and inducible nitric oxide synthase mRNA levels. These results indicate IRF-1 is one of the key transcriptional factors for the prevention of neointimal formation involving AT(2) receptors. J Am Soc Hypertens 2016;10(10):811-818. (C) 2016 American Society of Hypertension. All rights reserved.

DOI： 10.1016/j.jash.2016.07.005

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC  

Fractional flow reserve (FFR) is widely used for the assessment of myocardial ischemia. However, it has the disadvantage of cost and invasive complication risks. We investigated the usefulness of quantitative coronary angiography derived translesional pressure (QCA-TP) for predicting functional myocardial ischemia, using FFR as the gold standard. We retrospectively analyzed 152 coronary narrowings (98 left anterior descending arteries, 28 left circumflex arteries, and 26 right) in 132 patients with mild-severe coronary stenosis who underwent coronary angiography and FFR measurements simultaneously. QCA-TP was calculated using software implemented in the QCA software. Coronary morphology was calculated using both densitometry and lumen edges. Functional myocardial ischemia was defined as an FFR of 0.8 or less. The mean values of diameter stenosis by QCA and FFR were 48.9% +/- 14.9 and 0.76 +/- 0.14, respectively. QCA-TP was significantly correlated with FFR (r = 0.76, p &lt;0.01). The cut-off values of QCA-TP for predicting functional myocardial ischemia based on FFR were 72.8 mm Hg for the left, anterior descending arteries (accuracy, 86.7%; area under the curve [AUC], 0.93), 60.5 mm Hg for the left circumflex arteries (accuracy, 89.3%; AUC, 0.88), and 64.4 mm Hg for the right (accuracy, 88.5%; AUC, 0.94). Therefore, our data suggest that QCA-TP can predict myocardial ischemia with high diagnostic accuracy. (C) 2016 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.amjcard.2016.07.026

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPANESE CIRCULATION SOC  

Background: In patients who have atrial fibrillation (AF) with CHADS2 score of 0-1 (categorized as low-to-intermediate risk), there is little information on stratifying the risk of stroke. This study aimed to determine whether impaired endothelial function assessed by reactive hyperemia-peripheral arterial tonometry (RH-PAT) predicted left atrial blood stagnation in these patients.
Methods and Results: We enrolled 81 consecutive patients with nonvalvular AF. The reactive hyperemia index (RHI) was measured using RH-PAT. Transesophageal echocardiography was performed to determine spontaneous echo contrast (SEC) before direct-current cardioversion or radiofrequency catheter ablation. SEC was found in 49 patients (60%). The RHI was significantly lower in patients with than without SEC. Multivariate analysis demonstrated that RHI was one of the independent determinants of SEC (OR per 0.1, 1.26; 95% CI, 1.11-1.49; P= 0.002) in all patients. In addition, RHI was a significant determinant of SEC (AUC, 0.73; 95% CI, 0.63-0.89; P= 0.0017) in patients with low-to-intermediate risk. At an RHI cut-off &lt; 1.62, the sensitivity and specificity for the identification of patients with SEC were 58% and 89%, respectively.
Conclusions: Impaired endothelial function assessed by RH-PAT might help to predict the presence of SEC in patients with low-to-intermediate risk of stroke.

DOI： 10.1253/circj.CJ-16-0176

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL  

Purpose: Our recent report demonstrated that atrial electromechanical conduction time (EMT-epsilon) measured with speckle tracking echocardiography could predict cardiac events in patients with pathological left ventricular hypertrophy. This study aimed to validate EMT-epsilon by comparison with electroanatomical mapping and to investigate the clinical utility of EMT-epsilon in patients with atrial fibrillation (AF) undergoing catheter ablation. Methods: Forty-six patients with preserved LV ejection fraction (LVEF &gt;= 50%) undergoing pulmonary vein isolation (PVI) for AF were studied. Atrial electrical conduction delay was determined by measuring atrial electrical activation time (EAT) using three-dimensional electroanatomical mapping just after PVI. Echocardiographic parameters were acquired within 24 hours and at 6 months after PVI. The study also included 10 control subjects. Results: AF patients had a larger left atrial (LA) volume index (LAVI) and more prolonged EMT-epsilon compared with control subjects. According to the validation study, EAT was closely related to EMT-epsilon and a', and this association was independent of LAVI and the presence of persistent AF (EMT-epsilon: R-2 = 0.342, P &lt; 0.0001, a': R-2 = 0.337, P &lt; 0.0001). At 6 months after PVI, LAVI and EMT-epsilon were significantly improved. During continued follow-up beyond 6 months (total follow-up, 26 +/- 12 months), the EMT-epsilon shortening at 6 months after PVI was significantly greater in AF-free patients than patients with AF recurrence. Conclusions: This study suggested that the EMT-epsilon could be a useful echocardiographic marker of LA electromechanical abnormalities in patients with AF.

DOI： 10.1111/echo.13259

Web of Science

PubMed

researchmap

Language：English   Publisher：ELSEVIER IRELAND LTD  

DOI： 10.1016/j.ijcard.2015.11.069

Web of Science

PubMed

researchmap

Language：English  

This case report describes sustained monomorphic ventricular tachycardia (VT) caused by a large epicardial scar, related to dilated-phase hypertrophic cardiomyopathy mimicking VT originating from the apical septum. VT resolved with epicardial catheter ablation. The exit of the VT circuit suggested that a 12-lead electrocardiogram can be remote with respect to the critical isthmus in this case. In patients with structural heart disease, it is difficult to identify the VT reentrant circuit by surface electrocardiography, which shows only the exit site. VT originating in the epicardium should be considered, even if the suspected origin is another ventricular site.

DOI： 10.1016/j.joa.2015.06.003

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL  

Background: The pathological process of left ventricular (LV) hypertrophy is associated with left atrial (LA) remodeling. This study was aimed to evaluate the prognostic value of LA strain parameters in patients with pathological LV hypertrophy. Methods: This study included 95 patients with hypertensive heart disease (HHD: n = 24), hypertrophic cardiomyopathy (HCM: n = 56), cardiac amyloidosis (CA: n = 15), and control subjects (n = 20). We used two-dimensional speckle tracking echocardiography (STE) to analyze LA global strain. LA electromechanical conduction time (EMT) at the septal (EMT-septal) and lateral wall (EMT-lateral), and their time difference (EMT-diff) were calculated. The incidence of cardiac death and heart failure hospitalization was defined as major cardiac events and that of atrial fibrillation as secondary outcome. Results: Left atrial volume index was increased and LA booster strain was decreased in the HCM and CA groups compared with the HHD group. EMT-lateral was increased in the diseased groups compared with the control. EMT-diff was prolonged in the CA group compared with the HCM group. During the follow-up period (mean 3.4 years), major cardiac events and atrial fibrillation occurred in 17 and 13 patients, respectively. The occurrence of atrial fibrillation was associated with CA etiology, E/e', LA volume index, LAa, and EMT-lateral. The incidence of major cardiac events was independently correlated with LA volume index and EMT-diff in multivariate analysis. Conclusion: This study suggested that the EMT-diff could discriminate patients with a high risk of cardiac events among patients with pathological LV hypertrophy.

DOI： 10.1111/echo.12961

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：INT HEART JOURNAL ASSOC  

Arrhythmias are associated with reduced quality of life and poor prognosis in patients with hypertrophic cardiomyopathy (HCM). Recent genome-wide association studies revealed that a nonsynonymous single nucleotide polymorphism, rs6795970, in the SCN10A gene was associated with the PR interval. We examined whether the PR prolonging allele (A allele) in the SCN10A gene may be associated with cardiac conduction abnormalities in HCM patients.
We genotyped the polymorphism in 149 HCM patients. Conduction abnormalities were defined as first-degree heart block, bundle-branch block, and bifascicular heart block. Patients were divided into two groups: group A consisted of 122 patients (82%) without a conduction abnormality; and group B consisted of 27 patients (18%) with one or more cardiac conduction abnormalities. The frequency distribution of the SCN10A genotypes (G/G, G/A, and A/A) among the patients with HCM was 71%, 26%, and 3%, respectively. A cardiac conduction abnormality was documented in 9% with GIG and 40% with G/A or A/A. There was a significant difference in the genotype distribution between the two groups (P = 0.0002). In the dominant A allele model, there was a significant difference in genotypes between the two groups (P &lt; 0.0001). In addition, the A allele remained significant after adjusting for other covariates in a multivariate model (odds ratio = 6.30 [95% confidence interval: 2.24 to 19.09], P = 0.0005).
The rs6795970 in the SCN10A gene, which is reported to carry a high risk of heart block, might be associated with cardiac conduction abnormalities in HCM patients.

DOI： 10.1536/ihj.14-411

Web of Science

PubMed

researchmap

Language：English   Publisher：ELSEVIER IRELAND LTD  

DOI： 10.1016/j.ijcard.2014.07.157

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Background: The aim of this study was to investigate the correlation of the qualitative transmural extent of hypoperfusion areas (HPA) using stress dynamic whole-heart computed tomography perfusion (CTP) imaging by 256-slice CT with CTP-derived myocardial blood flow (MBF) for the estimation of the severity of coronary artery stenosis. Methods and Results: Eleven patients underwent adenosine triphosphate (0.16 mg/kg/min, 5 min) stress dynamic CTP by 256-slice CT (coverage: 8 cm, 0.27 s/rotation), and 9 of the 11 patients underwent coronary angiography (CAG). Stress dynamic CTP (whole-heart datasets over 30 consecutive heart beats in systole without spatial and temporal gaps) was acquired with prospective ECG gating (effective radiation dose: 10.4 mSv). The extent of HPAs was visually graded using a 3-point score (normal, subendocardial, transmural). MBF (ml/100g/min) was measured by deconvolution. Differences in MBF (mean ± standard error) according to HPA and CAG results were evaluated. In 27 regions (3 major coronary territories in 9 patients), 11 coronary stenoses (&gt
50% reduction in diameter) were observed. In 353 myocardial segments, HPA was significantly related to MBF (P &lt
0.05
normal 295 ± 94
subendocardial 186 ± 67
and transmural 80 ± 53). Coronary territory analysis revealed a significant relationship between coronary stenosis severity and MBF (P &lt
0.05
non-significant stenosis [&lt
50%], 284 ± 97
moderate stenosis [50-70%], 184 ± 74
and severe stenosis [&gt
70%], 119 ± 69). Conclusion: The qualitative transmural extent of HPA using stress whole-heart dynamic CTP imaging by 256-slice CT exhibits a good correlation with quantitative CTP-derived MBF and may aid in assessing the hemodynamic significance of coronary artery disease. © 2013 Kurata et al.

DOI： 10.1371/journal.pone.0083950

Scopus

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPANESE CIRCULATION SOC  

Background: The interventricular septum in hypertrophic cardiomyopathy (HC) has a unique shape, which is characterized by the convex curvature toward the left ventricle (LV). The aim of this study was to examine the relationship between curvature of the LV wall and regional myocardial strain.
Methods and Results: Fifty-six patients with HC (mean age, 55 +/- 12 years) and 20 age- and sex-matched control subjects (mean age, 56 +/- 8 years) were enrolled. The curvature index (1/radius) was measured by drawing along the endocardial surface from the apical 4-chamber and short axis views. Peak systolic strain was calculated in the septal and lateral walls using 2-D speckle tracking echocardiography. The septal curvature index and septal longitudinal strain were significantly lower in the HC group than in the control group. A multivariate model using the HC patient data showed that the septal curvature index and septal thickness were the independent determinants of septal longitudinal strain (septa] curvature index: beta=-0.421, P&lt;0.001; septal thickness: beta=0.401, P=0.002). In addition, global longitudinal strain and E/e' were worse in the lower septal curvature index group compared with the higher group.
Conclusions: Septal longitudinal strain is associated with the degree of septal curvature. This indicates a possible link between LV wall configuration and regional myocardial function. (Circ J 2013; 77: 1040-1045)

DOI： 10.1253/circj.CJ-12-0752

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Resolution of the issue of nonresponsiveness to cardiac resynchronization therapy (CRT) remains crucial to the successful treatment of conduction disturbances in heart failure. In this study, a patient with refractory heart failure including left bundle branch block was treated via surgical CRT. The epicardial left ventricular (LV) lead, implanted using thoracoscopic guidance, was unexpectedly located on the apical side. Echocardiographic findings of the LV motion mimicked takotsubo cardiomyopathy. The LV lead was successfully re-implanted along a lateral branch of the cardiac vein using an endovascular approach, resulting in restored contractility and reversal of the LV remodeling. © 2012 Japanese Society of Echocardiography.

DOI： 10.1007/s12574-012-0132-2

Scopus

PubMed

researchmap

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPANESE CIRCULATION SOC  

Background: Sustained cardiac adrenergic stimulation has been implicated in the progression of cardiovascular events in patients with dilated cardiomyopathy (DCM). Our group hypothesized that a combination of polymorphisms that result in increased synaptic norepinephrine release and enhanced receptor function would predispose patients with DCM to cardiovascular events. The effect of polymorphisms in adrenergic receptor-related genes on cardiovascular event-free survival in patients with idiopathic DCM was evaluated.
Methods and Results: Genotyping at 3 loci (ADRB1 Ser49Gly and Arg389Gly, and NET T-182C) was performed in 83 patients with DCM. Patients were followed prospectively to the endpoint of cardiovascular events (mean follow-up, 45 months). Cardiovascular events were defined as cardiac death and emergent hospitalization as a result of congestive heart failure, arrhythmia, and cerebrovascular events. Analyses were conducted based on the number of predicted risk genotypes a patient carried. The ADRB1 Ser49 allele carrier, ADRB1 Arg389 allele carrier, and NET-182CC genotype were defined as the predicted risk genotypes. Cardiovascular event-free survival was compared based on the number of predicted risk genotypes. Cardiovascular event-free survival was significantly better in patients with fewer than 3 predicted risk genotypes than in those with 3 predicted risk genotypes.
Conclusions: Genotyping at these 3 loci might be a useful approach for identification of patients with DCM at risk for cardiovascular events. (Circ J 2012; 76: 2003-2008)

DOI： 10.1253/circj.CJ-11-1014

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Objective-Angiotensin II is involved in the genesis of atherosclerosis. As the role of the angiotensin II type 1a (AT(1a)) receptor in plaque rupture is poorly understood, we assessed the hypothesis that the AT(1a) receptor contributes to atherosclerotic plaque rupture.
Methods and Results-Atherosclerotic plaque rupture was induced by carotid artery ligation for 4 weeks followed by polyethylene cuff placement around the carotid in apolipoprotein E (ApoE)(-/-) and ApoE(-/-) AT(1a)(-/-) mice. The incidence of plaque rupture at 4 days after cuff placement was 72% in ApoE(-/-) mice compared with 24% in ApoE(-/-) AT(1a)(-/-) mice (P&lt;0.01). Lipid accumulation, macrophage infiltration, expression of inflammatory cytokines, nicotinamide adenine dinucleotide phosphate-oxidase activity, and matrix metalloproteinase-9 activity in atherosclerotic plaque were markedly attenuated in ApoE(-/-) AT(1a)(-/-) compared with ApoE(-/-) mice. Oxidized low-density lipoprotein inhibited macrophage migration in ApoE(-/-) macrophages. In contrast, oxidized low-density lipoprotein-induced macrophage trapping was abolished in ApoE(-/-) AT(1a)(-/-) macrophages, and this was associated with decreased CD36 expression and focal adhesion kinase activity.
Conclusion-These results suggest that blocking the AT(1) receptor may reduce atherosclerotic plaque rupture and that AT(1a) receptor-mediated macrophage trapping, inflammation, oxidative stress, and matrix metalloproteinase activation may play crucial roles in plaque vulnerability. (Arterioscler Thromb Vasc Biol. 2012;32:1453-1459.)

DOI： 10.1161/ATVBAHA.112.249516

Web of Science

PubMed

researchmap

Language：English   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

DOI： 10.1161/CIRCULATIONAHA.110.000315

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：JAPANESE CIRCULATION SOC  

Background: Right ventricular (RV) pacing alters left ventricular (LV) mechanical activation, resulting in adverse impacts on LV function. This study was aimed to investigate the acute effect of RV apical (RVA) and septal pacing (RVS) on LV dyssynchrony and function using speckle tracking echocardiography.
Methods and Results: The 103 patients (74 9 years) with symptomatic bradyarrhythmia and preserved LV ejection fraction, and 50 age-matched control subjects were studied. All patients received a permanent pacemaker and were randomly assigned into 2 groups (RVA: n=51, RVS: n=52). After insertion, patients underwent an echocardiographic study during RV pacing. LV dyssynchrony and global strain parameters were analyzed using speckle tracking echocardiography. The QRS width and dyssynchrony indices by longitudinal and radial strain were significantly greater in RVA than in both the control and RVS. The LV longitudinal dyssynchrony index was significantly related to global longitudinal strain (GLS) among 103 patients receiving RV pacing (R(2)=0.25, P&lt;0.0001). The GLS in RVA were the lowest among the 3 groups (GLS: Control: -18.2 +/- 2.4%, RVA: -14.3 +/- 3.1%, P&lt;0.001 vs. control, RVS: -16.8 +/- 2.7%, P&lt;0.01 vs. RVA).
Conclusions: RVA created heterogeneous LV contraction, which resulted in deteriorated LV longitudinal contraction. RVS could be a better pacing alternative in terms of less LV dyssynchrony and better longitudinal function compared to RVA. (Circ J 2011; 75: 1609-1615)

DOI： 10.1253/circj.CJ-10-1138

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER IRELAND LTD  

Background: We undertook a cross-sectional study to test the hypothesis that patients with hypertrophic cardiomyopathy (HCM) who have impaired left ventricular (LV) diastolic function are insulin resistant. We also evaluated the relation between the development of atrial fibrillation (AF) and insulin resistance (IR) in patients with HCM.
Methods and results: Eighty-eight patients with HCM (71 men, 17 women) were enrolled in the study. IR was estimated using the homeostasis model assessment (HOMA) index. Echocardiographically determined left atrial (LA) dimension was measured as a marker of LA size. The ratio of trasmitral early LV filling velocity to early diastolic mitral annulus velocity (E/e&apos;) was also measured as a marker of LV diastolic function. Twenty-seven patients (31%) had IR. Multivariate logistic regression analyses showed that independent determinants of AF were increased LA size [odds ratio (OR) 3.5, 95% confidence interval (CI) 1.2-9.8] and impaired LV diastolic function [OR 4.6, 95% CI 1.6-12.8]. The strongest determinant of LA size was the HOMA index (p = 0.0005). Similarly, the HOMA index (p = 0.0019) was an independent determinant of LV diastolic function.
Conclusion: IR is highly prevalent among non-diabetic patients with HCM. A possible mechanism by which IR affects the development of AF is mediated through its association with increased LA size or impaired LV diastolic function. IR may be an important underlying mechanism for the genesis of AF in HCM. (C) 2011 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.jjcc.2011.03.001

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)  

Technologies associated with cardiac resynchronization therapy (CRT) devices and lead systems have progressed. However, dislocation after coronary sinus (CS) lead placement continues to be a problem. Furthermore, CS lead positioning at the site of the ventricular latest activation (detected by echocardiography) is often problematic due to large vessel size leading to the lead placement (wedge site) near the apical site. The newly available active fixation CS lead (StarFix 4195) enabled us to anchor the CS lead at the target site regardless of vessel size and availability of a wedge site. We report on seven patients who had previously failed conventional CS lead positioning due to large vessel size and a low phrenic nerve stimulation threshold at the optimal site and lack of stabilization followed by dislocation at the target vein. We attempted to replace the original lead with the StarFix 4195. All patients successfully underwent StarFix 4195 lead replacement at the target site and responded to CRT in the long-term follow-up period. © 2010 Japanese College of Cardiology.

DOI： 10.1016/j.jccase.2009.12.007

Scopus

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Cibenzoline, a Class I antiarrhythmic agent, can attenuate the left ventricular pressure gradient (LVPG) in patients with hypertrophic obstructive cardiomyopathy (HOCM). An association between the insertion/deletion polymorphism of the angiotensin-converting enzyme (ACE) gene and the progression of left ventricular hypertrophy in patients with hypertrophic cardiomyopathy has been reported. The aim of this study was to investigate the pharmacogenetic interactions between the ACE insertion/deletion polymorphism and the response to cibenzoline in patients with HOCM. Twenty-four patients with HOCM participated in this study. The LVPG and left ventricular function were measured by echocardiography before and 2 hours after administration of a single oral dose of 200 mg cibenzoline. The ACE insertion/deletion polymorphism was genotyped. The frequencies of the genotypes D/D, D/I, and I/I were 16%, 42%, and 42%, respectively. Before administration of cibenzoline, the LVPG was higher in patients with the D allele than in those without it (105 6 47 mm Hg versus 64 6 24 mm Hg, P = 0.0195). After administration of cibenzoline, the LVPG significantly decreased to 41 6 27 mm Hg in those with the D allele (P = 0.0001) and to 33 6 24 mm Hg in those without it (P = 0.0003). The LVPG in patients with the D allele was significantly decreased by cibenzoline when compared with patients without the allele (64 6 45 mm Hg versus 31 6 17 mm Hg, P = 0.038). Patients with HOCM with the ACE D allele had a high LVPG. Cibenzoline was more effective in patients with HOCM with the ACE D allele.

DOI： 10.1097/FJC.0b013e3181d8bc4b

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER IRELAND LTD  

A 19-year-old mate was admitted to the emergency room of our hospital after a motor vehicle accident. During his first physical examination, a holosystolic murmur was heard at the fourth left parasternal border. Transthoracic echocardiography showed severe tricuspid insufficiency, but the cause of tricuspid insufficiency was unclear. Therefore, three-dimensional echocardiography was performed and demonstrated flail anterior, posterior and septal. leaflets of the tricuspid valve. The diagnosis was tricuspid insufficiency due to papillary muscle rupture secondary to chest blunt trauma. Surgical repair of the tricuspid valve was performed in this patient. After surgery, the signs and symptoms of right ventricular heart failure were relieved. In this case, three-dimensional echocardiography was very useful for the evaluation of spatial destruction of the tricuspid valve and papillary muscle. (C) 2009 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/j.jjcc.2009.04.007

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER IRELAND LTD  

Background: The cytotoxic action of leukocytes is known to be a probable cause of the cardiac myocyte damage seen in idiopathic dilated cardiomyopathy (IDC). Monocyte chemoattractant protein 1 (MCP-1) contributes to enhanced leukocyte recruitment and activation resulting in chronic damage of cardiomyocytes. MCP-1 has been reported to be dynamically regulated in IDC and may contribute to the deterioration of left ventricular function. In addition, a polymorphism at -2518 (G/A) in the MCP-1 gene affects the level of MCP-1 expression in response to an inflammatory stimulus.
Methods and results: We genotyped the polymorphism at -2518 G/A in the MCP-1 gene in 73 Japanese patients with nonfamilial IDC and 349 healthy controls. The distribution of the MCP-1 genotypes in the IDC patients differed significantly from the controls (p = 0.016). In a dominant G allele model, there was a significant difference in the distribution of genotypes between the two groups (p &lt; 0.01). The odds ratio for nonfamilial IDC associated with the GG vs. non-GG genotype was 10.4 (95% CI = 1.7-64.5) after adjustment for the confounding factors.
Conclusions: These findings suggest that the G allele at -2518 in the MCP-1 gene may be a novel genetic marker of susceptibility to nonfamilial IDC. (C) 2009 Japanese College of Cardiology. Published by Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/j.jjcc.2009.04.001

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Background-Oxidative stress, generated by excessive reactive oxygen species, promotes cardiovascular disease. Cyclophilin A (CyPA) is a 20-kDa chaperone protein secreted from vascular smooth muscle cells (VSMCs) in response to reactive oxygen species that stimulates VSMC proliferation and inflammatory cell migration in vitro; however, the role CyPA plays in vascular function in vivo remains unknown.
Methods and Results-We tested the hypothesis that CyPA contributes to vascular remodeling by analyzing the response to complete carotid ligation in CyPA knockout mice, wild-type mice, and mice that overexpress CyPA in VSMC (VSMC-Tg). After carotid ligation, CyPA expression in vessels of wild-type mice increased dramatically and was significantly greater in VSMC-Tg mice. Reactive oxygen species-induced secretion of CyPA from mouse VSMCs correlated significantly with intracellular CyPA expression. Intimal and medial hyperplasia correlated significantly with CyPA expression after 2 weeks of carotid ligation, with marked decreases in CyPA knockout mice and increases in VSMC-Tg mice. Inflammatory cell migration into the intima was significantly reduced in CyPA knockout mice and increased in VSMC-Tg mice. Additionally, VSMC proliferation assessed by Ki67(+) cells was significantly less in CyPA knockout mice and was increased in VSMC-Tg mice. The importance of CyPA for intimal and medial thickening was shown by strong correlations between CyPA expression and the number of both inflammatory cells and proliferating VSMCs in vivo and in vitro.
Conclusions-In response to low flow, CyPA plays a crucial role in VSMC migration and proliferation, as well as inflammatory cell accumulation, thereby regulating flow-mediated vascular remodeling and intima formation.

DOI： 10.1161/CIRCULATIONAHA.107.756106

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS  

The potential combined effect and mechanism of calcium channel blockers (CCB) and angiotensin II type 1 receptor blockers (ARB) to improve insulin resistance were investigated in type 2 diabetic KK-Ay mice, focusing on their antioxidative action. Treatment of KK-Ay mice with a CCB, azelnidipine (3 mg/kg/day), or with an ARB, olmesartan (3 mg/kg/day), for 2 weeks lowered the plasma concentrations of glucose and insulin in the fed state, attenuated the increase in plasma glucose in the oral glucose tolerance test (OGTT), and increased 2-[H-3]deoxy-D-glucose (2-[H-3]DG) uptake into skeletal muscle with the increase in translocation of glucose transporter 4 (GLUT4) to the plasma membrane. Both blockers also decreased the in situ superoxide production in skeletal muscle. The decrease in plasma concentrations of glucose and insulin in the fed state and superoxide production in skeletal muscle, as well as GLUT4 translocation to the plasma membrane, after azelnidipine administration was not significantly affected by coadministration of an antioxidant, 2,2,6,6-tetramethyl-1-piperidinyloxy (tempol). However, those changes caused by olmesartan were further improved by tempol. Moreover, olmesartan enhanced the insulin-induced tyrosine phosphorylation of insulin receptor substrate-1 induced in skeletal muscle, whereas azelnidipine did not change it. Coadministration of azelnidipine and olmesartan further decreased the plasma concentrations of glucose and insulin, improved OGTT, and increased 2-[H-3] DG uptake in skeletal muscle. These results suggest that azelnidipine improved glucose intolerance mainly through inhibition of oxidative stress and enhanced the inhibitory effects of olmesartan on glucose intolerance, as well as the clinical possibility that the combination of CCB and ARB could be more effective than monotherapy in the treatment of insulin resistance.

DOI： 10.1124/jpet.106.108894

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Objective-Angiotensin II contributes to atherogenesis, mainly through oxidative stress and inflammation. Recent data suggest that aldosterone is implicated in some effects of angiotensin II. We hypothesized that aldosterone could directly contribute to oxidative stress and atherosclerotic lesion formation.
Methods and Results-Male apolipoprotein E-deficient mice 6 weeks of age were placed on a normal diet or 1.25% high-cholesterol diet. After 6 weeks of the high-cholesterol diet, a marked increase in atherosclerotic lesion formation was observed in the aorta, accompanied by significant elevation of plasma cholesterol level. Production of superoxide anion and expression of NAD(P)H oxidase subunit p47(phox), tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 in the aorta were increased with the high-cholesterol diet. Eplerenone (1.67 g/kg in high-cholesterol diet) did not affect blood pressure or plasma cholesterol but decreased the atherosclerotic area by nearly 70% (P &lt; 0.05), associated with attenuation of oxidative stress and inflammatory response. Valsartan (0.5 mg/kg per day) also decreased the atherosclerotic lesion, whereas coadministration of valsartan and eplerenone further decreased it. Moreover, aldosterone (0.1 mu mol/L) enhanced NADPH oxidase activity in cultured vascular smooth muscle cells.
Conclusions-These results suggest that aldosterone may play a critical role in atherogenesis subsequent to oxidative stress in part independent of angiotensin II-mediated signaling, and that eplerenone could prevent atherosclerosis by attenuating oxidative stress and inflammation.

DOI： 10.1161/01.ATV.0000204635.75748.0f

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Reactive oxygen species (ROS) contribute to the pathogenesis of atherosclerosis in part by promoting vascular smooth muscle cell (VSMC) growth. Previously we demonstrated that cyclophilin A (CyPA) is a secreted oxidative stress-induced factor (SOXF) that promotes inflammation, VSMC growth, and endothelial cell apoptosis. However, the mechanisms that regulate CyPA secretion are unknown. In this study, we hypothesized that ROS-induced CyPA secretion from VSMC requires a highly regulated process of vesicle transport, docking, and fusion at the plasma membrane. Conditioned medium and plasma membrane sheets were prepared by exposing VSMC to 1 mu mol/L LY83583, which generates intracellular superoxide. A vesicular transport mechanism was confirmed by colocalization at the plasma membrane with vesicle-associated membrane protein ( VAMP). CyPA transport to the plasma membrane and secretion were significantly increased by LY83583. Reduction of VAMP-2 expression by small interfering RNA inhibited LY83583-induced CyPA secretion. Pretreatment with 3 mu mol/L cytochalasin D, an actin depolymerizing agent, abrogated CyPA secretion. Infection with dominant-negative RhoA and Cdc42 adenovirus inhibited CyPA secretion by 72% and 63%, respectively, whereas dominant-negative Rac1 had a small effect (11%). Pretreatment with the Rho kinase inhibitor Y27632 (3 to 30 mu mol/L) and myosin II inhibitor blebbistatin (1 to 10 mu mol/L) inhibited CyPA secretion in a dose-dependent manner. Simvastatin (3 to 30 mu mol/L) also dose-dependently inhibited LY83583-induced CyPA secretion likely via decreased isoprenylation of small GTPases. Our findings define a novel VSMC vesicular secretory pathway for CyPA that involves actin remodeling and myosin II activation via RhoA-, Cdc42-, and Rho kinase-dependent signaling events.

DOI： 10.1161/01.RES.0000216405.85080.a6

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：TAYLOR & FRANCIS INC  

Purpose : To investigate the role of angiotensin II (Ang II) receptor subtypes in subconjunctival injury. Methods : A wound-healing model was developed by subconjunctival blunt dissection in male wild-type, AT(1a) receptor-deficient (AT(1a)KO) and AT(2) receptor-deficient (AT(2)KO) mice. Collagen deposition and cell infiltration were evaluated histologically. Expression of collagen, matrix metalloproteinase (MMP), and tissue inhibitor of metalloproteinase-1 (TIMP-1) were determined by real-time PCR. Results : Subconjunctival injury increased the infiltration of inflammatory cells, collagen deposition in the subconjunctival space, and the expression of collagen type I and type III, TIMP-1 and MMP2. In AT(1a)KO mice, collagen deposition, cell infiltration, and expression of collagen and TIMP-1 were inhibited, but MMP2 expression was enhanced. In contrast, in AT(2)KO mice, the increase in collagen deposition, cell infiltration, and expression of collagen and TIMP-1 were further enhanced. Conclusions : These results indicate that AT(1a) and AT(2) receptor stimulation may in addition to other mechanisms be antagonistically involved in the wound-healing process after subconjunctival injury.

DOI： 10.1080/02713680500507200

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Background - The role of angiotensin II (Ang II) type 2 (AT(2)) receptor in atherosclerosis was explored with the use of AT2 receptor/apolipoprotein E (ApoE)-double-knockout (AT2/ApoE-DKO) mice, with a focus on oxidative stress.
Methods and Results - After treatment with a high-cholesterol diet (1.25% cholesterol) for 10 weeks, ApoE-knockout ( KO) mice developed atherosclerotic lesions in the aorta. In AT(2)/ApoE-DKO mice receiving a high-cholesterol diet, the atherosclerotic changes were further exaggerated, without significant changes in plasma cholesterol level and blood pressure. In the atherosclerotic lesion, an increase in superoxide production, NADPH oxidase activity, and expression of p47(phox) was observed. These changes were also greater in AT(2)/ApoE-DKO mice. An Ang II type 1 (AT(1)) receptor blocker, valsartan, inhibited atherosclerotic lesion formation, superoxide production, NADPH oxidase activity, and p47phox expression; these inhibitory effects were significantly weaker in AT(2)/ApoE-KO mice. We further examined the signaling mechanism of the AT(2) receptor-mediated antioxidative effect in cultured fetal vascular smooth muscle cells. NADPH oxidase activity and phosphorylation and translocation of p47(phox) induced by Ang II were inhibited by valsartan but enhanced by an AT(2) receptor blocker, PD123319.
Conclusions - These results suggest that AT(2) receptor stimulation attenuates atherosclerosis through inhibition of oxidative stress and that the antiatherosclerotic effect of valsartan could be at least partly due to AT2 receptor stimulation by unbound Ang II.

DOI： 10.1161/CIRCULATIONAHA.104.525550

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Background - Recent studies suggest that angiotensin type 1 receptor (AT1R) blockers have vascular protective effects beyond blood pressure lowering. Because of the importance of endothelial nitric oxide synthase ( eNOS) in vascular and platelet function, we hypothesized that losartan and its metabolites would stimulate eNOS and its upstream activators Akt and phosphatidylinositol 3-kinase (PI3K).
Methods and Results - Losartan is metabolized into EXP3174 (AT1R-blocking metabolite) and EXP3179 ( no AT1R-blocking properties). Treatment of endothelial cells (ECs) with losartan and both metabolites stimulated phosphorylation of Akt and eNOS in the absence of angiotensin II. However, the magnitude for EXP3179 was much greater than EXP3174, and the EC50 was significantly lower (-logEC(50), 8.2 +/- 0.1 versus 5.4 +/- 0.2 mol/L), suggesting an AT1R-independent effect. Inhibiting PI3K or vascular endothelial growth factor receptor 2 (VEGFR2) tyrosine phosphorylation abrogated EXP3179-induced eNOS phosphorylation. In endothelium of intact rat aorta, EXP3179 also stimulated Akt and eNOS phosphorylation. VEGFR2 activation was shown to be calcium and Src family kinase dependent by use of specific drug inhibitors and dominant negative kinase transfection. EXP3179 significantly inhibited tumor necrosis factor alpha-induced apoptosis by approximate to 60% ( from 30.1 +/- 5.8% to 12.2 +/- 2.0% TUNEL-positive cells), which was abolished by pretreatment with the PI3K inhibitor LY294002. Cleaved caspase-3 was suppressed by 48% with EXP3179.
Conclusions - The losartan metabolite EXP3179 stimulates eNOS phosphorylation and suppresses tumor necrosis factor alpha-induced EC apoptosis by activating the VEGFR2/PI3K/Akt pathway.

DOI： 10.1161/CIRCULATIONHA.204.509760

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Objective Angiotensin II type 1 receptor blockers (ARB) are widely recognized to have a vasculoprotective effect. Accumulating data have revealed that calcium antagonists also retard atherosclerosis. We examined the possibility that combination therapy of ARB and calcium antagonists could more effectively prevent atherosclerosis than monotherapy.
Methods and results We observed a marked increase in the atherosclerotic area, associated with the exaggerated expression of nicotinamide adenine dinucleotide (phosphate), reduced form [NAD(P)H] oxidase subunits (P22(phox) and p47(phox)) and superoxide anion production, in the aorta of apolipoprotein E-deficient mice maintained on a 1.25% high-cholesterol diet for 10 weeks. A calcium antagonist, azelnidipine, at a dose of 1 mg/kg a day or an ARB, olmesartan, at a dose of 3 mg/kg a day, significantly inhibited these parameters, with no change in systolic blood pressure and the blood cholesterol level. Moreover, the co-administration of lower doses of azelnidipine (0.1 mg/kg a day) and olmesartan (11 mg/kg a day) significantly inhibited the atherosclerotic area and oxidative stress, whereas azelnidipine or olmesartan alone at these doses did not affect these parameters. Furthermore, we observed similar inhibitory effects of azelnidipine or olmesartan on angiotensin II-induced NADPH oxidase activity and Akt activity in cultured vascular smooth muscle cells.
Conclusion These results suggest that the co-administration of calcium antagonists and ARB synergistically blunts oxidative stress at least partly through the inhibition of Akt activity and enhances the beneficial effects of these drugs on atherosclerosis compared with monotherapy. (c) 2005 Lippincott Williams & Wilkins.

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE BV  

Background and aims: It has been proven that a disturbance in angiogenesis contributes to the progression of myocardial interstitial fibrosis in idiopathic dilated cardiomyopathy (DCM). This study was designed to evaluate the relationship between serum activity of angiogenic factors and myocardial ultrasonic tissue characterization in patients with DCNI.
Methods and results: We studied 30 patients with DCM and 15 healthy control subjects. Serum levels of vascular endothelial growth factor (VEGF), interleukin (IL)-4 and IL-13 were measured using enzyme-linked immunosorbent assay. We determined calibrated myocardial integrated backscatter (IB) as the value of myocardial interstitial fibrosis using ultrasonic tissue characterization and also quantified the magnitude of cyclic variations in IB (CV-IB). Serum levels of VEGF and IL-13 were significantly higher in patients with DCM than in control subjects (both P &lt; 0.05). Calibrated IB was significantly higher and CV-IB was markedly lower in patients with DCM than in control subjects (both P &lt; 0.01). In patients with DCM, the levels of IL-13 significantly correlated with calibrated IB (r = 0.520, P = 0.018). In addition, there was a significant negative correlation between levels of VEGF and CV-IB (r = -0.611, P = 0.007).
Conclusion: The increase in serum VEGF and IL-13 may be closely related to alterations in myocardial texture in DCM. (c) 2004 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.

DOI： 10.1016/j.ejheart.2004.09.011

Web of Science

PubMed

researchmap

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC PHARMACOLOGY EXPERIMENTAL THERAPEUTICS  

The detailed mechanism of the effects of extracellular Ca2+ entry blockade on angiotensin II ( Ang II) type 1 ( AT1) receptor-mediated growth-promoting signals in vascular smooth muscle cells (VSMCs) is not fully understood. Ang II stimulation caused biphasic activation of growth-promoting signals, reaching a peak at 5 to 10 min followed by a decrease and a second peak at around 2 to 4 h. Addition of PD98059 (2'-amino-3'- methoxyflavone), a mitogen-activated protein kinase/extracellular signal-regulated kinase kinase inhibitor, or AG490 [alpha-cyano-(3,4-dihydroxy)-N-benzylcinnamide], a Janus-activated kinase 2 (Jak2) inhibitor, even 4 h after Ang II treatment inhibited [H-3] thymidine incorporation. The calcium channel blocker azelnidipine attenuated the later peaks of extracellular signal-regulated kinasenase (ERK), tyrosine kinase 2, Jak2 activation, and phosphorylation of signal transducer and activator of transcription (STAT) 1 and STAT3. Interestingly, azelnidipine increased rather than decreased the later ERK peaks in cells treated with small interfering RNA against mitogen-activated protein kinase phosphatase-1. Ang II-mediated [H-3] thymidine incorporation was inhibited dose dependently by azelnidipine and also by azelnidipine, plus olmesartan, whereas olmesartan or azelnidipine alone at such lower doses did not affect [H-3] thymidine incorporation. These data provide new insight into the manner in which calcium channels exert an essential action in the AT1 receptor-mediated growth-promoting actions in VSMCs.

DOI： 10.1124/mol.104.008144

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

The present study explored the possibility that estrogen enhances the inhibitory effect of an angiotensin II type-1 (AT(1)) receptor blocker (ARB), olmesartan, on atherosclerosis, focusing on oxidative stress using apolipoprotein E knockout mice (ApoEKO). After 6 weeks on a high-cholesterol diet, marked atherosclerotic lesion formation with an increase in oxidative stress, such as superoxide production, NAD(P)H oxidase activity and expression of p47(phox) mRNA and rac-1 mRNA, were observed in the proximal aorta in both male and female ApoEKO mice, whereas these changes were less marked in female mice. Ovariectomy enhanced these parameters, the changes of which were reversed by 17 beta-estradiol (80 mu g/kg per day) replacement. Treatment with olmesartan (3 mg/kg per day) significantly inhibited oxidative stress and atherosclerosis, whereas its inhibitory effects were more marked in female than in male or ovariectomized mice. Smaller doses of olmesartan (0.5 mg/kg per day) or 17 beta-estradiol (20 mu g/kg per day) did not influence atherosclerosis and oxidative stress in ovariectomized mice, whereas co-administration of olmesartan and 17 beta-estradiol at these doses attenuated these parameters. An angiotensin-converting enzyme (ACE) inhibitor, temocapril, also inhibited atherosclerotic changes similarly to olmesartan. Moreover, angiotensin II-mediated activation of NAD( P) H oxidase in cultured vascular smooth muscle cells was attenuated by 17 beta-estradiol. These results indicate that estrogen and an ARB synergistically attenuate atherosclerosis at least partly via inhibition of oxidative stress.

DOI： 10.1161/01.HYP.0000157409.88971.fc

Web of Science

PubMed

researchmap

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

We investigated the effects of a 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor ( statin) on the inhibitory effects of an angiotensin II type-1 receptor (AT(1)) blocker on atherosclerosis and explored cellular mechanisms. We gave apolipoprotein E null mice a high-cholesterol diet for 10 weeks and measured atherosclerotic plaque area and lipid deposition. Neither 1 mg/kg per day of valsartan nor 3 mg/kg per day of fluvastatin had any effect on blood pressure or cholesterol concentration; however, both drugs decreased plaque area and lipid deposition after 10 weeks. We then reduced the doses of both drugs to 0.1 mg/kg per day and 1 mg/kg per day, respectively. At these doses, neither drug had an effect on atherosclerotic lesions. When both drugs were combined at these doses, a significant reduction in atherosclerotic lesions was observed. Similar inhibitory effects of valsartan or fluvastatin on the expressions of nicotinamide-adenine dinucleotide/nicotinamide-adenine dinucleotide phosphate oxidase subunits p22(phox) and p47(phox), production of superoxide anion, the expression of monocyte chemoattractant protein-1, and intercellular adhesion molecule-1 expression were observed. These results suggest that concomitant AT(1) receptor and cholesterol biosynthesis blockade, particularly when given concomitantly, blunts oxidative stress and inflammation independent of blood pressure or cholesterol-related effects.

DOI： 10.1161/01.HYP.0000145179.441660f

Web of Science

PubMed

researchmap

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

To examine the possible role of the bradykinin-NO system in the action of ACE inhibitors, we studied the effects of imidapril, an ACE inhibitor, on inflammatory vascular injury by using AT(1)a-receptor-deficient (AT(1)aKO) mice. A polyethylene cuff was placed around the femoral artery of AT(1)aKO mice and wild-type (WT; C57BL/6J) mice. Neointimal area in cross sections of the artery was measured 14 days after cuff placement. A low dose of imidapril (1 mg/kg per day), which did not affect blood pressure, was administered by gavage. Expression of monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-alpha was detected by immunohistochemical staining and reverse transcriptase-polymerase chain reaction (RT-PCR) 7 days after the operation. Neointimal formation, vascular smooth muscle cell proliferation, and expression of MCP-1 and TNF-alpha were attenuated in the injured artery in AT(1)aKO mice compared with those in WT mice. Imidapril inhibited neointimal formation, DNA synthesis of vascular smooth muscle cells, and expression of MCP-1 and TNF-alpha in AT(1)aKO mice as well as in WT mice. In addition, imidapril increased tissue cGMP content after cuff placement. These inhibitory effects of imidapril were significantly reduced or abolished by a bradykinin receptor antagonist, Hoechst 140, or an NO synthase inhibitor, L-NAME, both in WT and AT(1)aKO mice. Treatment with imidapril did not change AT(2) receptor and ACE expression detected by RT-PCR in the injured artery. These results indicate that not only blockade of angiotensin II production but also activation of the bradykinin-NO system plays an important role in the beneficial effects of imidapril on vascular remodeling.

DOI： 10.1161/01.HYP.0000092440.52239.39

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER COLL CHEST PHYSICIANS  

Study objectives: Of the hypertrophic obstructive cardiomyopathies, midventricular obstruction (MVO) often has been overlooked. In this study, hemodynamic parameters in patients with MVO were compared with patients with idiopathic hypertrophic subaortic stenosis (HISS), following which the specific markers for diagnosis of MVO were examined.
Patients and design: Twenty healthy control subjects (mean [+/- SD] age, 54 +/- 8 years), 20 patients with MVO (mean age, 54 +/- 13 years), and 12 patients with HISS (mean age, 58 +/- 12 years) participated in this study. Hemodynamic parameters associated with carotid pulse tracing (CPT) and echocardiography were examined.
Measurement and results: Left ventricular ejection time (LVET) and left ventricular pressure gradient (LVPG) were greater in patients with HISS than in patients with MVO (p &lt; 0.0001 for both). However, left ventricular dimensions and interventricular septal thickness did not vary between patients with MVO and those with HISS. As specific markers for the diagnosis of patients with MVO, two specific CPT patterns, the "spike-and-dip pattern" and the "spike-and-half-dome pattern," were identified, but no specific markers were observed echocardiographically. Among patients with MVO, both LVPG and LVET were greater in patients with the spike-and-half-dome pattern than in patients with the spike-and-dip pattern (113 +/- 34 vs 57 +/- 17 mm Hg, respectively [p &lt; 0.0001]; 318 +/- 19 vs 281 +/- 27 ins, respectively [p = 0.0033]), but echocardiographic parameters revealed no significant differences between the two types of MVOs. The pattern of continuous-wave Doppler recordings of the left ventricle in patients with the spike-and-half-dome pattern was identical to that of patients with HISS, but that of patients with the spike-and-dip pattern exhibited concavity from the onset of systole to the point of maximal velocity.
Conclusions: Two specific patterns for the diagnosis of patients with MVO were identified by CPT. These patterns may be strongly related to differences in ejection dynamics.

DOI： 10.1378/chest.124.4.1275

Web of Science

PubMed

researchmap

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCI IRELAND LTD  

Although beta-blockers can not be used for the treatment of vasospastic angina, the effect of beta-blockers with vasorelaxant property on coronary vasospasm remains uncertain. In this study, we evaluated the effect of betaxolol, a new beta-blocker with calcium antagonistic property, as an additional therapy on vasospastic angina (VSA) with anginal attacks on effort. We enrolled 12 patients with VSA and anginal attacks with ST segment depression during exercise stress test. All patients received 1.25-5 mg of betaxolol for 3 months. Treadmill exercise stress test and adenosine triphosphate stress thallium-201 myocardial scintigraphy were performed before and 3 months after the onset of the betaxolol treatment. The other drugs including calcium antagonists, nitrates and nicorandil were continued. No patients experienced the exacerbation of angina during the betaxolol treatment. Exercise time to chest pain (317.5+/-72.1-454.2+/-75.5 s, P&lt;0.01) and maximal ST segment depression (1.67+/-0.67-1.16+/-0.46 mm, P&lt;0.01) obtained by exercise stress test, the defect score (8.6&PLUSMN;2.7-53&PLUSMN;2.1, P&LT;0.01), the extent score (14.8&PLUSMN;5.8-8.8&PLUSMN;4.6%, P&LT;0.01), the severity score (17.5&PLUSMN;7.3-11.3&PLUSMN;5.2, P&lt;0.01) and washout rate (31.4+/-5.6-37.6+/-5.0%, P&lt;0.01) obtained by the scintigraphy were improved by betaxolol. Our results suggest that betaxolol increases regional myocardial blood flow and improves exercise capacity in patients with VSA. Betaxolol may become a drug for a new potential therapy for VSA. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

DOI： 10.1016/S0167-5273(03)00022-6

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：EXCERPTA MEDICA INC  

We examined the effects of cilostozol on impaired coronary arterial responses in patients with vasospastic angina (VSA). Thirty patients who were diagnosed with VSA based on an acetylcholine provocation test and 10 subjects with normal coronary arteries were enrolled. The patients were divided into the following 3 groups: no antiplatelet agent treatment group, aspirin treatment, or cilostozol treatment groups. Coronary flow reserve (CFR), coronary flow volume at maximum hyperemia, and epicardial coronary artery diameter after administration of N-G-monomethyl-L-arginine (L-NMMA) were examined using a Doppler flow wire before and 6 months after the start of this study. CFR, coronary flow volume at maximum hyperemia, and diameter changes by L-NMMA were significantly increased in the cilostazol treatment group compared with the other 2 groups. in conclusion, cilostazol increased CFR and flow-dependent coronary dilation; these changes were attributable to nitric oxide. Cilostazol may improve coronary vascular endothelial dysfunction and coronary hemodynamics in patients with VSA. (C)2003 by Excerpta Medica, Inc.

DOI： 10.1016/s0002-9149(03)00458-2

Web of Science

PubMed

researchmap

PubMed

researchmap

PubMed

researchmap

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：SPRINGER-VERLAG  

This study was designed to compare the efficacy of bevantolol, a beta(1)-selective blocker with alpha-blockade and vasodilating activity, with that of metoprolol, a beta(1)-selective receptor blocker, for the treatment of idiopathic dilated cardiomyopathy (DCM). Forty-one patients with DCM were enrolled to receive either bevantolol or metoprolol in addition to the standard therapy for DCM. They were classified into two groups: 16 patients were treated with bevantolol and 25 were treated with metoprolol. Echocardiographic parameters and atrial and brain natriuretic peptides (ANP, BNP) were measured before treatment and after 6 months of treatment. Left ventricular dimension at end-diastole and end-systole was significantly lower and fractional shortening was significantly higher after treatment than before treatment in both groups. The plasma ANP and BNP levels were significantly decreased in both groups. Changes in all variables, except for systolic blood pressure, showed no significant differences between the two groups. In conclusion, bevantolol showed parallel beneficial effects to those of metoprolol on cardiac function and natriuretic peptides in patients with DCM.

DOI： 10.1007/s003800200043

Web of Science

PubMed

researchmap

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：BLACKWELL PUBLISHING ASIA  

An 18-year-old male patient with biventricular hypertrophic obstructive cardiomyopathy (HOCM) had successful reduction of the pressure gradients by cibenzoline. At 11 months after birth, he was first diagnosed with cardiac murmurs and by the age of 5 years, he was diagnosed with subpulmonic infundibular stenosis with a pressure gradient of 10 mmHg by cardiac catheterization. At the age of 14, re-catherterization revealed hypertrophic cardiomyopathy with isolated obstruction of the right ventricular outflow tract, with a pressure gradient of 70 mmHg, but no obstruction in the left ventricle. He began daily treatment with 30 mg propranolol. At the age of 18, he was admitted for cardiac evaluation. An echocardiogram revealed left mid-ventricular and subpulmonic obstructions associated with pressure gradients of 88 mmHg and 65 mmHg, respectively. A single oral dose of 200 mg of cibenzoline decreased the pressure gradients in the left and right ventricles (38 mmHg and 36 mmHg, respectively). He was then given 300 mg daily of cibenzoline, and both pressure gradients remained low without any complications 8 months later at the time of discharge.

Web of Science

PubMed

researchmap

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

Background-In vitro studies suggest that angiotensin II type 1 and type 2 (AT(1) and AT(2)) receptors exert opposite effects in terms of vasoconstriction, natriuresis, and cell growth, but the role of these receptors in cardiovascular remodeling in vivo is still an enigma. In this study, we tested the hypothesis that AT(2) exerts an antiproliferative effect by inducing apoptosis, thereby antagonizing AT(1a) in vascular remodeling.
Methods and Results-Vascular injury was induced by polyethylene cuff placement around the left femoral artery of AT(1a)-null (AT(1a)KO), AT(2)-null (AT(2)KO), and wild-type mice. Neointimal formation as well as DNA synthesis in vascular smooth-muscle cells (VSMC) after vascular injury was exaggerated in AT(2)KO mice, but they were both suppressed in AT(1a)KO mice compared with those in wild-type mice. In contrast, the number of apoptotic cells in the injured artery in VSMC was significantly increased in AT(1a)KO mice but decreased in AT(2)KO mice. Reverse transcriptase-polymerase chain reaction analysis revealed that the expression of bax rnRNA was attenuated in AT(2)KO mice. On the other hand, the expression of bcl-2 and bcl-x(L) mRNA was enhanced in AT(2)KO mice but attenuated in AT(1a)KO mice. Immunohistochemical staining with antibody to the bcl-2 protein family supported these results.
Conclusions-Our results suggest that AT2 exerts antiproliferative effects and proapoptotic changes in VSMC by counteracting AT(1a) in the process of neointimal formation after vascular injury.

DOI： 10.1161/01.CIR.0000024103.04821.86

Web of Science

PubMed

researchmap

Language：English   Publishing type：Research paper (scientific journal)   Publisher：LIPPINCOTT WILLIAMS & WILKINS  

To clarify the possible involvement of uninhibited angiotensin II (Ang II) type 2 (AT(2)) receptor stimulation in the effects of an Ang II type 1 (AT(1)) receptor blocker, valsartan, we examined the cardiovascular remodeling induced by aortic banding with the use of wild-type (Agtr2+) and AT(2) receptor null (Agtr2-) mice. Aortic banding caused cardiac hypertrophy in Agtr2+ and Agtr2- mice to a similar degree 6 weeks after surgery, whereas coronary arterial thickening and perivascular fibrosis were more exaggerated in Agtr2- mice. The AT(2) receptor was observed predominantly in the coronary arteries and perivascular region of Agtr2+ mice. Valsartan at a dose of 1 mg/kg per day, which did not influence systolic blood pressure, suppressed cardiac hypertrophy similarly in both strains. Valsartan inhibited coronary arterial thickening and perivascular fibrosis in both groups; however, the inhibitory effects of valsartan were significantly weaker in Agtr2- trice. The inhibitory effects of a nonselective Ang II receptor antagonist, [Sar(1),Ile(8)]-Ang II, on cardiac hypertrophy, coronary artery thickening, and perivascular fibrosis were not significantly different in Agtr2+ and Agtr2- mice. These results suggest that the improvement by valsartan of coronary arterial thickening and perivascular fibrosis after pressure overload is caused by uninhibited AT(2) receptor stimulation in addition to AT(1) receptor blockade.

Web of Science

PubMed

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(一社)医療の質・安全学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)医療の質・安全学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本医薬品情報学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：English   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本不整脈心電学会  

【背景】植込みデバイス治療の安全性向上のためには、心臓解剖の習熟と手術手技の修練が不可欠である。本邦でも、手術手技習得を目的としたカダバートレーニング(死体を使った手術研修)が始まっており、今回デバイス植込み手技習得のためのカダバートレーニングを施行したため、報告する。【方法】Thiel固定液で固定された献体を対象とした。解剖室に放射線管理区域を設定し、X線透視を使用できる環境を整えた。実際のデバイス植込みと同様に鎖骨下静脈から心房・心室リードを留置し、その後解剖を行った。【結果】実臨床と同様に鎖骨下静脈からのリード留置が可能であった。しかしながら、非拍動下では心耳の同定が難しく、右心耳へのリード留置は困難であった。リード留置後の解剖では、解剖学的に組織が薄い部位を確認することができた。また、透視では心尖部と思われたリードは実際には心尖部近傍中隔に留置されており、透視上と解剖上の留置部位が異なっていた。真の解剖学的心尖部は、透視のみでは把握困難と考えられた。【結語】カダバートレーニングは心臓の構造を理解し、手技の安全性を向上させるうえで有用であると考えられた。(著者抄録)

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：English   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心血管インターベンション治療学会  

researchmap

Language：Japanese   Publisher：(一社)日本超音波検査学会  

researchmap

Language：Japanese   Publisher：(公財)日本心臓財団  

症例は75歳、男性。失神発作を伴うBrugada症候群に対して2012年9月に植込み型除細動器(implantable cardioverter defibrillator;ICD)移植術を施行した。ICD植込み8ヵ月後に草刈り機を使用し、約5時間の草刈り作業を行った。植込み部位に軽い違和感があったが放置し、数日後挫創ができていることに気付き近医を受診した。創部は徐々に拡大し、数日で創部が開放したためデバイス感染が強く疑われ精査加療目的で当院に入院した。左前胸部の創部に膿瘍を形成しており、鑷子で創部を観察すると容易にICD本体が外部と開通していたためデバイス感染と診断した。入院第2病日にICDを全抜去し、抗生剤による厳重な感染コントロールを行った後、反対側からICD再植込み術を施行した。デバイス感染予防には草刈り作業などの物理的刺激の回避も重要と考えられ、デバイス感染の診断・治療・管理についても文献的考察を加えて報告する。(著者抄録)

DOI： 10.11281/shinzo.47.166

researchmap

Other Link： http://search.jamas.or.jp/link/ui/2015217613

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公財)日本心臓財団  

症例は72歳、女性。当院膠原病内科で全身性エリテマトーデスに合併した血球貪食症候群に対して化学療法(CHOP療法)を施行後に心不全を発症しアドリアマイシン心筋症と診断された。また、心エコー上中等度の大動脈弁狭窄症を指摘された。以後心不全標準治療を継続したが、約10年の経過で徐々に心機能低下と大動脈弁狭窄症の重症度が進行し、心不全の増悪による入退院を繰り返した。内科的治療の限界と判断し、外科的大動脈弁置換術や経カテーテル的大動脈弁植込み術(Transcatheter Aortic Valve Implantation;TAVI)の適応を診断するため、低用量ドブタミン負荷心エコー検査を行った。本症例は偽性重症大動脈弁狭窄症の可能性があるため、Blaisらが提唱した予測有効大動脈弁口面積(projected effective orifice area;EOAproj)測定したところ、EOAproj 1.18cm2で境界所見であった。胸部CT検査から求めた大動脈弁石灰指数(Agatston&#039;s score)は659であり、強い石灰化は指摘できなかった。カテコラミンを含む心不全治療を行ったが、心不全の改善を認めず死亡した。剖検を行った結果、大動脈弁は弁腹の石灰化を認めたが、弁尖の変性は軽度であった。今回われわれは低左心機能を伴う大動脈弁狭窄症例におけるドブタミン負荷心エコー検査の有用性、限界について検討したので報告する。(著者抄録)

researchmap

Language：Japanese   Publisher：(株)メディカルレビュー社  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(公財)日本心臓財団  

症例は73歳、女性。2005年に検診の胸部X線検査で胸部異常陰影を指摘され、気管支鏡下肺生検で肺サルコイドーシスと確定診断された。以降、他科にて経過観察中であったが、2011年に施行した心エコー図検査で心室中隔中部の壁菲薄化を認め、心サルコイドーシスが疑われたため、当科に入院した。冠動脈造影では異常を認めなかったが、心筋血流シンチグラムにて菲薄化部位に一致して灌流異常を認め、ヘパリン負荷下の18F-FDG-PETでは同部位を中心に心臓への異常集積を認めた。心サルコイドーシスの可能性が高いと考えられたため、ステロイド加療を開始した。心サルコイドーシスの特徴的形態としては心室中隔基部の壁菲薄化があげられているが、現在までに心室中隔中部の壁菲薄化をきたした報告はない。心サルコイドーシスの表現型として心室中隔中部の菲薄化・憩室があることを念頭におき、各種モダリティでの精査を行い、早期に診断することが重要と考えられたため、文献的考察を加え報告する。(著者抄録)

researchmap

Language：Japanese   Publisher：(一社)日本超音波検査学会  

researchmap

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(株)日本臨床社  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(株)新興医学出版社  

70代男。失神と呼吸困難を主訴とした。X線で心拡大と左第2弓・右第2弓の突出を認め、心電図では心拍数61/minの正常洞調律、不完全右脚ブロック、Is、IIIQ、陰性T波(II、III、aVF、V1〜4)を認めた。心エコーでは、右室拡大と左室圧排所見、三尖弁逆流圧較差の上昇を認めた。食後低血圧による失神を繰り返したため、糖尿病に伴う自立神経障害からの食後低血圧も合併していると診断し、頻回少量の食事に変更したが、効果がなかった。肺血流シンチグラフィー、造影CT、血液検査で異常所見は認めず、associated肺動脈性肺高血圧症(PAH)は否定的であった。その後、右心カテーテル検査で肺動脈圧と肺血管抵抗の上昇を認めたため、PAHと診断した。酸素療法や抗凝固療法、ベラプロスト投与を開始したが、三尖弁逆流圧較差が改善しなかったため、ボセンタンを追加投与した。右室拡大は改善し、三尖弁逆流圧較差が半減、失神も消失し、第53病日に退院となった。

researchmap

Language：Japanese   Publisher：(公財)日本応用酵素協会  

researchmap

Language：Japanese   Publisher：(公財)日本心臓財団  

症例は64歳、女性。2005年に完全房室ブロックのため、DDDペースメーカー植え込み術を施行された。2008年に左前脛骨部の皮膚生検からサルコイドーシスと確定診断された。2009年4月より労作時呼吸困難が出現し、徐々に増悪した。2010年1月には軽労作でも呼吸困難が出現するようになったため、精査目的で当院に紹介された。心エコー図検査で左室拡大、び漫性の壁運動低下(特に心室中隔基部と後壁の菲薄化)、Gaシンチグラフィや18F-FDG-PETで心臓への集積を認め心サルコイドーシスと診断した。心エコー図検査で右室心尖部ペーシングによる左室同期不全も認めたため、心臓再同期療法およびステロイド療法を開始した。また、終夜睡眠検査で中枢性優位の睡眠時無呼吸症候群の合併を認めたため、陽圧換気療法(adaptive servo-ventilation;ASV)も開始した。治療後、左室駆出率は22.5%から29.7%に、拡張末期左室容積も148mLから104mLに軽度改善したが、reverse remodelingは認めず心機能改善効果は軽度であった。心筋障害や左室remodelingの高度な症例での治療には一定の効果が認められたが限定的であった。このため、心不全早期からの治療介入が重要と考えられたため、文献的考察を加えて報告する。(著者抄録)

researchmap

Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2012&ichushi_jid=J00679&link_issn=&doc_id=20120124160016&doc_link_id=%2Fah2sinzd%2F2012%2F004401%2F018%2F0062-0068%26dl%3D0&url=http%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fah2sinzd%2F2012%2F004401%2F018%2F0062-0068%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：愛媛医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：(一社)日本不整脈心電学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本不整脈心電学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：バイエル薬品(株)  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(公社)日本薬理学会  

researchmap

Language：Japanese   Publisher：(株)日本臨床社  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(株)先端医学社  

VALUEは,同等の降圧効果で治療した場合,バルサルタンの心血管イベント抑制効果はアムロジピンよりも優れているという仮説を検証する目的でおこなわれた.血圧値は観察期間のいずれの時点でもアムロジピン群で有意に低値であったが,一次エンドポイントである心疾患死および心疾患発症の複合エンドポイントには両群間で差を認めなかった.心筋梗塞の発症率はバルサルタン群で有意に高かった.一方,糖尿病の新規発症率はバルサルタン群で有意なリスク低下が認められた.血圧補正後の解析では,心筋梗塞の発症率は両群間で差はなく,心不全の予防効果はバルサルタンが有意に優れていた.VALUEの結果から,ハイリスク高血圧患者に対する降圧の重要性が再認識されたとともに,バルサルタンの降圧を超えた心不全および糖尿病発症予防効果が確認された(著者抄録)

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：愛媛医学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(公財)臨床薬理研究振興財団  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(株)先端医学社  

アンジオテンシンIIの受容体サブタイプには,主としてAT1受容体とAT2受容体が存在する.AT1受容体刺激は血管収縮作用や水・Na貯留作用に加え,炎症,細胞増殖,肥大作用を引き起こすことが知られている.一方,AT2受容体は血管障害や心筋梗塞などの臓器障害に伴って特異的に発現し,AT1受容体を介したシグナルに拮抗してはたらくことで心血管リモデリングに深く関与していることが明らかとなり,その心血管保護作用が注目されている

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：(株)メジカルビュー社  

researchmap

Language：Japanese   Publisher：(有)科学評論社  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：ライフサイエンス出版(株)  

2型糖尿病モデルマウスを用いて,耐糖能異常及び血管傷害に対するピタバスタチンの効果を検討した.グルコース取り込み測定に先立ち,マウスを用いて,経口糖負荷試験(OGTT)を行った.KK-A yマウスを一晩絶食させた後,2g/kgのグルコースを経口投与し,その前後において血漿のグルコース濃度を測定した.正常マウスでは,30分値をピークにして血糖が変化するのに対して,KK-A yマウスでは,正常マウスに比べて,30〜120分迄,著明な血糖値の上昇が認められた.このKK-A yマウスに対して,ピタバスタチン3mg/kg/日を2週間,前投与した後にOGTTを行うと,特に30分値,60分値の血糖値の上昇を有意に抑制するという結果が得られた.以上より,ピタバスタチンは耐糖能異常,或いはインスリン抵抗性に対して改善効果をもつ可能性が示唆された

researchmap

Language：Japanese   Publisher：(株)日本臨床社  

researchmap

Language：Japanese   Publisher：(株)日本臨床社  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：日本臨床生理学会  

researchmap

Language：Japanese   Publisher：(一社)日本リウマチ学会  

49歳女.35歳時に完全房室ブロックで恒久的ペースメーカー植込み術を施行された.39歳時に拡張型心筋症による左心不全で入院し,入退院を繰り返した.45歳時に,右眼隅角にサルコイド結節の存在を疑われたが確診に至らなかった.ツベリクリン反応陰性,血清リゾチーム高値で,Gaシンチで心への軽度集積を認めた.また,心不全に対し強心剤,利尿剤,ACE阻害剤,β遮断剤を投与したが,入院間隔が徐々に短縮し,保存的にコントロール困難と判断され,三尖弁閉鎖不全に対し,僧帽弁および三尖弁輪縫縮術を施行し,ワーファリン投与となったが心症状の改善はなかった.入院後,心不全は軽快傾向にあったが,咳嗽後,突然喀血し呼吸困難なため緊急気管支鏡検査を施行した.止血は困難で,処置中にショック状態となり死亡した.全身性サルコイドーシスで,喀血の原因はサルコイドーシスに伴う肉芽腫性肺動脈炎と考えられた

researchmap

Language：Japanese   Publisher：(公社)日本超音波医学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：日本臨床生理学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：愛媛医学会  

冠攣縮性狭心症患者86例を対象に外来受診時の胸部症状と診断確定迄の過程を分析した.その結果,典型的な夜間・早朝の安静時胸痛例は27例(31%)と少なく,又,以外の安静時胸痛例も14%に認めた.労作時胸痛を約14%の症例に,急性冠症候群を9%に認め胸部症状持続時間は10分以内が45例,10分以上30分未満が31例,30分以上が5例であった.発作時の硝酸薬の効果は,30例中8例が有効であった.明らかな胸痛発作の誘因は飲酒3例,喫煙後1例,パチンコ中1例と入浴後3例であった.心臓カテーテル検査施行理由は胸痛・胸部圧迫感20例(23%),胸部症状増悪15例(17%),心電図異常18例(21%)で心筋血流イメージ又は心筋脂肪酸代謝イメージ異常所見33例(39%)であった.86例中8例が,受診前に他の病院を受診し,非観血的検査後に異常なしと診断されていた

researchmap

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(NPO)日本高血圧学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：愛媛医学会  

動脈穿刺と共に静脈穿刺も必要な患者50例に対して上腕動脈穿刺+橈側・尺側皮静脈穿刺を試みた.その結果,静脈穿刺に失敗した1例を除く49例(98%)で穿刺に成功した.失敗した1例には対側の静脈穿刺を行い手技成功率は100%であった.動脈・静脈穿刺に伴う合併症は全く生じず,穿刺部位からの出血もみられなかった

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：愛媛医学会  

1年間に選択的冠動脈造影検査と同時に頸部動脈DSA・下肢動脈・上肢動脈造影検査を施行した虚血性心疾患患者144例の全身動脈硬化所見を検討した.検査に伴う合併症は認められなかった.冠動脈・内頸動脈・下肢動脈・上肢動脈の動脈狭窄の有無で冠危険因子,血清脂質値,血糖値,HbA1c値に差異を認めなかった.冠動脈病変指数増加に伴い,内頸動脈狭窄と下肢動脈狭窄症例数は有意に増加を認めたが,上肢動脈狭窄との間に相関関係はなかった.頸部DSAと上肢動脈造影検査で,動脈瘤は認められなかったが,下肢血管造影検査で無症状の動脈瘤を7例認め,内2例に手術を施行した

researchmap

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：(一社)日本内科学会  

researchmap

Language：Japanese   Publisher：日本臨床生理学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：日本心血管インターベンション学会  

4F診断的カテーテル検査施行時にジェットバランス(M群n=50),現行型ピッグカテーテル(C群n=50)を使用し,臨床成績を比較検討した. 1)M群において有意の心室性不整脈の抑制効果が認められた. 2)カテーテル安定性(遊走スコア),左室造影性(造影性スコア)共にM群が優れていた. 3)4F診断的カテーテル検査におけるジェットバランスの有用性が示唆された

researchmap

Language：Japanese   Publisher：臨床心臓電気生理研究会  

71歳男.発作時心拍数は150bpmのnarrow QRS tachycardiaであった.ATP或いはverapamil 5mg静注にて2:1〜4:1房室ブロックが出現しても頻拍は継続し心房性頻拍(AT-1)と診断した.AT-1はペーシングにて誘発停止が可能で,電気生理学的反応から機序はリエントリーと考えられた.最早期興奮部位は三尖弁輪上右房外側11時の位置で,同部位より高周波通電を行ったところ心房頻拍が停止した.以後AT-1は誘発されず成功と考えた.しかし退院1週間後異なるAT-2が出現した.AT-2の機序もリエントリーが考えられたが最早期興奮部位は洞結節近傍であった.高周波通電にて頻拍は停止し以後誘発されなくなったが,退院後再び新たなAT-3が出現した.患者の希望にてこの頻拍に対するアブレーションは断念した

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

CiNii Books

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：日本臨床生理学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本心臓病学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：(一社)日本老年医学会  

researchmap

Language：Japanese   Publisher：(一社)日本循環器学会  

researchmap