Biomedical subjects

Tomohiro Sakamoto

Publications and source records attributed to Tomohiro Sakamoto.

66 records · Page 4Linked to original sources

PubMed2003

Plasma thioredoxin levels and platelet aggregability in patients with acute myocardial infarction.

BACKGROUND: Oxidative stress is thought to play an important role in atherosclerotic vascular disease. Recently, it has become possible to quantitatively measure thioredoxin, a marker of oxidative stress in human plasma. A platelet aggregometer that uses laser-light scattering enables minimal changes in platelet aggregability to be monitored; however, the relationship between oxidative stress and platelet aggregability in vivo is not well understood. METHODS: We investigated plasma thioredoxin levels and platelet aggregability, in particular small platelet aggregates, in 45 patients with acute myocardial infarction (AMI); we compared the results with 33 patients with stable exertional angina (SEA) and 30 patients with chest pain syndrome (CPS). RESULTS: The plasma thioredoxin levels and the degree of small platelet aggregates were higher in the AMI group than in the SEA and the CPS groups: in the AMI group, at 4 weeks after admission, both of those parameters were significantly decreased (P <.01), but they were still higher (P <.05) than in the SEA or the CPS group. There was a significant positive correlation between small platelet aggregates and plasma thioredoxin levels (rho = 0.354, P =.0002). We divided the AMI patients into 2 groups according to the 75 percentile of plasma thioredoxin levels on admission. At the chronic phase, the left ventricular ejection fraction was significantly higher in the lower thioredoxin group than in the higher thioredoxin group. CONCLUSIONS: We showed that plasma thioredoxin levels and platelet aggregability increased concomitantly in patients with AMI. In these patients, increased plasma thioredoxin was associated with platelet hyperaggregability and lower left ventricular ejection fraction.

Adult↗

PubMed2003

Synergistic interaction of T-786-->C polymorphism in the endothelial nitric oxide synthase gene and smoking for an enhanced risk for coronary spasm.

OBJECTIVE: We previously reported that a T-786-->C polymorphism in the 5'-flanking region of the endothelial nitric oxide synthase gene and smoking were independently associated with coronary spasm; however, the interaction between this polymorphism and smoking remains to be elucidated. METHODS: We analyzed 209 men and 238 women who were admitted consecutively at our institution; all subjects received an intracoronary injection of acetylcholine (ACh) while undergoing coronary angiography for evaluation of chest pain: all subjects had no significant coronary stenosis. We divided these subjects into four groups: non-smokers with T/T genotype (Control Group A); non-smokers with C/T or C/C genotype (Group B); smokers with T/T genotype (Group C); and smokers with C/T or C/C genotype (Group D). We further examined quantitative coronary angiographies of the left anterior descending coronary artery in a subset of 54 consecutive men and 53 consecutive women. RESULTS: The frequencies of coronary spasm in Group B (male: 61%, female: 78%), Group C (62%, 59%) and Group D (91%, 92%) were significantly higher than in Group A (30%, 38%). In the males, ACh-induced vasoconstriction was greatest in Group D, and the change was weakest in Group A. In the females, ACh-induced vasoconstrictions were significantly greater in Groups B, C and D than in Group A. The T-786-->C polymorphism and smoking combine to increase the risk of coronary spasm.

Acetylcholine↗

PubMed2003

Platypnea - orthodeoxia syndrome with atrial septal defect.

A 75-year old man was referred to hospital for symptomatic hypoxemia. He did not complain of dyspnea while supine, but while sitting or standing, he experienced dyspnea with severe hypoxemia. He did not have any pulmonary diseases that could cause dyspnea. Transesophageal echocardiography revealed an atrial septal aneurysm with a small atrial septal defect (ASD) and a mild left-to-right shunt through the ASD when the patient was supine. However, when he became upright, a severe right-to-left shunt occurred and the arterial oxygen saturation decreased from 96% to 80% with dyspnea. Cardiac catheterization revealed normal pulmonary artery pressure. He was therefore diagnosed as having platypnea - orthodeoxia syndrome. Magnetic resonance imaging of the chest showed a deformity of the atrium associated with elongation of the ascending aorta. The ASD was closed surgically and the dyspnea and hypoxemia that occurred while he was upright completely resolved.

Aged↗

PubMed2003

Increased serum matrix metalloproteinase-1 concentration predicts advanced left ventricular remodeling in patients with acute myocardial infarction.

The left ventricular ejection fraction (LVEF) is one of the major prognostic factors after acute myocardial infarction (AMI) and matrix metalloproteinase-1 (MMP-1) is an enzyme responsible for extracellular collagen degradation and remodeling. The present study investigated whether the concentration of serum MMP-1 was associated with the LVEF after AMI. Blood was sampled on admission, and at 24 h, 3 days, 7 days, 2 weeks and 4 weeks in 24 patients with their first AMI. Left ventriculography was performed 4 weeks after the onset of AMI and the LVEF was calculated by center line method. MMP-1 concentrations were higher at 7 days and at 2 weeks than on admission (p<0.001), and at 7 days (r=-0.655, p=0.0005) and at 2 weeks (r=-0.636, p=0.0008) were negatively correlated with the LVEF. The patients with AMI were divided into high and low LVEF groups according to the results of left ventriculography. Although there were no differences in the clinical characteristics between the 2 LVEF groups, the MMP-1 concentrations at 24 h (p<0.01), 7 days (p<0.01) and 2 weeks (p<0.05) were lower in the high LVEF group than in low LVEF group. A high concentration of MMP-1 at the subacute phase after AMI predicts advanced left ventricular remodeling.

Aged↗

PubMed2003

Formation of platelet microaggregates correlates with adverse clinical outcome in patients with coronary artery disease.

Platelet activation plays a pivotal role in the pathogenesis of acute coronary syndromes. Laser-light scattering in a platelet aggregometer was used to evaluate aggregate size and number quantitatively. Small platelet aggregates ultimately develop into medium and then large platelet aggregates. Thus the measurement of small platelet aggregates is important in the evaluation of thrombus formation. We examined the relationship between small platelet aggregates and the occurrence of subsequent cardiovascular events. We followed-up 204 patients (149 men and 55 women, mean age 68 +/- 9 years) with coronary artery disease (CAD) for 48 months. Blood sampling to determine platelet aggregation was performed on the day of hospital discharge. The degree of small platelet aggregates [relative risk 4.34, 95% confidence interval (1.62-11.7), p = 0.004] and low left-ventricular ejection fraction [relative risk 2.88, 95% confidence interval (1.23-6.73), p = 0.015] were independent predictors of the occurrence of cardiovascular events in multivariate Cox hazard analysis. In Kaplan-Meier analysis, the degree of small platelet aggregates correlated with the probability of cardiovascular event occurrence. In patients with CAD, an increase in small platelet aggregates is closely correlated with the future occurrence of cardiovascular events

Adult↗

PubMed2002

Comparison of urinary biopyrrin levels in acute myocardial infarction (after reperfusion therapy) versus stable angina pectoris and their usefulness in predicting subsequent cardiac events.

We examined the relation between oxidative stress and cardiac events in patients with acute myocardial infarction (AMI). There is now increasing evidence that reactive oxygen species cause reperfusion injury to the previously ischemic myocardium after reperfusion. We measured urinary biopyrrin/creatinine levels, an oxidative stress marker, in 41 patients with AMI, 34 patients with stable angina pectoris (SAP), and 29 control subjects. In the patients with AMI, urine samples were taken before, at 4 and 24 hours, and at 1 and 2 weeks after reperfusion therapy. Of these 41 patients with AMI, 38 received reperfusion therapy, and the urinary biopyrrin/creatinine levels (micromol/g.creatinine) before reperfusion were significantly higher than those of the other 2 groups (AMI 4.24 +/- 0.49, SAP 2.45 +/- 0.15, control subjects 2.31 +/- 0.16; p = 0.0003 vs AMI). The onset of reperfusion significantly increased the levels of urinary biopyrrins/creatinine, and this time course was mapped out, peaking at 4 hours (8.21 +/- 0.96 vs 4.24 +/- 0.49 before, p = 0.0001), and decreasing to control levels between 24 hours and 7 days. The peak levels of urinary biopyrrins/creatinine were higher in the positive cardiac event group than in the negative cardiac event group (11.89 +/- 1.77 vs 7.57 +/- 1.00 micromol/g.creatinine, p = 0.029). These findings add further evidence that oxidative stress contributes to the complications of reperfusion injury, and suggest that urinary assessment of biopyrrins may be useful in predicting subsequent cardiac events after reperfusion in AMI.

Aged↗

PubMed2002

B-type natriuretic peptide as a marker of the effects of enalapril in patients with heart failure.

BACKGROUND: A-Type and B-type natriuretic peptides are cardiac hormones whose circulating levels reflect the severity of heart failure. It is not known how plasma levels of these hormones respond to changes in cardiac function that occur as a result of treatment with angiotensin-converting enzyme (ACE) inhibitors. METHODS: Enalapril was administered at 5 mg/d for 3 months in 24 patients with chronic heart failure, and for the next 3 months at 15 mg/d in the high-dose group (n = 12) and 5 mg/d in the low-dose group (n = 12). We measured plasma levels of A-type or B-type natriuretic peptides, as well as conventional measures of cardiac function, such as the cardiothoracic ratio, left ventricular end-diastolic volume, and percent fractional shortening. RESULTS: Mean (+/- SD) plasma levels of both hormones decreased promptly after 2 weeks of therapy (A-type natriuretic peptide: 140 +/- 107 pg/mL to 81 +/- 68 pg/mL, P = 0.01; B-type natriuretic peptide: 305 +/- 278 pg/mL to 190 +/- 178 pg/mL, P = 0.01). These reductions were sustained throughout therapy. In contrast, the cardiothoracic ratio, left ventricular end-diastolic dimension, and percent fractional shortening had not changed significantly after 3 months of treatment, although improvements were seen after 6 months of treatment. After 6 months, plasma levels of both A-type and B-type natriuretic peptides were significantly lower in the high-dose group than in the low-dose group (A-type natriuretic peptide: 48 +/- 25 pg/mL vs. 57 +/- 27 pg/mL, P = 0.01; B-type natriuretic peptide: 78 +/- 58 pg/mL vs. 139 +/- 61 pg/mL, P = 0.005), whereas no significant differences were observed in the other measures of cardiac function. CONCLUSION: Plasma levels of A-type and B-type natriuretic peptides appear to be more sensitive markers of heart failure than conventional echocardiographic parameters and cardiothoracic ratios. Measurement of these hormones might be useful for monitoring the effects of treatment with ACE inhibitors.

Aged↗

PubMed2002

Effects of perindopril on aldosterone production in the failing human heart.

The present study was designed to examine whether the production of aldosterone from the heart is suppressed by angiotensin-converting enzyme (ACE) inhibition in patients with heart failure. Forty-one patients with left ventricular systolic dysfunction were randomly divided into either the perindopril group (n = 21, perindopril 4 mg/day) or the placebo group (n = 20). Plasma levels of aldosterone and ACE activity were measured in the anterior interventricular vein, coronary sinus, and aortic root during cardiac catheterization. The levels of aldosterone as well as ACE activity were significantly higher at the anterior interventricular vein and the coronary sinus than at the aortic root in the placebo group (aldosterone: 92.1 +/- 9.0 vs 70.6 +/- 8.3 pg/ml [p <0.001]; 90.3 +/- 9.2 vs 70.6 +/- 8.3 pg/ml [p <0.001], respectively; ACE activity: 13.6 +/- 0.8 vs 12.2 +/- 0.7 IU/L [p <0.001], 13.4 +/- 0.8 vs 12.2 +/- 0.7 IU/L [p <0.001], respectively). On the other hand, there were no differences in the levels of aldosterone or ACE activity between the anterior interventricular vein and aortic root or between the coronary sinus and aortic root (aldosterone: 68.1 +/- 8.4 vs 69.9 +/- 9.4 pg/ml [p = NS]; 67.3 +/- 8.9 vs 69.9 +/- 9.4 pg/ml [p = NS], respectively; ACE activity: 9.7 +/- 0.8 vs 9.9 +/- 0.8 IU/L [p = NS]; 9.8 +/- 0.8 vs 9.9 +/- 0.8 IU/L, respectively) in the perindopril group. The levels of aldosterone as well as ACE activity were significantly lower at the anterior interventricular vein and coronary sinus in the perindopril group than in the placebo group. The difference in the level of aldosterone between the anterior interventricular vein and aortic root (Delta aldosterone [anterior interventricular vein - aortic root]) had a significant positive correlation with that of ACE activity (Delta ACE [anterior interventricular vein - aortic root]) (r = 0.536, p <0.001), whereas ACE activity in the aortic root had no significant correlation with either the aldosterone levels in the aortic root or Delta aldosterone (anterior interventricular vein - aortic root). Perindopril suppressed cardiac aldosterone production by mainly suppressing cardiac ACE activity in patients with heart failure. Thus, aldosterone production is activated in the failing ventricle and is suppressed by perindopril mainly via the suppression of cardiac ACE activity in patients with heart failure.

Aldosterone↗

PubMed2002

B-type natriuretic peptide after percutaneous transluminal septal myocardial ablation.

BACKGROUND: Plasma level of B-type natriuretic peptide is a sensitive marker of left ventricular dysfunction and the level is markedly elevated in patients with hypertrophic obstructive cardiomyopathy. Percutaneous transluminal septal myocardial ablation, a catheter-based treatment of hypertrophic obstructive cardiomyopathy, has been widely used as a new therapeutic option for the disease. This study was designed to evaluate clinical implications of natriuretic peptides after the new treatment. METHODS: Seven consecutive patients with hypertrophic obstructive cardiomyopathy unresponsive to usual medical treatments (age: 57.9+/-22.0 years) were enrolled in the study. Serial changes in atrial and B-type natriuretic peptide in plasma were examined after percutaneous transluminal septal myocardial ablation. RESULTS: Atrial and B-type natriuretic peptides levels (pg/ml, mean+/-S.D.) at baseline were higher in hypertrophic obstructive cardiomyopathy than in control (80.0+/-43.0 vs. 12.8+/-5.2, P<0.0001; 858.0+/-458.4 vs. 12.4+/-7.0, P<0.0001; respectively). Left ventricular outflow-tract pressure gradient (mmHg) immediately decreased from 115.3+/-23.3 to 30.6+/-12.4 (P<0.0001) after the treatment and concomitantly B-type natriuretic peptide level decreased (858.0+/-458.4 to 264.1+/-137.7, P=0.0084). The level re-increased and peaked at the 2nd day (634.4+/-429.6) and gradually decreased again until 4 weeks. Reduction rate of left ventricular outflow-tract pressure gradient between before and 4 weeks after percutaneous transluminal septal myocardial ablation positively correlated with that of B-type natriuretic peptide (r(2)=0.817, P=0.0053). Changes in atrial natriuretic peptide were not significant in contrast to those of B-type natriuretic peptide. CONCLUSIONS: Plasma B-type natriuretic peptide level could be useful to predict the effects of percutaneous transluminal septal myocardial ablation in patients with hypertrophic obstructive cardiomyopathy.

Adolescent↗

PubMed2002

Expression of aldosterone synthase gene in failing human heart: quantitative analysis using modified real-time polymerase chain reaction.

We have shown that aldosterone, previously thought to be synthesized solely in the adrenal cortex, is also produced in the failing human heart. One way to induce aldosterone synthesis in the heart would be to increase the expression of CYP11B2, the enzyme catalyzing the terminal step in aldosterone synthesis. However, CYP11B2 expression has never been examined in cardiac tissue from patients with heart failure. We assayed CYP11B2 expression in left ventricular tissue obtained at autopsy from seven patients. Total RNA was extracted from frozen samples. CYP11B2 gene expression was then quantitatively analyzed using a modified real-time PCR method that enabled assay of samples containing very small amounts of template DNA. The template DNA was initially amplified 1024-fold by subjecting it to 10 PCR cycles in the absence of the TaqMan probe. Thereafter, conventional real-time PCR was simultaneously performed on both target and standard samples. We measured the small quantities of CYP11B2 gene transcript and found the levels to be significantly higher in samples from heart failure patients than in those from cardiovascular disease-free patients. Our modified real-time PCR method enables quantitative analysis of gene expression using very small amounts of template DNA. CYP11B2 expression is up-regulated in the failing human heart.

Cytochrome P-450 CYP11B2↗

PubMed2002

Infective endocarditis with perivalvular pseudoaneurysm.

A 16-year-old Japanese woman with infective endocarditis was admitted to hospital. An echocardiography exhibited a perivalvular pseudoaneurysm just under the mitral valve. Left ventriculography demonstrated that the aneurysm had a small neck and dyskinetic motion with oppression to the coronary sinus and right coronary artery.

Adolescent↗

PubMedDate not supplied

Cardiac displacement with a congenital complete left-sided pericardial defect in a patient with exertional angina pectoris--a case report.

A 71-year-old man with exertional chest pain was admitted to the hospital. A chest roentgenogram exhibited levoposition of the heart. An electrocardiogram showed clockwise rotation in the precordial leads and ST depression in V6, V7, V8, and V9 as well as in II, III, aVF leads associated with chest pain in a treadmill exercise test. The congenital complete left-sided pericardial defect could not be diagnosed preoperatively, but it was confirmed by thoracotomy.

Aged↗