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Biomedical subjects

Fumitaka Ohsuzu

Publications and source records attributed to Fumitaka Ohsuzu.

At least 19 recordsLinked to original sources
PubMed2007

Effect of bezafibrate therapy on atherosclerotic aortic plaques detected by MRI in dyslipidemic patients with hypertriglyceridemia.

Fibrates reduce triglycerides (TG) and increase HDL-cholesterol levels, but there was no report showing plaque regression by fibrates. Using MRI, we investigated the effects of bezafibrate on aortic plaques in 22 dyslipidemic patients. All patients were asked to receive 400mg bezafibrate, but 8 who declined to have bezafibrate became the control group. Changes in vessel wall area (VWA) and lumen area (LA) from baseline to 1-year were evaluated. Bezafibrate reduced TG (-55%) and increased HDL-cholesterol levels (+29%). Bezafibrate reduced HDL size and increased LDL size. In thoracic plaques, bezafibrate reduced VWA (-6%, P<0.001) with no LA change, but VWA slightly progressed without bezafibrate (+5%). In abdominal plaques, bezafibrate reduced VWA (-8%, P<0.001) with LA increase (+3%, P<0.02), but VWA progressed without bezafibrate (+6%). VWA changes in thoracic and abdominal plaques correlated with TG reduction and HDL-cholesterol increase. Notably, VWA change in only abdominal plaques correlated with HDL size reduction and LDL size increase. Thus, bezafibrate induced plaque regression in thoracic and abdominal aortas with marked TG reduction and HDL-cholesterol increase, but the processes of plaque regression and vascular remodeling may differ between thoracic and abdominal aortas. However, because our study was not a controlled, randomized trial, further study is needed.

Aged↗
PubMed2006

A low level of C-reactive protein in Japanese adults and its association with cardiovascular risk factors: the Japan NCVC-Collaborative Inflammation Cohort (JNIC) study.

High-sensitivity C-reactive protein (hs-CRP) levels vary remarkably by race and ethnic group. We examined hs-CRP levels and their association with cardiovascular risk factors in the Japanese general population. The Japan National Cardiovascular Center (NCVC)-collaborative Inflammation Cohort (JNIC) Study recruited 5213 men and 7071 women aged > or = 40 years from seven communities in Japan during 2002-2004. hs-CRP was measured using nephelometry calibrated with CRM 470, the international plasma protein reference material. Traditional cardiovascular risk factors and their aggregation were studied in multivariate logistic models, stratified by overweight status. Median hs-CRP levels in men and women were 0.60 and 0.45 mg/L, respectively. The percentage of subjects with hs-CRP levels < 1.0, 1.0-3.0, and > 3.0 mg/L was 67.4%, 22.0%, and 10.6% in men, respectively, and 76.3%, 16.7%, and 7.0% in women. hs-CRP levels showed significant linear associations with traditional risk factors. Overweight, hypertension, dyslipidemia (men only), smoking (men only), and diabetes (women only) contributed significantly to elevated hs-CRP levels. Overweight individuals with hypertension, dyslipidemia, and diabetes had a high prevalence of elevated hs-CRP levels in both sexes. Japanese adults have very low hs-CRP levels. An aggregation of metabolic risk factors is associated with elevated hs-CRP levels among overweight individuals, particularly in women.

Aged↗
PubMed2006

Left ventricular hypertrophy in mice with a cardiac-specific overexpression of interleukin-1.

Recent studies have identified the importance of proinflammatory cytokines in the development of left ventricular (LV) hypertrophy. However, the precise role of interleukin-1 (IL-1), one of the major proinflammatory cytokines, in the myocardium is not fully understood. In this study, we investigated the pathophysiological consequences of cardiac expression of IL-1 in vivo. We generated mice with a cardiac-specific overexpression of human IL-1alpha. We then analyzed their heart morphology and functions. Histological and echocardiographic analyses revealed concentric LV hypertrophy with preserved LV systolic function in the mice. Our results suggest that myocardial expression of IL-1 is sufficient to cause LV hypertrophy.

Animals↗
PubMed2006

A possible association between coronary plaque instability and complex plaques in abdominal aorta.

OBJECTIVE: Coronary plaque instability causes myocardial infarction (MI). Angiographic lesions with such instability are complex lesions. Complex carotid plaques were reported to be prevalent in unstable angina. We investigated associations between coronary plaque instability, such as MI and angiographic complex coronary lesions, and aortic plaques. METHODS AND RESULTS: Aortic MRI was performed in 146 patients undergoing coronary angiography, of whom 108 had coronary artery disease (CAD) and 44 also had MI. Prevalence of plaques in thoracic and abdominal aortas was higher in patients with than without CAD (73% and 94% versus 32% and 79%), but it was similar in CAD patients with and without MI. Notably, complex plaques in abdominal aorta were more prevalent in CAD patients with than without MI (36% versus 14%; P<0.025). In multivariate analysis, abdominal complex plaques were associated with MI (odds ratio [OR], 4.5; 95% CI, 1.5 to 13.8). Among patients without MI, thoracic and abdominal complex plaques were more prevalent in patients with than without complex coronary lesions (22% and 33% versus 2% and 7%; P<0.05). Abdominal complex plaques were also associated with complex coronary lesions (OR, 9.8; 95% CI, 1.1 to 85.9). CONCLUSIONS: Complex plaques in abdominal aorta were associated with MI and complex coronary lesions, suggesting a link between coronary and aortic plaque instability.

Adult↗
PubMed2006

Usefulness of cardiac magnetic resonance imaging for detecting acute myocardial infarction in patients with no significant electrocardiogram changes.

A 73-year-old man presented with suspected acute myocardial infarction at the outpatient clinic. However, the clinical symptoms and the laboratory findings were not diagnostic. Only emergency cardiac magnetic resonance imaging (MRI) was helpful in making a definitive diagnosis of acute myocardial infarction. Cardiac MRI is a useful diagnostic tool for suspected acute coronary syndrome in emergency room settings when conventional modalities do not provide a definitive diagnosis.

Aged↗
PubMed2006

QT peak dispersion, not QT dispersion, is a more useful diagnostic marker for detecting exercise-induced myocardial ischemia.

BACKGROUND: The electrocardiographic indices of QT dispersion (QTd), QT peak dispersion (QTpd), and the principal component analysis ratio (PCAr) are related to the occurrence of fatal arrhythmia and are influenced by physical exercise. OBJECTIVE: The purpose of this study was to investigate whether or not the QT parameters can be used as markers for exercise-induced myocardial ischemia. METHODS: We measured these QT parameters at rest and at 3 minutes after exercise using exercise-stress thallium-201 scintigraphy (SPECT), compared with conventional ST segment changes in 161 patients with suspected or known coronary artery disease. The patients were classified into four groups (normal, redistribution, fixed defect, and redistribution with fixed defect) according to SPECT. RESULTS: At rest, QTd and PCAr were greater in the fixed defect and redistribution with fixed defect groups. PCAr, however, increased after exercise in the redistribution and redistribution with fixed defect groups. Although QTpd at rest was not significantly different among the four groups, it increased in the redistribution and redistribution with fixed defect groups after exercise (QTpd after exercise: normal, 36 +/- 16 ms vs. redistribution, 51 +/- 23 ms, redistribution with fixed defect, 53 +/- 19 ms; P<.05). For myocardial infarction reflected by fixed defect, QTd at rest was the most useful indicator, while QTpd after exercise was the most useful indicator for exercise-induced myocardial ischemia according to multiple logistic regression analysis with receiver operating characteristic curves. In addition, the change in PCAr by exercise was an independent predictor for exercise-induced ischemia. CONCLUSIONS: QTpd and PCAr could be useful indices for exercise-induced myocardial ischemia. Determining the QTpd of a patient after exercising can improve the diagnostic accuracy of ischemia in a routine clinical setting.

Adolescent↗
PubMed2006

Vagal nerve-mediated vasospasm-induced lethal ventricular fibrillation.

We report a case of variant angina complicated by lethal ventricular fibrillation. Serial ambulatory electrocardiogram monitoring revealed high-frequency spectra reflecting augmented vagal nerve activity preceding the vasospastic episodes. Our case suggests that heart rate variability analysis can help identify potential unexpected sudden cardiac death in patients with variant angina.

Angina Pectoris↗
PubMed2006

Altered action potential dynamics in electrically remodeled canine atria: evidence for altered intracellular Ca2+ handling.

BACKGROUND: Electrical instability following sustained rapid excitation has been attributed to altered ion channels. Alterations of Ca(2+) handling could also contribute to abnormal dynamics of action potential, favoring the initiation and perpetuation of arrhythmia. METHODS AND RESULTS: Transmembrane action potentials and twitch force (TF) were recorded from normal (n=6) and remodeled (6-week atrial pacing at 400 beats/min, n=6) canine atria. When the cycle length (CL) was suddenly prolonged in normal atria, both TF and action potential duration (APD) increased on the first beat, and decreased subsequently. Opposite changes were observed with sudden CL shortening. These dynamics in both APD and TF were abolished by ryanodine, but augmented by cyclopiazonic acid, an inhibitor of the sarcoplasmic reticulum (SR) Ca(2+) pump. In remodeled atria (RA), dynamic changes in APD were also concordant with dynamic changes in TF. The transient increases in APD and TF were enhanced, and the transient decreases were reduced compared to normal atria. The maximal slopes of APD and TF restitution curves were flatter and the magnitude of alternans was reduced in RA. The protein expression of SR Ca(2+) ATPase and SR Ca(2+)-release channel in RA was significantly reduced. CONCLUSION: Altered Ca(2+) handling may underlie abnormal APD dynamics in RA.

Action Potentials↗
PubMed2006

Comparable prognostic value of vasodilator response to acetylcholine in brachial and coronary arteries for predicting long-term cardiovascular events in suspected coronary artery disease.

BACKGROUND: Vasodilator response to acetylcholine (ACh) (ie, endothelium-dependent dilation) is impaired in the peripheral and coronary circulation of patients with coronary risk factors and coronary artery disease (CAD). There is a close relationship of vasodilator response to ACh in both the coronary artery (CA) and the brachial artery (BA), but the comparative prognostic importance of these responses has not been fully investigated in relatively low-risk suspected CAD. METHODS AND RESULTS: The flow responses of both the CA and BA were measured in 70 patients with suspected CAD, excluding patients with triple-vessel disease and known peripheral or cerebrovascular disorders. A Doppler guidewire was placed into a major branch of the CA and a proximal portion of the left BA. ACh was infused at 10(-8), 10(-7) and 10(-6) mol/L for 3 min into the CA and at 7.5, 15, and 30 mug/min for 5 min into BA. The flow response was obtained by multiplying the average peak velocity by the cross-sectional area from quantitative angiography. Vasodilator response to ACh was assessed by the ratio of ACh-induced flow/baseline flow, expressed as coronary blood flow index (CBFI) or brachial blood flow index (BBFI). There were 39 CAD patients (61 +/- 8 years old) and 31 normal coronary patients (NL, 58 +/- 11 years old) who were followed up for 53 +/- 17 months. Eleven patients had coronary events (CE) during this period: 1 case of nonfatal myocardial infarction and 10 cases of unstable angina. A strong correlation between CBFI and BBFI was observed at middle-and high-doses of ACh (r=0.72, p<0.0001, 15 microg/min vs 10(-7) mol/L; r=0.76, p<0.0001, 30 microg/min vs 10(-6) mol/L). Kaplan-Meier analysis, using the best cut-off values obtained from receiver-operating characteristic curves for CE, revealed that both CBFI and CAFI were significant predictors for CE. CONCLUSIONS: The BA vasodilator response to optimal ACh dosage can be used as a surrogate prognostic predictor for coronary endothelial function tests in patients with suspected CAD.

Acetylcholine↗
PubMed2006

Interleukin-1 and occlusive arterial diseases.

Interleukin (IL)-1 is a pro-inflammatory cytokine and a central mediator in the cytokine network, and is known to control important functions both in the immune system and inflammation. The activity of IL-1 is counter-regulated by its endogenous inhibitor, IL-1 receptor antagonist (IL-1Ra). IL-1 and IL-1Ra are produced and secreted by a variety of cells including those responsible for controlling immunity. A recent study indicated that IL-1 and IL-1Ra transcripts were expressed in the vessel wall, suggesting that these cytokines contribute to the development and progression of vascular diseases. In this review, we will discuss the recent advances in our understanding of the mechanism of action of IL-1 in occlusive arterial diseases such as neointimal hyperplasia and atherosclerosis, specifically in a mouse model.

Animals↗
PubMed2006

The effect of interleukin-1 receptor antagonist on arteries and cholesterol metabolism.

This review summarizes both the structure and function of IL-1 receptor antagonist (IL-1Ra), and relates our new findings, particularly those obtained in IL-1Ra-deficient mice (IL-1Ra(-/-)), to the role of IL-1Ra in arterial diseases and cholesterol metabolism. IL-1Ra(-/-) mice show an increase in neointima-formation after arterial injury. Heterozygosity in the IL-1Ra gene against the apolipoprotein E-deficient background revealed a role for IL-1 in promoting atherogenic cell signaling and that the larger lesions of IL-1Ra(-/-) mice are enriched in macrophages and depleted of smooth muscle cells. Furthermore, IL-1Ra(-/-) mice developed severe fatty livers and hypercholesteroremia following 20 weeks on a atherogenic diet compared to WT mice. Taken together, these results suggest that IL-1Ra plays important roles in restenosis after angioplasty, the development of atherosclerosis, and the metabolism of cholesterol in vivo.

Animals↗
PubMed2005

Beneficial effects of nifedipine on vasodilator response to acetylcholine in coronary and brachial arteries in the patients with coronary artery disease.

BACKGROUND: Nifedipine has been reported to improve endothelial function. However, there are few simultaneous studies on the effects of nifedipine on coronary and peripheral endothelial function in humans. METHODS: To investigate the effects of nifedipine on endothelial function in coronary artery (CA) and brachial artery (BA) in coronary artery disease (CAD), we measured vasodilator responses of CA and BA to acetylcholine (ACh, endothelium-dependent dilation) in 13 patients (63+/-10 years old) with CAD before and after sublingual administration of nifedipine 10 mg. To measure blood flow, a Doppler guidewire was inserted into the major branch of CA and the left BA. ACh was infused at 10(-7) mol/l for 3 min into CA and at 15.0 microg/ml for 5 min into BA, respectively. The vasodilator response to ACh was assessed by the ratio of ACh-induced flow/baseline flow (CAVR index, the ratio of CA flow changed by ACh; BAVR index, the ratio of BA flow changed by ACh). RESULTS: Nifedipine significantly increased both the CAVR and BAVR index:CAVR index, from 1.33+/-0.54 to 1.76+/-0.52 (32%) and BAVR index, from 1.74+/-0.83 to 2.18+/-0.93 (25%), respectively, p<0.05. In addition, nifedipine-induced changes in CAVR tended to correlate with those of BAVR (r=0.42. p=0.06). CONCLUSIONS: Acute administration of nifedipine improves both coronary and brachial artery vasodilator responses to ACh. Nifedipine improves coronary and peripheral endothelial function in patients with CAD.

Acetylcholine↗
PubMed2005

Glucocorticoid receptor regulates ATP-binding cassette transporter-A1 expression and apolipoprotein-mediated cholesterol efflux from macrophages.

OBJECTIVE: The ATP-binding cassette transporter-A1 (ABCA1) regulates cholesterol efflux from cells and is involved in high-density lipoprotein metabolism and atherogenesis. The objective of this study was to investigate the effect of dexamethasone (Dex) and other glucocorticoid receptor (GR) ligands on apolipoprotein AI-mediated cholesterol efflux from macrophages and ABCA1 expression in them. METHODS AND RESULTS: Dex, a GR agonist, decreased ABCA1 mRNA levels in a dose- and time-dependent fashion, and RU486, a GR antagonist, reversed the inhibitory effect of Dex. The effects of Dex and RU486 on ABCA1 protein levels and apolipoprotein AI-mediated cholesterol efflux from the macrophages were consistent with these changes in mRNA levels. Transfected RAW264.7, together with a human ABCA1 promoter-luciferase construct, inhibited transcriptional activity by Dex and overexpression of human GR. Transrepression by GR was not mediated by liver X receptor (LXR), because there were no differences in the effects of the GR ligands on promoter activity between a reporter construct with mutations at the LXR binding site and one without the mutations, and no changes were brought about in ABCG1 and ABCG4 expression by GR ligands. CONCLUSIONS: Our results showed that GR ligands affected ABCA1 expression and cholesterol efflux from macrophages, which are regulated by GR through a LXR-independent mechanism.

ATP Binding Cassette Transporter 1↗