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Biomedical subjects

Yoichi Goto

Publications and source records attributed to Yoichi Goto.

At least 19 recordsLinked to original sources
PubMed2007

Enhanced cardiac production of matrix metalloproteinase-2 and -9 and its attenuation associated with pravastatin treatment in patients with acute myocardial infarction.

Previous experimental studies have demonstrated that MMPs (matrix metalloproteinases) contribute to LV (left ventricular) remodelling. We hypothesized that cardiac MMPs are activated in patients with AMI (acute myocardial infarction) and, if so, MMP production may be attenuated by statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) through their cardiovascular protective actions. We studied 30 patients, ten control patients with stable angina pectoris and 20 patients with AMI, in whom LV catheterization at the chronic stage was performed 22+/-12 days (value is mean+/-S.D.) after the onset of AMI. Blood samples were collected from the CS (coronary sinus) and a peripheral artery. In patients with AMI, the levels of MMP-2 and MMP-9 were significantly (P<0.05) higher in the CS than the peripheral artery (MMP-2, 853+/-199 compared with 716+/-127 ng/ml; MMP-9, 165+/-129 compared with 98+/-82 ng/ml), whereas no significant differences were observed in the patients with angina pectoris. The CS-arterial concentration gradients of MMP-2 and MMP-9 correlated positively with BNP (brain natriuretic peptide) levels (MMP-2, R=0.68, P<0.01; MMP-9, R=0.59, P<0.05) and LV end-diastolic volume index (MMP-2, R=0.70, P<0.01; MMP-9, R=0.70, P<0.01). When patients with AMI treated with 10 mg of pravastatin or without (n=10 in each group) were compared, this statin therapy significantly (P<0.05) decreased the CS-arterial concentration gradients of MMP-2 (69+/-43 compared with 213+/-185 ng/ml) and MMP-9 (14+/-27 compared with 119+/-84 ng/ml). In conclusion, the enhanced production of cardiac MMP-2 and MMP-9 is associated with LV enlargement and elevated BNP levels in patients with AMI. A pleiotropic effect of statins appears to be associated with the modulation of cardiac MMP activation, which may be potentially beneficial in the attenuation of post-infarction LV remodelling.

Aged↗
PubMed2006

Intensive treatment of risk factors in patients with type-2 diabetes mellitus is associated with improvement of endothelial function coupled with a reduction in the levels of plasma asymmetric dimethylarginine and endogenous inhibitor of nitric oxide synthase.

AIMS: Vascular endothelium is a major organ involved in hyperglycaemia and is affected by plasma asymmetric dimethylarginine (ADMA). ADMA is an endogenous, competitive inhibitor of nitric oxide synthase and is induced by inflammatory cytokines of tumour necrosis factor (TNF)-alpha in vitro. We hypothesized that a tight glycaemic control may restore endothelial function in patients with type-2 diabetes mellitus (DM), in association with modulation of TNF-alpha and/or reduction of ADMA level. METHODS AND RESULTS: In 24 patients with type-2 DM, the flow-mediated, endothelium-dependent dilation (FMD: %) of brachial arteries during reactive hyperaemia was determined by a high-resolution ultrasound method. Blood samples for glucose, cholesterol, TNF-alpha, and ADMA analyses were also collected from these patients after fasting. No significant glycaemic or FMD changes were observed in 10 patients receiving the conventional therapy. In 14 patients who were hospitalized and intensively treated, there was a significant decrease in glucose level after the treatment [from 190+/-55 to 117+/-21 (mean+/-SD) mg/dL, P<0.01]. After the intensive control of glucose level, FMD increased significantly (from 2.5+/-0.9 to 7.2+/-3.0%), accompanied by a significant (P<0.01) decrease in TNF-alpha (from 29+/-16 to 11+/-9 pg/dL) and ADMA (from 4.8+/-1.5 to 3.5+/-1.1 microM/L) levels. The changes in FMD after treatment correlated inversely with those in TNF-alpha (R=-0.711, P<0.01) and ADMA (R=-0.717, P<0.01) levels. CONCLUSION: The intensive correction of hyperglycaemia is associated with the improvement of endothelial function, which is coupled with the decrease in the levels of reduction of plasma TNF-alpha and ADMA in patients with type-2 DM. A strict glycaemic control may exert anti-cytokine and anti-atherogenic effects and may therefore be pathophysiologically important.

Arginine↗
PubMed2006

B-type natriuretic peptide strongly reflects diastolic wall stress in patients with chronic heart failure: comparison between systolic and diastolic heart failure.

OBJECTIVES: We explored the stimulus for B-type natriuretic peptide (BNP) secretion in the clinical setting of heart failure (HF). BACKGROUND: Increasingly, plasma BNP levels are being incorporated into the clinical assessment and management of systolic heart failure (SHF) as well as diastolic heart failure (DHF). However, heterogeneity in BNP levels among individuals with HF can cause some confusion in interpreting results. METHODS: In 160 consecutive patients presenting with HF, we measured plasma BNP levels and performed echocardiography and cardiac catheterization. Systolic and diastolic meridional wall stress was calculated from echocardiographic and hemodynamic data. RESULTS: Although plasma BNP had a significant correlation (r2 = 0.296 [p < 0.001]) with left ventricular end-diastolic pressure (EDP) as previously reported, the correlation between plasma BNP and end-diastolic wall stress (EDWS) (r2 = 0.887 [p < 0.001]) was more robust. In a subanalysis of 62 patients with DHF, a similar result was obtained (r2 = 0.143 for EDP and r2 = 0.704 for EDWS). In a comparison between SHF and DHF, the BNP level was significantly higher in SHF (p < 0.001). Although EDP did not show any difference, EDWS was significantly higher in SHF than in DHF (p < 0.001). CONCLUSIONS: The present study shows that plasma BNP levels reflect left ventricular EDWS more than any other parameter previously reported, not only in patients with SHF, but also in patients with DHF. The relationship of left ventricular EDWS to plasma BNP may provide a better fundamental understanding of the interindividual heterogeneity in BNP levels and their clinical utility in the diagnosis and management of HF.

Adult↗
PubMed2006

Postinfarction cardiac rupture despite immediate reperfusion therapy in a patient with severe aortic valve stenosis.

A 74-year-old woman with severe aortic valve stenosis (AS) was admitted to our hospital because of dyspnea on exertion. On day 2, she developed acute anterior wall myocardial infarction (MI) with ST elevation. Tissue plasminogen activator (tPA) was administered 10 min after the onset of chest pain, and emergency percutaneous coronary intervention was performed to induce coronary reperfusion after another 50 min. Five hours after MI onset, however, she suddenly went into electromechanical dissociation and died from cardiac rupture. This is the first case report of postinfarct cardiac rupture with severe AS occurring in spite of instituting immediate reperfusion therapy. High intraventricular pressure may be a critical risk factor for cardiac rupture in patients with AS complicated with acute MI. Further studies are required to clarify the risk and benefit of tPA administration before percutaneous coronary intervention and the necessity of the emergency correction of AS to prevent cardiac rupture.

Aged↗
PubMed2006

Assessment of genetic effects of polymorphisms in the MCP-1 gene on serum MCP-1 levels and myocardial infarction in Japanese.

BACKGROUND: Recently, the Framingham Heart Study reported that genetic variations in CCL2 influence serum levels of monocyte chemoattractant protein-1 (MCP-1) and the incidence of myocardial infarction (MI). The purpose of the present study was to investigate the possible involvement of CCL2 in the pathogenesis of atherosclerosis and MI in Japanese. METHODS AND RESULTS: Multiple regression analysis indicated that the MCP-1 levels were significantly influenced by various factors including age, body mass index, smoking, alcohol intake, high density lipoprotein-cholesterol, and systolic blood pressure. Moreover, the serum MCP-1 level was significantly correlated with intima - media thickness (p < 0.0001). However, this association disappeared when other clinical confounding factors were included in the analyses. Comprehensive analysis of common polymorphisms of CCL2 in a large community-based population and in subjects with MI found that the A(-2138)T polymorphism affected the serum MCP-1 level in a subgroup of subjects 65 years and older. However, no significant differences in the frequencies of any of the polymorphisms or haplotypes were found between subjects with and without MI. None of the polymorphisms in CCL2 affected carotid atherosclerosis. CONCLUSIONS: The serum MCP-1 level was a good surrogate marker of atherosclerosis in the present study population. Although genetic variations in CCL2 may have some influence on MCP-1 production, their influence does not seem to contribute appreciably to atherosclerosis in Japanese. The present results did not support the recently published findings from the Framingham Heart Study. The discrepancy between the 2 studies may be related to differences in confounding factors that contribute to MCP-1 levels and in the haplotype structure of the 2 populations.

Aged↗
PubMed2005

Postexercise VO2 "Hump" phenomenon as an indicator for inducible myocardial ischemia in patients with acute anterior myocardial infarction.

OBJECTIVES: At exercise testing with respiratory gas analysis in patients with inducible myocardial ischemia, we have occasionally observed abnormal transient oxygen uptake (VO2) components with a characteristic "Hump"-shaped morphology early after exercise, which may serve as an index for inducible ischemia. We examined this hypothesis in patients with anterior q-wave myocardial infarction in whom the accuracy to identify ischemia by exercise ECG is limited. DESIGN: From patients with acute anterior q-wave infarction but without clinically overt heart failure who underwent pre-discharge exercise testing, we examined patients with (Group-I, n = 30) and without (Group-N, n = 29) inducible ischemia. To identify "Hump", postexercise VO2 (up to 4 min) standardized for peak VO2 was exponentially fitted with use of peak VO2 and VO2 of 90-240 s, yielding "expected VO2". "D-curve" was obtained by subtracting "expected VO2" from measured VO2. RESULTS: Although exercise-induced ST depressions more frequently appeared in Group-I (27%) than in Group-N (3%, p < 0.05), the prevalence was low. D-curve peaked later (p < 0.01) and its value was greater (p < 0.05) in Group-I than in Group-N. When "Hump" was defined to be present if D-curve peaked > or =40 s and its peak value > or =15%, it was far more frequently found in Group-I (n = 17/30) than in Group-N (n = 1/29, p < 0.01). Thus, "Hump" could diagnose inducible ischemia with a sensitivity of 57% and a specificity of 97%. CONCLUSIONS: Although not highly sensitive, postexercise VO2 "Hump" with its peak occurring around 60 s after exercise is a specific marker for inducible ischemia. The identification may be useful, particularly in patients with limited accuracy of exercise ECG such as those with q-wave anterior infarction.

Exercise Test↗
PubMed2005

Validation of the association between the gene encoding 5-lipoxygenase-activating protein and myocardial infarction in a Japanese population.

BACKGROUND: Recently, the 5-lipoxygenase activating protein gene (ALOX5AP) was reported to confer a risk of myocardial infarction (MI) and stroke, independent of conventional risk factors. The purpose of the present study was to validate those findings in a Japanese population. METHODS AND RESULTS: The study population consisted of 1,875 subjects (males 871, females 1,004) recruited from the Suita study (control group) and 353 subjects (males 306, females 47) with MI. The promoter, all of the exons, and 3'UTR regions of ALOX5AP were sequenced in 96 subjects, and 8 polymorphisms were found. There were significant differences in the frequencies of the haplotypes constructed from the 2 SNPs (A162C and T8733A) between the control and MI groups. Multiple logistic analysis indicated that the homozygous genotype of the (CA) haplotype was significantly associated with a reduced risk for MI. CONCLUSION: The hypothesis that ALOX5AP contributes to susceptibility for MI was validated in a Japanese population.

3' Untranslated Regions↗
PubMed2005

Assessment of MEF2A mutations in myocardial infarction in Japanese patients.

BACKGROUND: Recently, a mutation in the human MEF2A gene was reported to be responsible for an autosomal dominant form of coronary artery disease, so the purpose of the present study was to assess the significance of MEF2A mutations in Japanese subjects with myocardial infarction (MI). METHODS AND RESULTS: The study population consisted of 589 control subjects recruited from the Suita study and 379 subjects with MI. The promoter, all the exons, and 3'-UTR regions of MEF2A were sequenced in 190 subjects with myocardial infarction. We found 2 amino acid length polymorphisms, a 7-amino acid deletion polymorphism, and a nonsense mutation (R447X) in exon 12. The length and deletion polymorphisms did not confer susceptibility to MI. Although the nonsense mutation was detected in 1 subject with MI, and in none of the control subjects, the impact of this mutation does not appear to be great; the subject had the MI while in his 70 s, had 2 major risk factors, and no family history of ischemic heart disease. CONCLUSION: MEF2A polymorphism does not contribute appreciably to MI in the Japanese population.

3' Untranslated Regions↗
PubMed2005

Angiotensin-converting enzyme genotype is not associated with exercise capacity or the training effect of cardiac rehabilitation in patients after acute myocardial infarction.

BACKGROUND: The relationship of the genotype for the angiotensin-converting enzyme (ACE) with exercise capacity or training effects has been studied in athletes or healthy persons, but recently the ACE DD genotype was reported to be associated with decreased exercise capacity in patients with congestive heart failure. Therefore, in the present study the association between the ACE genotype and exercise capacity was investigated in patients with acute myocardial infarction (AMI) participating in cardiac rehabilitation (CR) for 3 months. METHODS AND RESULTS: The study population comprised 168 patients stratified as II (n=75), ID (n=67), and DD (n=26) according to ACE genotype. Baseline left ventricular ejection fraction (LVEF) was similar among the genotype groups. In all patients, exercise capacity (peak work rate (PWR) and peak oxygen uptake (PVO 2)) significantly increased after CR. However, no differences were observed in PWR and PVO2 among the genotype groups at baseline or after CR. The results were similar even when analyzed in 60 patients with left ventricular (LV) dysfunction (LVEF <45%). CONCLUSION: The present study suggests that there is no association between ACE I/D polymorphism and exercise capacity in patients after AMI, even with LV dysfunction. Furthermore, ACE genotype may have no influence on the effects of CR after AMI.

Exercise Test↗
PubMed2005

Assessment of quality of life with 5 different scales in patients participating in comprehensive cardiac rehabilitation after acute myocardial infarction.

BACKGROUND: Measures assessing quality of life (QOL) in patients participating in comprehensive cardiac rehabilitation (CCR) have not been established in Japan. METHODS AND RESULTS: To compare different types of QOL scales and to determine the impact of CCR on QOL in Japanese cardiac patients, 5 different types of questionnaires were assessed in 44 patients participating in CCR after acute myocardial infarction (AMI). After 3-month CCR, peak oxygen uptake (PVO2, p<0.01), Sickness Impact Profile (SIP) total score (p<0.05) and physical function-related QOL scores (Specific Activity Scale (SAS), p<0.01; SIP physical score, p<0.01) significantly improved, whereas psychosocial/mental aspect-related QOL scores (Ministry of Health and Welfare (MHW)-QOL score, SIP psychosocial score, State-Trait Anxiety Inventory, Self-rating Depression Scale) did not change on the average. However, patients with low PVO2 (<21.7 ml.min-1.kg-1) showed significant improvements in all scores after CCR, whereas patients with preserved exercise capacity showed improvements only in physical function-related scores (SAS and physical SIP). Furthermore, patients with anxiety and depression showed significant improvements in these respective measures after CCR. CONCLUSION: In patients with AMI, physical function-related QOL scores improve after a 3-month CCR program, but psychosocial/mental aspect-related QOL scores improve only in those with impaired exercise tolerance or anxiety/depression. Thus, changes in QOL after CCR depend on type of QOL scale used and the baseline status of the patient. In addition, in Japanese cardiac patients MHW-QOL mainly reflects psychosocial/mental aspect-related QOL, as well as overall QOL.

Activities of Daily Living↗
PubMed2005

[Fulminant myocarditis causing severe left heart failure and massive thrombus formation following cardiac tamponade: a case report].

A woman aged middle thirties presented with common cold-like symptoms, and was hospitalized due to hypotension and tachycardia. Echocardiography revealed pericardial effusion and preserved left ventricular fractional shortening (28%). Cardiac index, pulmonary capillary wedge and right atrial pressure were 1.8 l/min/m2, 15 and 13 mmHg, respectively. After drainage of pericardial effusion, cardiac index increased to 3.4 l/min/m2. On the fifth hospital day, left ventricular dysfunction developed (fractional shortening: 16%, cardiac index: 1.5 l/min/m2, pulmonary capillary wedge pressure: 18 mmHg, right atrial pressure: 12 mmHg), so percutaneous cardiopulmonary support was introduced. However, the heart failed in asystole and the cavity was occupied by massive thrombus, probably related to heparin-induced thrombocytopenia. This case of fulminant myocarditis passed through various clinical features of heart failure. She died on the 12th hospital day.

Adult↗
PubMed2004

An association analysis between ApoA1 polymorphisms and the high-density lipoprotein (HDL) cholesterol level and myocardial infarction (MI) in Japanese.

Association studies were performed to confirm the effect of polymorphisms in apolipoprotein A1 ( ApoA1) on the high-density lipoprotein cholesterol (HDL-C) level and the incidence of myocardial infarction (MI). A sequence analysis identified nine polymorphisms in ApoA1. After considering linkage disequilibrium, four polymorphisms in ApoA1 and four polymorphisms in the 5'-flanking regions and 3'-flanking regions from the JSNP database were determined in 1,880 subjects recruited from the Suita study, which represents the general population in Japan. Of the eight polymorphisms tested, the ApoA1 T84C polymorphism had the greatest effect on the levels of HDL-C ( P=0.0005, P(c)=0.0040 corrected by the Bonferroni method) and triglyceride ( P<0.0001, P(c)=0.0008). The ApoA1 MspI polymorphism was not associated with HDL-C or triglyceride levels. We confirmed that the ApoA1 T84C polymorphism was associated with the HDL-C level but not the triglyceride level in patients with MI ( n=637). Moreover, this polymorphism was associated with the incidence of MI in male subjects ( P=0.0326). A logistic analysis indicated that the frequency of MI in the CC genotype was lower than that in the CT+TT genotype ( P=0.0145, OR=0.4955, 95% CI: 0.2746-0.8525). The ApoA1 T84C polymorphism is an important marker for the HDL-C level and may be a new risk marker for MI in Japanese.

Aged↗
PubMed2004

A promoter variant of the ATP-binding cassette transporter A1 gene alters the HDL cholesterol level in the general Japanese population.

To investigate the effects of polymorphisms in the ATP-binding cassette transporter A1 ( ABCA1) gene on the high-density lipoprotein cholesterol (HDL-C) level and the incidence of myocardial infarction (MI), we performed association studies. Sequence analysis identified 14 polymorphisms in the promoter region of ABCA1. After considering linkage disequilibrium, three polymorphisms in the promoter region and 11 polymorphisms from the JSNP database were determined in 1,880 subjects recruited from the Suita Study, representing the general population in Japan. We evaluated the association between the ABCA1 genotype and HDL-C level adjusted not only for standard factors, but also for genetic factors including ApoA1 and ApoE genotypes. Of the 14 polymorphisms tested, the G(-273)C ( P=0.0074), C(-297)T ( P=0.0195), and IMS-JST071749 ( P=0.0093) polymorphisms were significantly associated with the HDL-C level in the Suita population. We could reconfirm that the G(-273)C genotype was influential in another set of subjects ( P=0.0310, n=743). However, the distribution of the ABCA1 G(-273)C genotype in subjects with MI ( n=598) was not different from that in the control population ( n=801). These results indicate that ABCA1 G(-273)C has a significant effect on the HDL-C level in the general Japanese population, but not on the incidence of MI.

ATP Binding Cassette Transporter 1↗
PubMed2004

Genetic variants in PCSK9 affect the cholesterol level in Japanese.

Mutations in the proprotein convertase subtilisin/kexin 9 ( PCSK9) gene have been reported in affected members of two families with autosomal dominant hypercholesterolemia. To investigate the effects of common variants in PCSK9 on the cholesterol level, we conducted an association study using a large cohort representing the general population in Japan (n=1,793). Direct sequencing in all of the exonic regions identified 21 polymorphisms. After consideration of linkage disequilibrium among these polymorphisms, we selected and genotyped nine polymorphisms by the TaqMan method. The intron 1/C(-161)T and exon 9/I474 V polymorphisms were associated with levels of total cholesterol (TC) [C(-161)T, P=0.0285; I474 V, P=0.0069] and low-density lipoprotein cholesterol (LDL-C) [C(-161)T, P=0.0257; I474 V, P=0.0007]. The distributions of these polymorphisms in subjects with miocardial infarction (MI) (n=649) were not different from those in the control population. These results provide the first evidence that common variants intron 1/C(-161)T and exon 9/I474 V in PCSK9 significantly affect TC and LDL-C levels in the general population in Japan.

Base Sequence↗
PubMed2004

A promoter variant of the heme oxygenase-1 gene may reduce the incidence of ischemic heart disease in Japanese.

Heme oxygenase-1 (HO-1) has been suggested to have antiatherogenic properties. This study was designed to examine the relationship between the HO-1 gene (HMOX1) and ischemic heart disease. The study population consisted of 1972 control subjects and 597 subjects with ischemic heart disease (myocardial infarction (MI) n = 393, HMOX1 n = 204). The control subjects were consecutively selected from the Suita study, an epidemiological cohort representing the general population in Japan. Patients with ischemic heart disease were recruited from the outpatient clinic of the National Cardiovascular Center (NCVC). We sequenced HMOX1 and found a T(-413)A polymorphism in the promoter region. Multiple logistic analyses indicated that the T(-413)A (T(-413)A (TA + TT/AA) polymorphism, sex, smoking habit, DM and BMI affected the occurrence of ischemic heart disease. The odds ratios of the TA + TT allele for MI and AP were 1.42 (P = 0.0468, 95% confidence interval: 0.01-0.35) and 1.86 (P = 0.0096, 95% confidence interval: 0.08-0.55), respectively. Luciferase reporter assay indicated that the A allele promoter had significantly higher activity than the T allele promoter. The AA genotype of HMOX1 reduced the incidence of ischemic heart disease, possibly due to the high expression level of HMOX1.

Base Sequence↗