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Biomedical subjects

B Takase

Publications and source records attributed to B Takase.

At least 37 records · Page 2Linked to original sources
PubMed2000

Endothelial function and peripheral vasomotion in the brachial artery in neurally mediated syncope.

BACKGROUND: Paradoxical peripheral vasodilation is one of the suspected mechanisms of neurally mediated syncope. Parasympathetic stimulation following sympathetic activation during orthostatic stress mainly contributes to this vasodilation. HYPOTHESIS: Since endothelial function modulates peripheral vascular tone, this study aimed to determine whether endothelial function and inappropriate peripheral vasomotion has a significant role in the pathogenesis of neurally mediated syncope. METHODS: To investigate whether endothelial function is augmented or whether abnormal peripheral vasomotion exits, flow-mediated dilation (FMD, endothelium-dependent vasodilation) and sublingual glyceryl trinitrate-induced dilation (0.3 mg, GTN-D, endothelium-independent vasodilation) were measured in the brachial artery in 16 patients with neurally mediated syncope, aged 33 +/- 10 years, by using high-resolution ultrasound. All patients underwent positive head-up tilt testing. These measures were compared with those in 16 control subjects matched with the patients by age, gender, and coronary risk factors. For FMD, percent diameter changes were obtained from baseline to hyperemic conditions (1 min after 5 min occlusion of the forearm artery). There were five smokers in both the patient and the control groups, but there was no structural heart disease in either group. RESULTS: Baseline brachial artery diameters were comparable (3.8 +/- 0.6 vs. 3.8 +/- 0.7 mm, NS). Flow-mediated dilation in patients with neurally mediated syncope had a normal value of 9.8 +/- 5.0% despite the inclusion of five smokers. Flow-mediated dilation and GTN-D in patients with neurally mediated syncope were significantly greater than those in controls (9.0 +/- 5.0 vs. 3.0 +/- 3.5%, p<0.05; 18.4 +/- 5.5 vs. 14.1 +/- 4.4%, p<0.05). CONCLUSIONS: Augmented endothelial function and/or abnormal peripheral vasomotion in peripheral arteries are important in patients with neurally mediated syncope in selected populations.

Adult↗
PubMed1999

Effect of aprindine on heart rate variability indices in patients with ischemic heart disease.

BACKGROUND: Decreased heart rate variability indices (HRV) are associated with untoward outcome of patients with ischemic heart disease (IHD). Most class I antiarrhythmic agents decrease HRV, but aprindine (a new class I antiarrhythmic agent) is reported to increase HRV in patients without ischemia. HYPOTHESIS: The study was undertaken to determine whether apridine might increase HRV in patients with IHD. METHODS: To investigate the effect of aprindine on HRV in patients with IHD, we performed 24-h ambulatory electrocardiogram (ECG) at the end of placebo and aprindine (60 mg daily) treatment phases on 38 patients with IHD and at least isolated premature ventricular contractions (PVC). The study protocol utilized a single blind, 4-week, placebo-controlled design. Heart rate variability from ambulatory ECG included SDNN (ms), SDANN (ms), SD (ms), rMSSD (ms), pNN50 (%); frequency analysis of HRV consisting of total (ms, 0.01-1.00 Hz), low (ms, 0.04-0.15 Hz), and high (ms, 0.15-0.40 Hz) components. RESULTS: Study patients were divided into three groups according to the severity of IHD and antiarrhythmic efficacy of aprindine. Group 1 consisted of 15 patients with angina with single-vessel disease, and Group 2 was composed of 10 patients with either multivessel disease or post myocardial infarction; PVCs decreased in both groups as result of aprindine treatment. Group 3 consisted of 13 patients who showed no decreased PVC after aprindine treatment. RMSSD increased, and pNN50 and high-frequency spectra tended to increase in Group 1, while SD, rMSSD, pNN50, and total and low-frequency spectra decreased in Group 3; no significant changes were observed in Group 2. Aprindine significantly augments vagal activity, as reflected by the increase of rMSSD, pNN50, and high-frequency spectra in mild IHD. CONCLUSION: These salutary effects are less in more severe IHD, but aprindine does not aggravate HRV. Thus, if there are salutary effects on arrhythmias and no proarrhythmic effects, aprindine could be prescribed to patients with IHD without concern about decreasing HRV.

Adult↗
PubMed1999

Frequency domain heart rate variability and plasma norepinephrine level in the coronary sinus during handgrip exercise.

BACKGROUND: Heart rate (HR) variability has been recognized as an important noninvasive index of autonomic nervous activities. However, the relationship between HR variability and cardiac circulating norepinephrine (NE), especially with respect to coronary ischemia, remains unclear. HYPOTHESIS: This study was undertaken to determine whether HR variability indices can reflect cardiac NE levels during handgrip exercise. METHODS: We simultaneously measured HR variability and cardiac NE overflow rate in 32 patients (30 men, 2 women) during a 6-min isometric handgrip exercise. Among the 32 subjects, 20 (19 men, 1 woman) had coronary artery disease (CAD) and 12 (control group; 11 men, 1 woman) did not. RESULTS: Hemodynamics and cardiac NE overflow rates among subjects at rest were not significantly different between the two groups. In the normal subjects, low-frequency (LF) spectra and LF/HF (high-frequency) ratios were not significantly changed during handgrip exercise, but HF spectra significantly increased from 10.1 +/- 4.5 to 12.2 +/- 7.0 ms (p < 0.05). In the subjects with CAD, LF and LF/HF spectra were significantly (p < 0.05 and 0.01, respectively) increased by handgrip exercise. High-frequency spectra were not significantly changed by handgrip exercise. In the normal subjects, a significant negative relation (r = -0.76, p < 0.01) was obtained between HF change and cardiac NE overflow rate, whereas this relationship was not significant in the subjects with CAD. The correlation between changes of LF/HF and cardiac NE overflow rate was significant in the normal (r = 0.56, p < 0.05) but not in subjects with CAD. CONCLUSION: These results suggest that vagal modulation of HR variability is more prominent in normal coronary artery subjects than in CAD subjects during handgrip exercise. Heart rate variability indices may thus serve as adequate indicators of autonomic nerve activity in subjects with normal coronary arteries but not in those with CAD, probably due to decreased adaptation to physical stress during handgrip exercise.

Blood Pressure↗
PubMed1999

Morning attenuation of endothelium-dependent, flow-mediated dilation in healthy young men: possible connection to morning peak of cardiac events?

BACKGROUND AND HYPOTHESIS: Brachial artery flow-mediated dilation (FMD), a noninvasive, widely used clinical index of endothelial function and magnitude of FMD, has been reported to be closely related to many coronary risk factors and coronary atherosclerosis. However, there has been no study that examines the diurnal change of FMD. We designed this study to reveal the diurnal variation of FMD in healthy volunteers. METHODS: We examined FMD in response to reactive hyperemia by high resolution ultrasound in 13 healthy young men (age 25-32) at four different times over the course of a day. RESULTS: Mean measures of brachial artery FMD was 4.0% at 8:00, 5.3% at 12:00, 9.7% at 17:00, and 6.9% at 21:00 hours. Flow-mediated dilation at 8:00 and at 12:00 hours was significantly lower than that at 17:00 (p < 0.05). CONCLUSIONS: These results show that endothelial function has diurnal variation and is significantly attenuated in the morning. Morning attenuation of endothelial function should be recognized in clinical research and may play an important role in the circadian variation of the occurrence of acute cardiovascular events.

Adult↗
PubMed1999

Clinical validation of intravascular ultrasound imaging for assessment of coronary stenosis severity: comparison with stress myocardial perfusion imaging.

OBJECTIVES: To validate intravascular ultrasound (IVUS) measurements for differentiating functionally significant from nonsignificant coronary stenosis. BACKGROUND: To date, there are no validated criteria for the definition of a flow-limiting coronary artery stenosis by IVUS. METHODS: Preinterventional IVUS imaging (30-MHz imaging catheter) of 70 de novo coronary lesions was performed. The lesion lumen area and three IVUS-derived stenosis indixes comparing lesion lumen area with the lesion external elastic lamina (EEL) area, the mean reference lumen area and the mean reference EEL area were compared with the results of stress myocardial perfusion imaging. RESULTS: The lesion lumen area and three IVUS-derived stenosis indexes showed sensitivities and specificities ranging between 80% and 90% using stress myocardial perfusion imaging as the gold standard. The lesion lumen area < or =4 mm2 is a simple and highly accurate criterion for significant coronary narrowing. CONCLUSIONS: Quantitative IVUS indices can be reliably used for identifying significant epicardial coronary artery stenoses.

Aged↗
PubMed1998

Endothelium-dependent flow-mediated vasodilation in coronary and brachial arteries in suspected coronary artery disease.

Previous studies showed a weak correlation between endothelial function of the coronary arteries as assessed by acetylcholine and brachial artery vasomotion during reactive hyperemia. When the same stimulus was used, we obtained a strong correlation between flow-mediated dilation in the coronary and brachial arteries (r=0.78, p <0.001), so that noninvasive assessment of flow-mediated dilation in the brachial artery could be used as a surrogate measure for coronary artery endothelial function.

Adult↗
PubMed1998

Extent of ischemic stimulus and plasma beta-endorphin levels in silent myocardial ischemia.

BACKGROUND: Beta-endorphin has been reported to play a role in the mechanism of silent myocardial ischemia. OBJECTIVES: Plasma beta-endorphin levels during coronary angioplasty-induced silent and symptomatic myocardial ischemia were compared with those during exercise-induced silent ischemia. METHODS AND RESULTS: The study population consisted of 40 nondiabetic patients with angioplasty-indicated coronary artery disease. All patients underwent exercise treadmill testing 2 to 4 days before angioplasty. Patients were divided into three groups: group 1, 10 patients with silent ischemia during exercise and angioplasty; group 2, 15 patients with silent ischemia during exercise and symptomatic ischemia during angioplasty; and group 3, 15 patients with symptomatic ischemia during both exercise and angioplasty. In group 1, plasma beta-endorphin levels during balloon inflation were significantly higher than in groups 2 and 3 and also significantly higher than during exercise. In group 2, plasma beta-endorphin levels were significantly elevated at exercise-induced silent myocardial ischemia and balloon-induced symptomatic myocardial ischemia, but the levels between exercise and balloon inflation were not significantly different. CONCLUSIONS: For "silent" myocardial ischemia, it may be necessary for beta-endorphin levels to increase to sufficiently high levels to suppress anginal symptoms in response to the degree of ischemic stimuli.

Aged↗
PubMed1998

Differences in heart rate variability in the acute phase of first and second attacks of myocardial infarction.

The purpose of the study was to examine the differences between first and second myocardial infarctions with respect to improvement in measures of heart rate variability (HRV). The study population comprised 48 non-diabetic patients with acute myocardial infarction (AMI), and with angiographically documented coronary artery occlusion and successful reperfusion. The subjects were grouped as 35 cases with a first AMI attack and 13 with their second AMI. Two weeks after the onset of infarction, indices of HRV were higher in first infarction cases than in second infarction cases. In the latter, there were no significant increases in HRV indices from day of onset to 2 weeks later, nor were there any significant changes in left ventricular ejection fraction (LVEF) from onset to 3 weeks later. All patients studied had a patent infarct-related artery 3 weeks later. We found sustained low values of HRV after a second AMI. Different risk stratification may be needed between uncomplicated first AMI and second AMI cases.

Aged↗
PubMed1997

Autonomic responses to orthostatic stress in head-up tilt testing: relationship to test-induced prolonged asystole.

BACKGROUND: Prolonged asystole is sometimes an extreme manifestation of neurally mediated syncope. HYPOTHESIS: To investigate the mechanism of head-up tilt testing-induced prolonged (life-threatening) cardiac asystole, we measured temporal changes in frequency domain heart rate variability indices in 25 patients with syncope of undetermined etiology. METHODS: Head-up tilt testing (80 degrees) was performed in 25 patients for up to 40 min or until asystole or syncope occurred. Three patients (Group 1; 37 +/- 13 years, 1 man 2 women) had an episode of prolonged cardiac asystole (> or = 10 s) during testing, necessitating cardiopulmonary resuscitation. Syncope, but no asystole, was induced in 10 patients (Group 2; 48 +/- 31 years, 6 men, 4 women), and 12 patients (Group 3; 55 +/- 20 years, 5 men, 7 women) failed to show asystole or syncope during testing. Power spectra of low (0.04-0.15 Hz) and high (0.15-0.40 Hz) frequency, and total (0.01-1.00 Hz) frequency spectra were measured in consecutive 2 min segments throughout the test. RESULTS: Maximally changed values in heart rate, systolic blood pressure, and heart rate variability indices during testing were compared among the three groups (maximally changed values did not include the values during tilt-induced symptoms). High frequency spectra in Groups 2 and 3, but not in Group 1, decreased during the test. High frequency spectra, low frequency spectra, and total spectra in Group 1 were significantly higher than those in Groups 2 and 3 during testing. In Group 1 patients, findings at test-induced asystole were consistent with exaggerated sympathetic and concurrent persistent parasympathetic activity. CONCLUSION: Unusual autonomic responses to orthostatic stress can cause prolonged asystole, and this autonomic nerve dysregulation may relate to asystolic episodes associated with cardiovascular collapse.

Adult↗
PubMed1997

Effect of carteolol on silent myocardial ischemia, variability in heart rate, and the pain-modulating system.

To investigate the effects of carteolol, which is a nonselective beta-adrenergic agent with intrinsic sympathomimetic activity, on silent myocardial ischemia, exercise-induced myocardial ischemia, indexes of heart rate variability, and pain-modulating system, 20 patients (mean 60 +/- 9 years) with chronic stable angina underwent exercise treadmill testing and 24-hour ambulatory electrocardiographic monitoring during 2 weeks of carteolol administration (15 mg/day) in a double-blind, placebo-controlled design. Plasma levels of beta-endorphin and bradykinin and electrical pain stimulation to the skin were measured at rest and peak exercise. Indexes of heart rate variability of both time-domain and frequency-domain analysis were derived from 24-hour ambulatory electrocardiographic monitoring. Carteolol decreased maximal heart rate responses to daily activities during ambulatory monitoring and significantly reduced the median frequency and duration of silent myocardial ischemic episodes (from 1.0 to 0.0 events/24 hr and from 16 to 0 min/24 hr, respectively). Carteolol significantly decreased the rate-pressure product at rest and during exercise with improving maximal ST segment depression, suggesting amelioration of exercise-induced myocardial ischemia. Carteolol did not significantly affect plasma levels of beta-endorphin and bradykinin or pain threshold. It significantly decreased some indexes (standard deviation of all normal sinus R-R intervals in the entire 24-hour recording and standard deviation of the mean of all 5-minute segments of normal R-R intervals of a 24-hour recording) of heart rate variability. These results suggest that carteolol may reduce total myocardial ischemic burden by the reduction of cardiac oxygen demand during daily activities and exercise stress, while not affecting plasma levels of beta-endorphin, bradykinin, and pain threshold. Because carteolol tended to decrease indexes of heart rate variability, significant caution might be necessary in prescribing the beta-blocking agents with intrinsic sympathomimetic activity like carteolol to patients with potential serious arrhythmia.

Adrenergic beta-Antagonists↗
PubMed1997

Use of head-up tilt testing to determine a possible cause of unexpected cardiac asystole during epidural anesthesia.

Head-up tilt testing is widely used in the diagnosis of syncope of unknown origin. In this report, head-up tilt testing elucidated the etiology of cardiac asystole of unexpected and sudden onset during orthopedic surgery under epidural anesthesia in a 30-year-old woman. Conventional diagnostic approaches were ineffective. Venous pooling in the lower legs as a result of vasodilation and subsequent vagotony due to epidural anesthesia, a condition mimicking orthostatic stress, is proposed as the mechanism of asystole. Follow-up examinations over 16 months revealed no further syncope and a good clinical course. Head-up tilt testing was useful in determining etiology in this case.

Adult↗
PubMed1996

Change of plasma leukotriene C4 during myocardial ischemia in humans.

Changes in leukotriene C4 levels during different degrees of myocardial ischemia in humans were examined by comparing radioimmunoassay measures of leukotriene C4 plasma levels obtained during transient and prolonged myocardial ischemia. Leukotriene C4 levels in systemic arterial and coronary sinus blood were determined in patients with chronic stable angina before and after myocardial ischemia induced either by exercise (supine bicycle ergometer exercise stress testing; n = 14; age, 52 +/- 8 years) or by coronary occlusion during angioplasty (n = 14; age 53 +/- 7 years). Temporal changes of leukotriene C4 were also followed in arterial and pulmonary artery blood within 24 h after the onset of chest pain (acute phase), and 1 day, 1 week, and 1 month later in 22 patients with acute myocardial infarction (AMI) (12 patients with thrombolytic therapy, age 61 +/- 10 years; 10 patients without thrombolytic therapy, age 60 +/- 11 years). Clinical characteristics, including coronary risk factors and the severity of coronary artery disease, were not significantly different among the groups. Exercise-induced myocardial ischemia and coronary occlusion did not induce any significant leukotriene C4 changes in the chronic stable angina patients, whereas AMI patients had significantly higher plasma leukotriene C4 levels in both arterial and pulmonary artery blood in the acute phase compared with those of chronic stable angina patients (arterial blood, 471 +/- 164 pg/ml and 477 +/- 235 pg/ml vs. 275 +/- 254 pg/ml or 240 +/- 66 pg/ml, p < 0.05; pulmonary artery blood in AMI, 543 +/- 162 pg/ml vs. 234 +/- 125 pg/ml or 225 +/- 64 pg/ml, coronary sinus blood in chronic stable angina, p < 0.05). These results suggest that leukotriene C4 is involved more in prolonged myocardial ischemia than in transient myocardial ischemia, and that leukocyte function might play a significant role in the pathogenesis of patients with AMI.

Adult↗
PubMed1996

Effect of nipradilol on silent myocardial ischemia, plasma beta-endorphin, and bradykinin in chronic stable angina.

HYPOTHESIS: This study was undertaken to investigate the effect of nipradilol on the total ischemic burden and on plasma levels of beta-endorphin and bradykinin. METHODS: Sixteen patients with chronic stable angina were subjected to exercise treadmill testing and 24-h ambulatory electrocardiogram (ECG). RESULTS: Nipradilol significantly decreased both mean heart rate and mean pressure rate product at submaximal and maximal exercise. It significantly improved exercise-induced maximal ST-segment depression from -2.7 +/- 0.5 mm to -1.3 +/- 0.6 mm (p < 0.05) and reduced the number of leads with significant ST-segment depression (4.0 +/- 1.2 vs. 2.0 +/- 1.8, p < 0.05). Silent ischemic episodes recorded in 24-h ambulatory ECG were significantly decreased by nipradilol administration, concomitantly with a decrement of mean heart rate and observed maximal heart rate. Patients with exercise-induced silent myocardial ischemia showed significantly increased plasma levels of beta-endorphin during both the placebo and nipradilol phases of the study. However, during the nipradilol phase, bradykinin did not change significantly at rest and at peak exercise. CONCLUSION: Nipradilol effectively controls exercise-induced myocardial ischemia and silent myocardial ischemic episodes, and does not influence the response of plasma levels of beta-endorphin to exercise stress testing in patients with exercise-induced silent myocardial ischemia.

Adrenergic alpha-Antagonists↗
PubMed1996

Methodology of serial ECG classification using an adaptation of the NOVACODE for Q wave myocardial infarction in the Bypass Angioplasty Revascularization Investigation (BARI).

Serial electrocardiographic (ECG) changes are a critical component of the diagnostic algorithm for classification of myocardial ischemic events in large-scale clinical trials. This study describes a computerized serial ECG classification program developed at the St. Louis University Core ECG Laboratory for use in the Bypass Angioplasty Revascularization Investigation (BARI) trial, in which patients with multivessel coronary artery disease were randomized to receive either coronary artery bypass grafting or percutaneous transluminal coronary angioplasty. The St. Louis University program detects and codes serial changes in Q, ST, and T wave items according to Minnesota code (MC) criteria using a modified NOVACODE hierarchical classification system. Measurements using a seven-power calibrated coding loupe are used to generate the MC from a customized software program. Significant minor or major changes are detected by the serial comparison program and referred to a physician coder for verification. Serial comparison coding rules are used to adjust for weaknesses in the standard MC classification system resulting from instability at decision boundaries. Of 4,244 BARI randomized and registry study participants with follow-up ECGs received at the Core ECG Laboratory as of March 1995, a grade 2 MC Q wave progression was noted in 568 participants (13.4%) using MC criteria alone, as compared with 367 (8.6%) after the St. Louis University coding rules were applied. The incidence of grade 1 MC Q wave progressions was 16.4% (697/4,244) versus 6.1% (259/4,244) when the St. Louis University program was applied. Intraobserver variability for grade 2 Q wave progression codes determined from a sample of 812 serial.

Algorithms↗
PubMed1996

Arachidonic acid metabolites in acute myocardial infarction.

Abnormalities of arachidonic acid metabolism are implicated in spasm and thrombosis in coronary arteries. Therefore, arachidonic acid metabolites were examined in patients with acute myocardial infarction (AMI). Plasma levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6KPGF1 alpha), leukotriene B4 (LTB4), and slow reacting substance of anaphylaxis (SRS-A) composed of leukotriene C4 (LTC4), leukotriene D4 (LTD4) and leukotriene E4 (LTE4), were measured in 19 AMI patients. Plasma levels of TXB2, LTB4, and SRS-A in systemic artery blood were significantly elevated during the acute stage (within twenty-four hours after the onset of chest pain) of AMI (TXB2, 0.36 ng/mL; LTB4, 0.75 ng/mL; and SRS-A [LTC4+LTD4+LTE4], 0.96 ng/mL compared with those of normal controls (TXB2, 0.18 ng/mL; LTB4, 0.44 ng/mL; and SRS-A (LTC4+LTD4+LTE4], 0.31 ng/mL). These values decreased to near-normal control levels by one month after the AMI attack. The findings in this study suggest that abnormalities of arachidonic acid metabolism accompany, and may play a role in the pathogenesis of, AMI.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Heart rate variability and head-up tilt testing in patients with syncope of undetermined etiology.

Indices of heart rate variability are non-invasive indicators of neural control of the heart. To investigate the significance of changes in heart rate variability in neurally mediated syncope, we performed head-up tilt testing in 45 patients with syncope of undetermined etiology. Seventeen patients showed a negative response and 28 showed a positive response; 18 had a vasodepressor response (systolic blood pressure dropped > or = 50% without a decrease in heart rate) and 10 had a vasovagal response (systolic blood pressure dropped > or = 50% with a decrease in heart rate of > or = 30%). The mean RR-interval, the standard deviation of normal sinus RR-intervals (standard deviation of RR-interval) and power spectra were measured in consecutive 2 min periods throughout the study. Power spectra consisted of low frequency (0.04-0.15 Hz), high frequency (0.15-0.40 Hz) and total spectra (0.01-1.0 Hz). Both high frequency spectra and the low/high frequency spectra ratio significantly changed with head-up tilt testing regardless of the response. However, high frequency, low frequency and total spectra increased in relation to symptoms. These changes were most profound in the high frequency spectra of subjects with a vasovagal response. Since high frequency spectra reflect parasympathetic tone, a profound change in the high frequency spectra implies that parasympathetic activities play a significant role in patients with a vasovagal response. The assessment of heart rate variability during head-up tilt testing can provide new insight into the pathogenesis of syncope of undetermined etiology.

Adolescent↗
PubMed1996

Efficacy of direct injection of ethanol into the myocardium to control aconitine-induced ventricular tachycardia in anesthetized dogs.

The effect of injecting ethanol directly into the myocardium to control aconitine-induced ventricular tachycardia (VT) was evaluated in anesthetized dogs. In 17 dogs, VT was induced by injecting aconitine (1.0 microgram, median dose) directly into the epicardium. After inducing persistent VT for up to 3 min, 0.6 ml (median volume) of 96% ethanol was injected into the same epicardial region. Regular sinus rhythm reappeared in 15 dogs with no change in systolic blood pressure; the other 2 dogs died of ventricular fibrillation (VF). In another 13 dogs, VT was induced by injecting aconitine directly into the endocardium using a Variocath needle catheter. After persistent VT for up to 3 min, a regular sinus rhythm was restored in 7 dogs by injecting 2.0 ml (median volume) of 96% ethanol; the remaining 6 dogs died of VF. Histology showed no transmural necrosis and the subendocardial necrotic areas were essentially the same in the dogs that recovered from VT as in those that died. There was no statistically significant relationship between doses of ethanol and VT duration. These preliminary results suggest that the injection of ethanol into the myocardium may efficiently terminate VT when other techniques fail.

Aconitine↗