Biomedical subjects

Katsuji Inoue

Publications and source records attributed to Katsuji Inoue.

10 recordsLinked to original sources

PubMed2005

Effect of beta-blocker therapy on myocardial perfusion defects in thallium-201 scintigraphy in patients with dilated cardiomyopathy.

BACKGROUND: The beneficial effects of beta-blocker therapy in patients with heart failure have been confirmed. However, the effects of beta-blockers on myocardial perfusion defects are unclear. The aim of this study was to evaluate the effect of beta-blockers on myocardial perfusion defects estimated by thallium-201 myocardial scintigraphy in patients with dilated cardiomyopathy (DCM) and to investigate the relationships between beta-blocker treatment and myocardial damage and cardiac function. METHODS: 201Tl and echocardiography were performed in 37 patients before and after 6 months of beta-blocker therapy. Extent score (ES) by 201Tl was used to quantitate myocardial perfusion defects before and after treatment. RESULTS: ES was significantly decreased by beta-blocker therapy. According to the change in ES, DCM patients were classified into three groups, patients who improved, patients showing no change and patients who deteriorated. In the improvement and no-change groups, beta-blocker therapy induced a reduction in left ventricular dimensions and an associated increase in ejection fraction. However, in the deterioration group, left ventricular dimensions and ejection fraction were unchanged. There was a significant relationship between the change in left ventricular dimension at end-diastole and the change in ES. CONCLUSIONS: beta-Blocker therapy could attenuate myocardial perfusion defects in some patients with DCM. The improvement in left ventricular function associated with beta-blocker therapy may be related to the attenuation in myocardial perfusion defects.

Adolescent↗

PubMed2005

Relation of genetic predisposition and insulin resistance to left ventricular hypertrophy in hypertension.

BACKGROUND: The aim of the study was to determine whether genetic predisposition to hypertension and insulin resistance are related to left ventricular (LV) hypertrophy in essential hypertension. METHODS: The study included 72 nondiabetic patients with essential hypertension and 15 normotensive control (NC) subjects. The 72 patients were divided into two groups according to genetic predisposition to hypertension. The family history (FH)(+) group included 33 patients with at least one essential hypertensive parent or sibling. The FH(-) group included 39 patients with weak genetic predisposition to hypertension. Insulin resistance was estimated using the homeostasis model assessment (HOMA). Echocardiographically determined LV mass (LVM) and relative wall thickness (RWT) were measured as markers of LV hypertrophy. RESULTS: The HOMA values in the FH(+) group (2.00 +/- 0.89) were significantly higher than those in either the FH(-) group (1.21 +/- 0.44) or NC subject group (0.91 +/- 0.24). The HOMA values in the FH(-) group were significantly higher than those in NC subjects. The LVM and RWT were greatest in the FH(+) group, followed by those in the FH(-) group and NC subjects. There were no significant differences in LVM and RWT between the FH(-) group and NC subjects. By multivariate analysis, HOMA value (P = .0011), male sex (P = .0032), body mass index (P = .0061), systolic blood pressure (P = .0245), and genetic predisposition to hypertension (P = .0441) remained determinants of LVM in nondiabetic patients with essential hypertension. CONCLUSIONS: Genetic predisposition to hypertension and the HOMA value appear to have additive impact on LV hypertrophy. This relation is independent of well-known determinants of LVM such as male sex, overweight, and high blood pressure.

Adult↗

PubMed2005

Serum markers of angiogenesis and myocardial ultrasonic tissue characterization in patients with dilated cardiomyopathy.

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 DCM. 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<0.05). Calibrated IB was significantly higher and CV-IB was markedly lower in patients with DCM than in control subjects (both P<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.

Adult↗

PubMed2005

[A 73-year-old man with primary pulmonary hypertension].

A rare case of primary pulmonary hypertension was observed in a 73-year-old man. Angina pectoris was diagnosed at the age of 67 and he received several percutaneous coronary interventions because of refractory restenosis. He also had coronary artery bypass surgery at the age of 69. After 4 years, he again suffered from dyspnea and chest pain upon physical exertion. On admission to our hospital, a chest radiograph showed dilatation of bilateral pulmonary arteries. Moreover, echocardiography showed right ventricular dilatation and tricuspid regurgitation. Continuous wave Doppler imaging revealed a pressure gradient of 82.1 mmHg. Pulmonary capillary wedge pressure was normal, but pulmonary artery pressure was elevated upon cardiac catheterization. Because there was no apparent etiology of pulmonary hypertension, primary pulmonary hypertension was diagnosed and appropriate conventional therapy was started.

Aged↗

PubMed2004

Myocardial microvascular abnormalities observed by intravenous myocardial contrast echocardiography in patients with hypertrophic cardiomyopathy.

We tested the hypothesis that myocardial microvascular abnormalities occur and are influenced by clinical features in 30 patients with hypertrophic cardiomyopathy (HC) using intravenous myocardial contrast echocardiography. Patients with HC were subdivided into 3 groups: nonobstructive HC (n = 12), obstructive HC (n = 10), or HC with systolic dysfunction and heart failure (n = 8). In patients with nonobstructive HC and obstructive HC, subendocardial peak myocardial contrast intensity at the mid-septal area was significantly decreased and the transmyocardial difference of peak myocardial contrast intensity between subendocardial and periendocardial regions at the mid-septal area was significantly related to regional wall thickness. Reduced peak myocardial contrast intensities at the mid-septal subendocardial and periendocardial regions were observed in patients with HC and heart failure. Our study indicates that subendocardial microvascular abnormalities during end-systole may be associated with severity of regional myocardial hypertrophy in patients with nonobstructive HC and obstructive HC. In addition, progressive microvascular damage may occur in patients with HC and heart failure.

Aged↗

PubMed2004

Relation of circulating interleukin-6 to left ventricular remodeling in patients with reperfused anterior myocardial infarction.

BACKGROUND: During the remodeling process after myocardial infarction (MI), the expression of proinflammatory cytokines is enhanced in the myocardium. However, only a few clinical studies have been conducted on cytokine involvement in left ventricular (LV) remodeling after MI. HYPOTHESIS: Circulating proinflammatory cytokines may be involved in LV remodeling in patients with reperfused MI. METHODS: We studied 25 patients with acute anterior MI who had undergone coronary reperfusion therapy, and 10 normal control subjects with no cardiac disease. In all patients, LV ejection fraction, end-diastolic volume index (EDVI), and end-systolic volume index (ESVI) were determined using left ventriculography at the acute phase and 6 months after onset. The delta EDVI and delta ESVI were calculated as the value of LV volume reduction, suggesting LV reverse remodeling. Serum levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha were measured using enzyme-linked immunosorbent assay. RESULTS: Serum levels of IL-6 and TNF-alpha at the acute phase were significantly higher in patients with MI than in control subjects (both p < 0.05). The IL-6 levels correlated well negatively with delta EDVI (r = 0.779, p = 0.039), whereas no correlation was found for TNF-alpha. According to multivariate analysis, IL-6 at the acute phase was a significant independent predictor for LV remodeling after reperfused MI (p = 0.007). CONCLUSIONS: Circulating IL-6 levels correlated closely with LV geometric changes during the remodeling process in patients with reperfused MI. Our study addresses the usefulness of another marker for LV remodeling after MI.

Adrenergic beta-Antagonists↗

PubMed2004

Relation of myocardial blood volume to left ventricular function and future cardiac events in patients with idiopathic dilated cardiomyopathy.

BACKGROUND: The hypothesis that myocardial blood volume is associated with left ventricular (LV) dysfunction and future cardiovascular events in patients with idiopathic dilated cardiomyopathy (IDC) was tested using intravenous myocardial contrast echocardiography (MCE). METHODS AND RESULTS: Thirty-five patients with IDC and 10 age-matched healthy control subjects were enrolled. Using MCE, background-subtracted and peak myocardial contrast intensity (calibrated PMCI) were calculated as measures of myocardial blood volume. LV ejection fraction (LVEF) was calculated using the modified Simpson method. Patients with IDC were stratified into 2 groups according to the median value of the calibrated PMCI [high value group (n=17): calibrated PMCI > or = -22.7 dB, low value group (n=18): calibrated PMCI < -22.7 dB]. The calibrated PMCI was markedly reduced in patients with IDC compared with the control subjects (p=0.0025) and closely related to LVEF (r=0.688, p<0.0001). In the multivariate model, calibrated PMCI was the independent variable that predicted cardiac events in patients with IDC. According to the Kaplan-Meier analysis, cardiac event-free rates were significantly lower in the low-value group than in the high-value group (p<0.01). CONCLUSIONS: Myocardial blood volume is closely related to LV dysfunction and future cardiac events in patients with IDC.

Blood Volume↗

PubMed2002

Clinical and angiographical characteristics of acetylcholine- induced spasm: relationship to dose of intracoronary injection of acetylcholine.

OBJECTIVES: The purpose of this study was to clarify clinical and angiographical characteristics of acetylcholine (ACh)-induced spasm in the right and left coronary artery. METHODS AND RESULTS: We performed 557 consecutive procedures of spasm provocation tests of ACh from January 1991 to December 2000 in patients without significant stenosis. ACh was injected in incremental doses of 20, 50 and 80 microg into the right coronary artery and in incremental doses of 20, 50 and 100 microg into the left coronary artery if spasm had not been provoked. Coronary spasm was defined as positive with more than 99% transient luminal narrowing. Proximal spasm was defined as that of segments 1, 2, 5, 6, 7 and 11 and distal spasm as that of segments 3, 4, 8, 9, 12, 13 and 14. Low-ACh-dose-induced spasms showed the clinical findings and angiographical characteristics of higher incidence of variant angina, proximal spasms, focal spasms, more ST elevation and ischemic heart disease. In contrast, angiographical characteristics of high-Ach-dose-induced spasms were distal spasms and diffuse spasms and there was less variant angina and less ST elevation. CONCLUSIONS: Lower ACh doses induced spasms more proximally and focally in the coronary artery, while higher doses of ACh provoked spasms more distally and diffusely.

Acetylcholine↗

PubMed2002

Pure right ventricular infarction.

A 76-year-old man with chest pain was admitted to hospital where electrocardiography (ECG) showed ST-segment elevation in leads V1-4, indicative of acute anterior myocardial infarction. ST-segment elevation was also present in the right precordial leads V4R-6R. Emergency coronary angiography revealed that the left coronary artery was dominant and did not have significant stenosis. Aortography showed ostial occlusion of the right coronary artery (RCA). Left ventriculography showed normal function and right ventriculography showed a dilated right ventricle and severe hypokinesis of the right ventricular free wall. Conservative treatment was selected because the patient's symptoms soon ameliorated and his hemodynamics was stable. 99mTc-pyrophosphate and 201Tl dual single-photon emission computed tomography showed uptake of 99mTc-pyrophosphate in only the right ventricular free wall, but no uptake of 99mTc-pyrophosphate and no perfusion defect of 201Tl in the left ventricle. The peak creatine kinase (CK) and CK-MB were 1,381 IU/L and 127 IU/L, respectively. His natural course was favorable and the chest pain disappeared under medication. Two months after the onset, the ECG showed poor R progression in leads V1-4 indicating an old anterior infarction. Coronary angiography confirmed the ostial stenosis of the hypoplastic RCA. This was a case of pure right ventricular free wall infarction because of the occlusion of the ostium of the hypoplastic RCA, but not of the right ventricular branch. Because the electrocardiographic findings resemble those of an acute anterior infarction, it is important to consider pure right ventricular infarction in the differential diagnosis.

Aged↗

PubMed2002

Intracoronary administration of a thromboxane A2 synthase inhibitor relieves acetylcholine-induced coronary spasm.

This study sought to clarify the effectiveness of intracoronary administration of a thromboxane (TX) A2 synthase inhibitor, Ozagrel Na, to relieve coronary spasms induced by intracoronary injection of acetylcholine (ACh). An ACh spasm provocation test was performed in 92 consecutive patients with coronary spastic angina using incremental doses of 20, 50, and 80 microg into the right coronary artery, and 20, 50, and 100 microg into the left coronary artery within 20s. A coronary spasm was defined as TIMI 0 or 1 flow and an intracoronary injection of 20 mg Ozagrel Na was administered when it was provoked. Within 2 min of the administration of the TXA2 synthase inhibitor, ACh-induced coronary spasms were relieved (TIMI 3 flow) in 88.1% of procedures without complications. In only 4 cases (4.3%), it took more than 3 min to relieve the coronary spasms. Intracoronary administration of 20mg Ozagrel Na when ACh-induced spasms occurred, shortened the spasm relief time in all 7 patients (200 +/- 59s vs 111 +/- 23s, p < 0.01), improved the maximal ST segment elevation in 5 of them (3.9 +/- 3.7 mm vs 0.7 +/- 1.5 mm, p < 0.05), and stopped chest pain in 4 patients. In 4 patients who had ACh-induced coronary spasm of the left anterior descending artery, the TXB2 concentration in the coronary sinus decreased after intracoronary administration of Ozagrel Na into the left coronary artery (463 +/- 562 vs 96 +/- 45, p < 0.01). In conclusion, intracoronary administration of a TXA2 synthase inhibitor can relieve ACh-induced coronary spasms by inhibiting TXA2 synthesis in the local coronary circulation.

Acetylcholine↗