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Minoru Yoshiyama

Publications and source records attributed to Minoru Yoshiyama.

At least 37 records · Page 2Linked to original sources
PubMed2006

[Estimation of myocardial ischemia by diastolic strain analysis in exercise stress echocardiography: comparison with exercise thallium-201 single photon emission computed tomography].

OBJECTIVES: The feasibility of detecting persistent regional left ventricular abnormal relaxation due to myocardial ischemia using strain echocardiography several minutes after exercise was investigated. METHODS: Consecutive 27 patients (mean age 65 +/- 9 years, 21 males, 6 females) with suspected coronary artery disease were enrolled. Strain echocardiographic images were acquired at the mid segments of the left ventricular wall before and 5 min after exercise in the apical long-axis, two-chamber and four-chamber views. Strain curves were obtained at each segment, and peak values of strain at the closure of aortic valve (A) and at one third of diastolic duration (B) were measured. Strain diastolic index (SDI) was calculated as (A - B)/A X 100%. The ratio of SDI before exercise to that after exercise was defined as the SDI ratio and compared with exercise thallium-201 single photon emission computed tomography (SPECT) as the reference standard to detect myocardial ischemia. RESULTS: A total of 162 segments were evaluated. Based on the results of exercise SPECT, 119 segments were classified as non-ischemic segments, and 43 as ischemic segments. Ischemic segments showed significant decreases in SDI before and after exercise, whereas non-ischemic segments showed no significant differences in SDI before and after exercise. SDI ratio was significantly decreased in ischemic segments, but not in non-ischemic segments. SDI ratio with a cut off value of 0.51 had a sensitivity of 91% and a specificity of 89% to detect myocardial ischemia in the receiver-operating characteristics. Conclusions. Strain echocardiography can provide quantitative assessment of myocardial ischemia by detecting post-ischemic regional left ventricular delayed relaxation even 5 min after exercise.

Aged↗
PubMed2006

Activation of mitogen-activated protein kinases, activator protein-1, and nuclear factor-kappaB during acute rejection after heterotopic heart transplantation in rats.

BACKGROUND: Activation of mitogen-activated protein kinases (MAPKs), including c-Jun NH2-terminal kinases (JNKs), extracellular signal-regulated kinases (ERKs), and p38MAPK during acute cardiac rejection is not clear. This study aimed to determine whether MAPKs and transcriptional factors such as activator protein-1 (AP-1) and nuclear factor-kappaB (NF-kappaB) were involved in acute rejection after cardiac transplantation. METHODS: Hearts from Lewis (LEW) rats (group C) or DA rats (group R) were transplanted into the abdomen of recipients (LEW). Grafts were collected at the 1st, 3rd, or 5th postoperative day (POD). ERKs were measured by Western blot analysis, and JNKs were measured by in-gel kinase assay. AP-1 and NF-kappaB DNA binding activities were determined using an electrophoretic mobility shift assay. We assessed functions of donor hearts using echocardiography. RESULTS: Heart rates and myocardial contraction significantly decreased at POD 5 in group R. Phosphorylated p42ERK and p44ERK in the left ventricular free wall (FW) and septal wall (SW) of group R significantly increased at POD 5 compared to those of group C at POD 1. Activities of p46JNK and p55JNK in the FW and SW of group R also significantly increased at POD 5. AP-1 DNA binding activities in the FW and SW of group R significantly increased at POD 5, and NF-kappaB DNA binding activities of group R significantly increased at PODs 3 and 5. CONCLUSIONS: We conclude that ERK, JNK, AP-1, and NF-kappaB are activated during acute rejection. The MAPK pathways may play an important role in acute cardiac rejection.

Animals↗
PubMed2006

Endothelin-converting enzyme expression in the neointima after percutaneous coronary intervention.

Smooth muscle cells (SMCs) are the major cellular component of neointimal tissues after percutaneous coronary intervension (PCI). Endothelin-1 (ET-1) is a powerful vasoconstrictor and has a mitogenic effect on SMCs. Endothelin-converting enzyme (ECE) is a key enzyme in the process of ET-1 generation. However, the expression of ECE in association with post-PCI repair processes has not been reported. Thirteen coronary sites after PCI obtained at autopsy and 6 atherectomy specimens obtained from restenotic sites were investigated. Frozen sections were stained with antibodies against ECE, SMCs, macrophages, and endothelial cells. The immunoreactivity of ECE was quantified using computer-aided planimetry. At the early stage after PCI, most neointimal SMCs expressed ECE. The ECE-positive cell area was significantly (p<0.005) larger in the sites within 3 months after PCI than in the sites from 6 months onward. In atherectomy specimens, neointimal SMCs showed distinct ECE positivity. These findings suggest that ECE is upregulated in the neointima at early stages after PCI injury. ECE may be one of the mediators in the repair processes after PCI in humans.

Aged↗
PubMed2005

Comparison of levels of serum matrix metalloproteinase-9 in patients with acute myocardial infarction versus unstable angina pectoris versus stable angina pectoris.

Matrix metalloproteinases (MMPs) are important for resorption of extracellular matrixes and may degrade the fibrous cap of an atherosclerotic plaque, thus contributing to coronary plaque rupture. Histologic studies have shown MMP expression in lesions of acute coronary syndrome. In this study, we evaluated the relation between plaque morphology as obtained by intravascular ultrasound before percutaneous coronary intervention and serum MMP levels in patients who had coronary artery disease. We enrolled consecutive 47 patients who had acute myocardial infarction (AMI), 23 who had unstable angina pectoris (UAP), and 19 who had stable effort angina pectoris and underwent intravascular ultrasound before percutaneous coronary intervention followed by successful primary percutaneous coronary intervention. Peripheral blood was obtained from all patients before angiography and serum levels of MMP-1,-2, and -9 were analyzed. Serum levels of MMP-9 in the AMI and UAP groups were significantly higher than that in the stable effort angina pectoris group (p = 0.007 and 0.04, respectively). From the intravascular ultrasound findings before percutaneous coronary intervention, plaque rupture was detected in 26 patients (55%) in the AMI group and in 11 patients (48%) in the UAP group. In these 2 groups, patients with plaque rupture had significantly higher levels of MMP-9 than patients who did not have plaque rupture (p = 0.03 and 0.01, respectively). Multiple logistic regression analysis showed that MMP-9 was the only independent predictor of plaque rupture (p = 0.004). In conclusion, high levels of MMP-9 in patients who have AMI and UAP are related to the presence of plaque rupture in the culprit lesion.

Aged↗
PubMed2005

Granulocyte-colony stimulating factor augments neovascularization induced by bone marrow transplantation in rat hindlimb ischemia.

Because granulocyte-colony stimulating factor (G-CSF) mobilizes bone marrow cells including endothelial progenitor cells, we examined whether G-CSF augments angiogenesis and collateral vessel formation induced by bone marrow-mononuclear cells transplantation (BMT). Unilateral hindlimb ischemia was surgically induced in Lewis rats. One week after surgery, administration of 100 mg/kg per day G-CSF significantly increased the laser Doppler blood perfusion index (LDBPI), number of angiographically detectable collateral vessels (angiographic score), and capillary density determined by alkaline phosphatase staining. In the BMT group (1 x 10(7) cells/rat) and the group with combined G-CSF treatment and BMT, LDBPI was significantly increased compared with that in the vehicle-treated group. In the BMT group, neovascularization was significantly increased as evidenced by the angiographic score and capillary density compared with the vehicle-treated group. Furthermore, the combination of G-CSF treatment and BMT augmented neovascularization compared with BMT alone, as evidenced by the angiographic score and capillary density. Moreover, G-CSF significantly increased vascular endothelial growth factor mRNA and fibroblast growth factor-2 mRNA in hindlimb muscle. In conclusion, G-CSF was found to augment neovascularization in rat hindlimb ischemia. Combined use of G-CSF treatment and BMT may be a useful strategy for therapeutic neovascularization in ischemic tissues.

Alkaline Phosphatase↗
PubMed2005

Beneficial effect of candesartan on rat diastolic heart failure.

In this study, we examined whether an angiotensin II type 1 (AT1)-receptor blocker improves diastolic heart failure (DHF) in Dahl salt-sensitive (DS) rats. DHF was prepared by feeding DS rats on 8% NaCl diet from 7 weeks of age. DHF was estimated with echocardiography by measuring E velocity / A velocity (E/A) of left ventricular inflow. DS rats with established DHF were orally given candesartan (1 mg/kg per day) or vehicle. After 13 days of treatment, candesartan significantly improved DHF, as shown by the reduction of E/A from 4.49 +/- 1.04 to 1.98 +/- 0.54 (P<0.05) and prolonged survival rate more than the vehicle. Cardiac fibrosis, apoptosis, and gene expression were estimated by Sirius Red-staining, TUNEL-staining, and Northern blot analysis, respectively. The improvement of DHF by candesartan was accompanied by the decrease in cardiac hypertrophy, fibrosis, and apoptosis, and the reduction of gene expression of brain natriuretic peptide, collagen I, and monocyte chemoattractant protein-1. Moreover, candesartan decreased cardiac inflammatory cells and reactive oxygen species, estimated by counting ED-1-positive cells and the measurement of 4-hydroxy-2-nonenal staining, respectively. These results indicate that candesartan can improve diastolic dysfunction and may slow the progression of cardiac remodelling in DS rats with established DHF.

Aldehydes↗
PubMed2005

Acute hemodynamic benefits of bi-atrial atrioventricular sequential pacing with the optimal atrioventricular delay.

OBJECTIVES: We evaluate the acute effects on hemodynamics of bi-atrial (BiA) pacing with the optimal atrioventricular (AV) delays, in comparison with high right atrial (HRA) pacing and coronary sinus (CS) pacing. BACKGROUND: Bi-atrial pacing has been suggested as one of the alternative therapy for preventing the recurrence of atrial fibrillation (AF). There are, however, few reports on the hemodynamic effects of BiA pacing, and the results that exist are controversial. METHODS: Twenty patients were paced from HRA, left lateral site of CS, and both sites with the optimal AV delays at 80 and 100 beats/min, in random order. After 5-min pacing, maximal P-wave duration in a 12-lead electrocardiogram, cardiac output (CO), pulmonary capillary wedge pressure (PCWP), and the transmitral flow pattern by transthoracic echocardiography were measured. RESULTS: Compared with HRA and CS pacing, BiA pacing delivered the shortest P-wave duration (HRA: 130 +/- 14 ms, CS: 132 +/- 19 ms, and BiA: 94 +/- 8 ms, respectively, p < 0.001) and the most improvement in CO and PCWP (HRA: 3.63 +/- 0.67 l/min and 9.2 +/- 4.3 mm Hg, CS: 3.71 +/- 0.70 l/min and 8.8 +/- 3.4 mmHg, and BiA: 3.88 +/- 0.63 l/min and 8.0 +/- 3.1 mmHg, respectively, p < 0.01). Bi-atrial pacing also significantly increased the mitral flow time velocity integral and peak A-wave velocity by transthoracic echocardiography, compared with HRA and CS pacing (HRA: 7.6 +/- 1.4 cm and 68.8 +/- 12.2 cm/s, CS: 7.8 +/- 1.4 cm and 70.5 +/- 14.5 cm/s, and BiA: 8.2 +/- 1.2 cm and 76.3 +/- 14.2 cm/s, respectively, p < 0.01). Bi-atrial pacing most significantly decreased the intervals between the atrial pacing spike and the peak of A-wave (HRA: 180 +/- 28 ms, CS: 165 +/- 21 ms, and BiA: 157 +/- 19 ms, respectively, p < 0.01). These improvements in hemodynamics significantly correlated with interatrial conduction delay. CONCLUSIONS: Bi-atrial pacing made the most significant improvements of hemodynamics. These benefits may be due to the improvements in interatrial conduction delay and atrial dyssynchrony.

Aged↗
PubMed2005

Angiotensin blockade inhibits osteopontin expression in non-infarcted myocardium after myocardial infarction.

Osteopontin has been reported to have an important role in cardiac fibrosis. However, little is known about the effects of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin type 1 receptor blockers (ARB) on osteopontin expression in infarcted myocardium. The purpose of this study was to elucidate the effects of an ACEI (perindpril) and an ARB (candesartan cilexitil) on cardiac function as assessed by Doppler echocardiography and cardiac osteopontin expression associated with cardiac remodeling in myocardial infarcted rats. ACEI or ARB was administered after myocardial infarction (MI). At 4 weeks after MI, cardiac function, and mRNAs in non-infarcted myocardium were analyzed. ACEI and ARB equally prevented left ventricular dilatation, reduction of ejection fraction, and the increase in E/A wave velocity ratio and the rate of E wave deceleration by MI. ACEI and ARB significantly suppressed increased mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, osteopontin, and collagen I and III in the non-infarcted ventricle at 4 weeks. Immunohistochemically stained osteopontin was increased in interstitial fibrosis of non-infarcted myocardium. Both ACEI and ARB significantly prevented cardiac fibrosis and osteopontin expression. In conclusion, angiotensin blockade inhibits osteopontin expression in non-infarcted myocardium and prevents cardiac remodeling after MI.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Important role of apoptosis signal-regulating kinase 1 in ischemia-induced angiogenesis.

OBJECTIVE: We first examined the role of apoptosis signal-regulating kinase 1 (ASK1), one of mitogen-activated protein kinase kinase kinases, in ischemia-induced angiogenesis. METHODS AND RESULTS: Unilateral hindlimb ischemia was induced surgically in C57BL/6J wild-type (WT) mice or mice deficient in ASK1 (ASK1(-/-)). ASK1 activity in WT mouse hindlimb was increased dramatically after ischemia. By laser Doppler analysis, well-developed collateral vessels and angiogenesis were observed in WT mice in response to hindlimb ischemia, whereas these responses were reduced in ASK1(-/-) mice. Immunostaining revealed that infiltration of macrophages and T lymphocytes was suppressed in the ischemic tissues of ASK1(-/-) mice compared with WT mice. The expression of vascular endothelial growth factor (VEGF) and monocyte chemoattractant protein-1 (MCP-1) proteins in ischemic tissues was weaker in ASK1(-/-) mice compared with WT mice. In vitro study on endothelial cells indicated that dominant-negative ASK1 significantly attenuated hydrogen peroxide-induced VEGF and MCP-1 production. Furthermore, in vivo blockade of MCP-1 by its neutralizing antibody suppressed the recovery of the blood flow and capillary formation after ischemia. CONCLUSIONS: ASK1 pathway promotes early angiogenesis by inducing inflammatory cell infiltration and VEGF and MCP-1 expression. ASK1 may provide the basis for the development of new therapeutic strategy for angiogenesis.

Animals↗
PubMed2005

Vascular endothelial growth factor-expressing mesenchymal stem cell transplantation for the treatment of acute myocardial infarction.

OBJECTIVE: Vascular endothelial growth factor (VEGF) plays an important role in inducing angiogenesis. Mesenchymal stem cells (MSCs) may have potential for differentiation to several types of cells, including myocytes. We hypothesized that transplantation of VEGF-expressing MSCs could effectively treat acute myocardial infarction (MI) by providing enhanced cardioprotection, followed by angiogenic effects in salvaging ischemic myocardium. METHODS AND RESULTS: The human VEGF165 gene was transfected to cultured MSCs of Lewis rats using an adenoviral vector. Six million VEGF-transfected and LacZ-transfected MSCs (VEGF group), LacZ-transfected MSCs (control group), or serum-free medium only (medium group) were injected into syngeneic rat hearts 1 hour after left coronary artery occlusion. At 1 week after MI, MSCs were detected by X-gal staining in infarcted region. High expression of VEGF was immunostained in the VEGF group. At 28 days after MI, infarct size, left ventricular dimensions, ejection fraction, E wave/A wave ratio and capillary density of the infarcted region were most improved in the VEGF group, compared with the medium group. Immunohistochemically, alpha-smooth muscle actin-positive cells were most increased in the VEGF group. CONCLUSIONS: This combined strategy of cell transplantation with gene therapy could be a useful therapy for the treatment of acute MI.

Actin Cytoskeleton↗
PubMed2005

Non-invasive assessment of myocardial ischaemia using new real-time three-dimensional dobutamine stress echocardiography: comparison with conventional two-dimensional methods.

AIMS: Although two-dimensional-dobutamine stress echocardiography (2D-DSE) is useful for the diagnosis of myocardial ischaemia, it requires the acquisition of multiple cross-sections at each stage. The introduction of new real-time three-dimensional echocardiography (RT3DE) offers rapid acquisition and 3D display of the entire left ventricle (LV). The purpose was to evaluate real-time three-dimensional-dobutamine stress echocardiography (RT3D-DSE) for the diagnosis of ischaemia using exercise (201)Tl single-photon emission computed tomography (SPECT) as the reference standard, in comparison with 2D-DSE. METHODS AND RESULTS: We performed DSE in 56 consecutive patients who had undergone SPECT because of suspected ischaemia. 3D images by RT3DE were acquired from the apical window after the acquisition of cross-sectional images at every stage of 2D-DSE. Wall motion analysis in RT3DE was performed from anatomical images by cropping the acquired full volume data sets. Mean scanning time for adequate image acquisition at peak stress by RT3D-DSE was shorter than that by 2D-DSE (29+/-4 vs. 68+/-6 s, P<0.0001). RT3DE provided adequate images at success rate of 92% at rest and 89% at peak stress, whereas two-dimensional echocardiography did at 94 and 90%, respectively. The sensitivity, specificity, and accuracy of RT3D-DSE for the detection of coronary artery disease are 86, 80, and 82%, respectively. Those of 2D-DSE are 86, 83, and 84%, respectively. There were no significant differences in the sensitivity, specificity, and accuracy between these two methods (P=1.000). CONCLUSION: RT3D-DSE offers rapid and simple acquisition of the entire LV wall motion and provides feasible and accurate assessment of myocardial ischaemia.

Aged↗
PubMed2005

Protective effect of high diastolic blood pressure during exercise against exercise-induced myocardial ischemia.

BACKGROUND: Hypertension is one of the risk factors for coronary artery disease. However, because most coronary blood flow to the left ventricle occurs during diastole, high diastolic blood pressure during exercise may have a protective effect against exercise-induced myocardial ischemia. The aim of the present study was to test this hypothesis. METHODS AND RESULTS: We identified 469 patients with sinus rhythm and known or suspected coronary artery disease who underwent exercise thallium-201 myocardial single-photon emission computed tomography and coronary arteriography. High diastolic blood pressure during exercise was defined as diastolic blood pressure at peak exercise > or = 90 mm Hg. There was no significant difference in medications, number of diseased vessels, or Gensini score between patients with high (n = 228) and normal (n = 241) diastolic blood pressure during exercise, whereas patients with high diastolic blood pressure during exercise exhibited a higher pressure-rate product during exercise than patients with normal diastolic blood pressure during exercise. The reversibility score on thallium-201 myocardial scan was significantly smaller in patients with high diastolic blood pressure during exercise than in patients with normal diastolic blood pressure during exercise (P = .021). CONCLUSIONS: High diastolic blood pressure during exercise has a potential protective effect against exercise-induced ischemia, although the mechanism of such effects remains to be determined.

Adult↗
PubMed2005

A novel technique to detect total occlusion in the right coronary artery using retrograde flow by transthoracic Doppler echocardiography.

BACKGROUND: We hypothesized that detection of reverse flow in the distal right coronary artery (d-RCA) and the inferior septal branches (ISB) by transthoracic Doppler echocardiography (TTDE) would be useful for noninvasive diagnosis of the occluded right coronary artery (RCA). METHODS: Coronary angiography and TTDE were performed on 129 patients. Antegrade flows in the d-RCA and the ISB were defined as directions from the base to the apex in the posterior sulcus and from anterior to inferior in the inferior septum, respectively. Retrograde flow was defined as an inverse direction. RESULTS: Retrograde flow was obtained by TTDE in 14 patients (d-RCA:11, ISB:3) of 18 patients with occluded RCA. The sensitivity and the specificity for identification of occluded RCA were 100% and 97.8%, respectively. CONCLUSION: Detection of reverse flow in the d-RCA and the ISB using TTDE is a useful method for the noninvasive diagnosis of occluded RCA.

Aged↗
PubMed2005

Role of c-Jun NH2-terminal kinase in G-protein-coupled receptor agonist-induced cardiac plasminogen activator inhibitor-1 expression.

Plasminogen activator inhibitor-1 (PAI-1) has been implicated as a contributing risk factor for cardiovascular disease. However, little is known about molecular mechanisms of cardiac PAI-1 gene expression. To elucidate these mechanisms, dominant negative mutants of c-Jun NH(2)-terminal kinase (JNK), p38MAPK, apoptosis signal-regulating kinase-1 (ASK-1) and c-Jun were overexpressed in rat neonatal ventricular cardiac myocytes and fibroblasts by adenovirus vector to abrogate the activation of the corresponding endogenous proteins. One hundred nmol/l of angiotensin II significantly enhanced the JNK and p38MAPK activities of cardiomyocytes (2.3-fold and 1.9-fold, P < 0.05) and fibroblasts (3.2-fold and 2.5-fold, P < 0.05). At 3 h after stimulation, angiotensin II was found to have significantly increased PAI-1 mRNA, by 5.2-fold in cardiomyocytes and by 9.7-fold in fibroblasts. Dominant negative mutants of JNK, ASK-1 and c-Jun significantly inhibited PAI-1 mRNA expression and protein synthesis in both cardiomyocytes and fibroblasts, whereas a dominant negative mutant of p38MAPK did not change this expression. Moreover, a dominant negative mutant of JNK also significantly prevented the induction of PAI-1 mRNA expression by 100 nmol/l endothelin-1 and 10 micromol/l phenylephrine. In conclusion, G-protein-coupled receptor agonist-induced PAI-1 expression is partially mediated through JNK activation.

Angiotensin II↗
PubMed2005

Involvement of c-Jun NH2 terminal kinase and p38MAPK in rapamycin-mediated inhibition of neointimal formation in rat carotid arteries.

OBJECTIVE: Rapamycin-coated stents in coronary artery lesions have recently been shown to be effective in inhibiting neointimal formation. However, little is known about the effects of rapamycin on mitogen-activated protein kinase (MAPK), which is an important signal for neointimal formation. Therefore, we examined the effects of rapamycin on MAPK and transcriptional factors in cultured human coronary artery smooth muscle cells (CASMC) and in balloon-injured rat carotid arteries. METHODS AND RESULTS: Activation of ERK, JNK, p38MAPK, AP-1, and NF-kB in coronary artery smooth muscle cells was increased by 2% fetal bovine serum. Ten nmol/L of rapamycin prevented the activation of JNK, p38MAPK, AP-1, and NF-kB (65%, 65%, 67%, and 26% respectively, P<0.01). In an in vivo study, remarkable neointimal formation was observed 14 days after injury. Coating Pluronic gel with 20 and 50 mug rapamycin around the injured artery significantly decreased the intimal area/medial area ratio, compared with vehicle (0.75 vs. 1.2, P<0.01). Rapamycin prevented the increase in activation of JNK, p38MAPK, AP-1, and NF-kB in injured artery (42%, 70%, 75%, and 60% respectively, P<0.05). CONCLUSIONS: Neointimal formation after balloon injury is inhibited by rapamycin, which is partially mediated by inhibition of JNK and p38MAPK, followed by AP-1 and NF-kB.

Animals↗
PubMed2005

Freehand three-dimensional echocardiography with rotational scanning for measurements of left ventricular volume and ejection fraction in patients with coronary artery disease.

BACKGROUND: Measurement of left ventricular (LV) volumes and ejection fraction (EF) is important in managing patients with coronary artery disease (CAD). Introduction of free-hand three-dimensional echocardiography (3DE) system which is equipped with small magnetic tracking system and average rotational geometry for LV volumes may provide easy and accurate quantification of LV systolic function in CAD patients. PURPOSE: To evaluate the feasibility and accuracy of LV volumes and EF measurement by free-hand 3DE with rotational geometry in patients with CAD. METHODS AND RESULTS: The study subjects consisted of consecutive 25 patients with CAD who were scheduled for quantitative gated single-photon emission computed tomography (QGS). LV end-diastolic volume (EDV), end-systolic volume (ESV), and EF were determined by conventional two-dimensional echocardiography (2DE), 3DE, and QGS. Three-dimensional echocardiography data acquisition and analysis were possible in 22 of 25 subjects (feasibility 88%). In this 3DE system, image acquisition time was 2 minutes, and 5 minutes were needed for off-line analysis of LV volumes and EF. Correlations and the limits of agreement between 3DE and QGS (r = 0.97, 0.0 +/- 9.1 ml for EDV, r = 0.99, 0.0 +/- 5.0 ml for ESV, and r = 0.97, 0.5 +/- 3.3% for EF, respectively) were superior to those between 2DE and QGS (r = 0.85, 12.6 +/- 26.8 ml for EDV, r = 0.85, 9.7 +/- 26.1 ml for ESV, and r = 0.90, -1.3 +/- 6.9% for EF, respectively). Inter- and intra-observer variabilities of 3DE were smaller than that of 2DE (5% vs 10%, 5% vs 10% for EDV, 6% vs 13%, 5% vs 9% for ESV, and 4% vs 11%, 4% vs 6% for EF, respectively). CONCLUSION: Three-dimensional echocardiography using magnetic tracking system and average rotational geometry offered a feasible and accurate method for quantification of LV volumes and EF in patients with CAD.

Aged↗
PubMed2005

No positive association between adrenergic receptor variants of alpha2cDel322-325, beta1Ser49, beta1Arg389 and the risk for heart failure in the Japanese population.

AIMS: We investigated the correlation of adrenergic receptor polymorphisms, alpha(2c)Del322-325, beta(1)Ser49Gly and beta(1)Arg389Gly, with the risk of heart failure in the Japanese population. METHODS: These polymorphisms were analysed by polymerase chain reaction-restriction fragment length polymorphism in patients with chronic heart failure due to idiopathic dilated cardiomyopathy (DCM) and compared with the control group. RESULTS: There were no differences or any trends in the allele and genotype frequencies of the beta(1)Ser49Gly and beta(1)Arg389Gly polymorphisms. The allele frequency of the alpha(2c)Del322-325 variant was lower in patients than in controls (0.11 vs. 0.04, P = 0.011 < 0.017, by Bonferroni correction), while the genotype frequency just failed to reach significance (P = 0.022 > 0.017, by Bonferroni correction). CONCLUSIONS: In this population, the variants beta(1)Ser49, beta(1)Arg389, and alpha(2c)Del322-325 do not appear to be risk factors for chronic heart failure due to DCM. The alpha(2c)Del322-325 variant may in fact confer some protection.

Aged↗