Software tool for gene mapping: gRanch.
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Animals↗
Biomedical subjects
H Yasue
Publications and source records attributed to H Yasue.
The upper turnover site in the reentry circuit of common atrial flutter.
The upper turnover site of the reentry circuit of common atrial flutter was examined with the uses of atrial activation mapping and extrastimulus techniques during atrial flutter. The findings suggest that it is anterior to the orifice of the superior vena cava, i.e., between the superior vena cava and tricuspid annulus.
Adult↗
Deficiency in nitric oxide bioactivity in epicardial coronary arteries of cigarette smokers.
OBJECTIVES: This study sought to examine nitric oxide-mediated regulation of epicardial coronary arterial tone in cigarette smokers. BACKGROUND: Cigarette smoking is a major risk factor for coronary artery disease and is highly prevalent in patients with coronary spastic angina. Long-term exposure to cigarette smoking has been recently reported to suppress endothelium-dependent arterial relaxation in vivo humans. METHODS: Responses of epicardial coronary artery diameter to single or combined infusion of acetylcholine and NG-monomethyl-L-arginine (L-NMMA) into the left main coronary artery were examined in 11 current smokers and 17 nonsmokers using quantitative coronary angiography. RESULTS: Acetylcholine dilated one-third of the proximal segments and most of the distal segments of coronary arteries in nonsmokers, whereas it constricted most of the proximal and distal segments in smokers. L-NMMA decreased the basal diameter of coronary arteries in nonsmokers but had minimal effect on the basal diameter in smokers. L-NMMA abolished the dilator response to acetylcholine in the coronary arteries of nonsmokers but had minimal effect on the constrictor response to acetylcholine in the arteries of smokers. The dilator response to nitroglycerin was significantly increased in the coronary arteries of smokers compared with in those of nonsmokers. The constrictor response to L-NMMA at rest was significantly correlated with the dilator response to nitroglycerin and with the diameter changes to acetylcholine in both smokers and nonsmokers. CONCLUSIONS: Nitric oxide bioactivity at rest and at acetylcholine-stimulated conditions in smokers was decreased, leading to the supersensitivity of the artery to the dilator effect of nitroglycerin as well as the constrictor effect of acetylcholine in smokers. Cigarette smoking affects nitric oxide-mediated regulation of coronary artery tone.
Acetylcholine↗
Expression of angiotensin-converting enzyme in remaining viable myocytes of human ventricles after myocardial infarction.
BACKGROUND: Local ACE in the heart may be important in the pathophysiological state after myocardial infarction (MI). It is unknown, however, whether ACE is expressed in myocytes of the human heart. METHODS AND RESULTS: Using a newly generated polyclonal antibody to a synthetic peptide corresponding to part of the human endothelial ACE sequence, we examined the localization of ACE in left ventricles of patients (n = 10) with MI obtained at left ventricular aneurysmectomy or autopsy and in the hearts of control subjects at autopsy (n = 10). The avidinbiotinylated peroxidase complex method was used for the immunohistochemical staining for ACE. In the left ventricles, positively stained myocytes for ACE were found in 8 of the 10 patients with MI. ACE immunoreactivity was seen in the remaining viable myocytes located near the infarct scar of the aneurysmal left ventricle and in nonmyocytes such as fibroblasts, macrophages, vascular smooth muscle cells, and endothelial cells within the scarred tissue. On the other hand, no immunoreactivity for ACE was detected in the ventricular myocytes of all control hearts obtained at autopsy. CONCLUSIONS: We observe immunohistochemical staining for ACE in the left ventricular myocytes of the region adjacent to the infarct scar and in nonmyocytes. These results indicate that ACE is markedly increased on the edge of the infarct scar and suggest that local ACE may be important in the ventricular remodeling after MI.
Aged↗
Effects of enalapril on tissue factor in patients with uncomplicated acute myocardial infarction.
In a randomized, double-blind, placebo-controlled study beginning 4 weeks after uncomplicated acute myocardial infarction, it was established that the baseline plasma tissue factor antigen level was significantly higher in patients with myocardial infarction than in control subjects, and enalapril therapy significantly reduced the elevated plasma tissue factor antigen level. This may be associated with the reduction in the risk of coronary thrombosis seen with the use of angiotensin-converting enzyme inhibitors.
Angiotensin-Converting Enzyme Inhibitors↗
Nitric oxide activity is deficient in spasm arteries of patients with coronary spastic angina.
BACKGROUND: Coronary spasm can be induced by acetylcholine, serotonin, ergonovine, or histamine, all of which cause vasodilation when the endothelium is intact by releasing nitric oxide (NO). Coronary spasm is promptly relieved by nitroglycerin, which vasodilates through its conversion to NO. It is thus possible that NO release may be deficient in the spasm arteries in patients with coronary spastic angina (CSA). The aim of this study was to determine whether NO release is deficient in coronary arteries of patients with CSA. METHODS AND RESULTS: NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, was infused into coronary arteries in 21 patients with coronary spastic angina (CSA) and in 28 control patients. Coronary spasm was induced by intracoronary injection of acetylcholine and was documented angiographically in all patients with CSA. L-NMMA dose-dependently decreased basal luminal diameter of coronary arteries in control patients, whereas it had no effect on basal diameter of the spasm arteries in patients with CSA. L-NMMA abolished the dilator response to acetylcholine and enhanced the constrictor response to acetylcholine in control arteries, whereas it had no effect on the constrictor response to acetylcholine in spasm arteries. Intracoronary infusion of L-arginine did not affect the diameter of spasm or control arteries. The dilator response to nitroglycerin was increased markedly in spasm arteries compared with control arteries, whereas response to diltiazem did not differ between them. CONCLUSIONS: There is a deficiency in endothelial NO activity in spasm arteries, which leads to the supersensitivity of the artery to the vasodilator effect of nitroglycerin and to the vasoconstrictor effect of acetylcholine in patients with CSA. This deficient endothelial NO activity plays an important role in the pathogenesis of coronary spasm.
Acetylcholine↗
Effects of angiotensin-converting enzyme inhibitor alacepril in patients with stable effort angina during chronic isosorbide dinitrate treatment.
Nitrate tolerance has been reported to be reversed by certain types of angiotensin-converting enzyme (ACE) inhibitors. We examined whether alacepril, a new long-acting oral ACE inhibitor, has beneficial effects against exercise-induced angina in patients with stable effort angina after substantial isosorbide dinitrate (ISDN) treatment. Thirteen men with stable effort angina were treated with oral ISDN (80 mg/d) for >3 weeks. After this period, efficacy of single oral administration of either alacepril (50 mg) or its placebo on exercise-induced angina and electrocardiographic changes was examined by treadmill exercise test in a double-blind crossover design. Alacepril significantly improved the exercise duration by 9.1% (p=0.03), the time to 1 mm ST-segment depression by 19% (p<0.01), and the maximal ST-segment depression by 33% (p=0.015) compared with placebo. Alacepril did not significantly alter the rate-pressure product, a marker of myocardial oxygen demand, during exercise test compared with placebo. Plasma renin activity was significantly increased (p<0.05) after administration of alacepril, indicating that alacepril significantly blocked ACE activity in our patients. In conclusion, a single oral administration of the ACE inhibitor alacepril (50mg) elicited beneficial effects against exercise-induced myocardial ischemia in patients with stable effort angina during chronic nitrate treatment. These effects may be mediated by increased coronary blood flow.
Aged↗
Neutral endopeptidase 24.11 in neutrophils modulates protective effects of natriuretic peptides against neutrophils-induced endothelial cytotoxity.
This study was performed to determine effects of atrial and brain natriuretic peptides (ANP, BNP) on neutrophils-induced endothelial injury which is known to play a role in the pathophysiology of ischemia/reperfusion myocardial injury and to examine whether the effects of ANP and BNP on neutrophils are modulated by neutral endopeptidase 24.11 (NEP) in neutrophils themselves. The incubation of human neutrophils with ANP and BNP inhibited the neutrophils-induced detachment of cultured human endothelial cells (HEC). The inhibitory effect of ANP and BNP was associated with the suppressions of the neutrophils adhesiveness to HEC, CD18 expression on the neutrophils and elastase release from the neutrophils. Coincubation with UK73967 or phosphoramidon, inhibitors of NEP, potentiated all of the effects of ANP and BNP on the neutrophil functions, and the NEP inhibitors protected degradation of ANP and BNP by the neutrophils. NEP enzymatic activity in the particulate fractions and immunoreactive NEP expression were found to increase in the neutrophils from patients with early phase of acute myocardial infarction (AMI) by 5.2- and by 4.2-fold of the neutrophils from patients with late phase of AMI, respectively. In an in vivo canine model of myocardial ischemia/reperfusion, the intravenous administration of UK73967 suppressed the neutrophil adherence to endothelium and the neutrophil accumulation in the ischemic/reperfused myocardium. The results indicate that ANP and BNP, which are known to increase in AMI, modulate the neutrophil functions and exert protective effects against the neutrophils-induced endothelial cytotoxity. But the effects are suppressed due to their degradation by the neutrophil own NEP. Thus, neutrophil NEP, which also increases in AMI, may play a role in the pathophysiology of neutrophils-mediated ischemia/reperfusion endothelial and myocardial injury.
Animals↗
Heart period variability in patients with variant angina.
To clarify how cardiac autonomic control is affected in variant angina, we analyzed heart period variability in 35 patients with variant angina and in 19 control subjects. Patients with variant angina were divided into 1-vessel (group S, n = 17) and multivessel spasm groups (group M, n = 18) according to the site(s) of ST elevation on the electrocardiogram during attacks. The 24-hour Holter electrocardiogram recorded 6 +/- 3 days after the treatment with calcium antagonist was analyzed to avoid the possible influence of spontaneous attacks. In 5 group M patients, the electrocardiogram recorded 1 month after the treatment was also analyzed. There was no difference in the number of spontaneous attacks between groups S and M. The standard deviation of all normal RR intervals (SDNN) and the percentage of differences between adjacent normal RR intervals >50 (pNN50) in variant angina were slightly but significantly lower than those in controls. There were no differences in other indexes between variant angina and controls. When the data were analyzed separately in groups S and M, averaged RR intervals (MN), SDNN, pNN50, high-frequency power, and low-frequency power in group M were significantly lower than those in group S and controls, and the ratio of low- to high-frequency power in group M was significantly higher than that in group S and controls. There was no difference in any index between group S and controls. All abnormal indexes in group M recovered to levels similar to those in controls 1 month after the treatment. In conclusion, depressed cardiac vagal control and sympathetic-dominant sympathovagal interaction were present in patients with variant angina, especially in those with multivessel spasm.
Aged↗
Characteristics of slow conduction zone demonstrated during entrainment of idiopathic ventricular tachycardia of left ventricular origin.
Idiopathic ventricular tachycardia (VT) with the right bundle branch block pattern and left-axis deviation has been shown to be due to reentry, but the property of the slow conduction zone within the reentry circuit is little understood. In 7 patients (mean VT cycle length [CL]: 361 +/- 49 ms), rapid pacing from the right ventricular outflow tract was performed during VT while recording electrograms at the early activation site in the left ventricle and at the right ventricular apex; also, conduction times from the pacing site to these recording sits (St-A and St-B intervals, respectively) were measured. Both constant fusion (except for the last paced beat) and progressive fusion were seen in all patients, indicating VT entrainment. The left ventricular site was captured orthodromically with an St-A of 394 +/- 57 ms at the pacing CL of 351 +/- 47 ms during entrainment, while the right ventricular apex was captured directly with an St-B interval of 63 +/- 19 ms. The St-A interval was gradually prolonged with the shortening of the pacing CL, whereas the St-B interval remained unchanged. VT was interrupted in all patients at the pacing CL of 279 +/- 39 ms. The effects of intravenous lidocaine (1 mg/kg) and verapamil (1 mg) were examined in 5 and 7 patients, respectively. Neither drug terminated VT but the VT-CL was increased to 369 +/- 57 ms after lidocaine (p <0.05) and to 413 +/- 69 ms after verapamil (p <0.05) (p <0.05 vs after lidocaine). The St-A interval was significantly increased after lidocaine (p <0.05) and after verapamil (p <0.05), while the St-B interval remained unchanged. A significant correlation between changes in St-A interval and VT-CL after verapamil was noted (p <0.001). In conclusion, the slow conduction zone of this VT shows tachycardia-dependent conduction delay, and the mechanism of this slow conduction involves mainly calcium channel-dependent conduction and partly depressed sodium channel-dependent conduction.
Adolescent↗
[Humoral and metabolic changes in cardiogenic shock].
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Acidosis, Lactic↗
Assignment of c-KIT gene to swine chromosome 8p12-p21 by fluorescence in situ hybridization.
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Animals↗
Assignment of the choline acetyltransferase gene to porcine chromosome 14q25-27 by fluorescence in situ hybridization.
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Animals↗
Diffuse disorder of coronary artery vasomotility in patients with coronary spastic angina. Hyperreactivity to the constrictor effects of acetylcholine and the dilator effects of nitroglycerin.
OBJECTIVES: We examined the vasomotility of the entire epicardial coronary artery system in patients with and without coronary spastic angina. BACKGROUND: The coronary arteries of patients with variant angina are hyperreactive to diverse constrictor stimuli. It is unclear whether the abnormal responses to constrictive or dilative stimuli, or both, result from a localized or diffuse disorder in the coronary artery tree. METHODS: Coronary artery diameter responses to intracoronary acetylcholine and nitroglycerin were examined at the proximal, middle and distal segments of three principal coronary arteries in 36 patients with coronary spastic angina without significant stenosis and in 12 young (< or = 30 years old) and 20 older control subjects (> 30 years old) with normal coronary arteriographic findings. In 10 patients with significant coronary stenosis, the responses of the prestenotic segments were also examined. RESULTS: In patients with coronary spastic angina, coronary spasm was induced in 23 left anterior descending, 13 left circumflex and 17 right coronary arteries by acetylcholine. Multivessel spasm was observed in 15 patients. Acetylcholine had a dilator effect on most segments in young control subjects and a mild constrictor effect in older control subjects and in patients with significant stenosis. Comparison of the responses to acetylcholine among groups demonstrated that the constrictor response of the artery with spasm was enhanced significantly and diffusely. That of the artery without spasm also tended to be enhanced. Coronary artery diameters after nitroglycerin did not differ in any segment among patients with coronary spastic angina and both control groups. In patients with coronary spastic angina, nitroglycerin significantly enhanced dilation in all segments of the artery with spasm compared with that observed in both control groups and in most segments of the artery without spasm. Patients with significant coronary stenosis had a reduced response compared with that in control subjects. CONCLUSIONS: Hyperreactive responses not only to the constrictor effects of acetylcholine, but also the dilator effects of nitroglycerin were detected diffusely in the epicardial coronary arteries of patients with coronary spastic angina. This finding indicates that a diffuse, not localized, disorder in vasomotility is involved in the pathogenesis of coronary spastic angina.
Acetylcholine↗
Increased plasma levels of B-type natriuretic peptide in patients with unstable angina.
This study was designed to examine the plasma levels of B-type or brain natriuretic peptide (BNP), as well as A-type or atrial natriuretic peptide (ANP) in patients with unstable angina as compared with those in patients with stable exertional angina and control subjects. We measured the plasma levels of BNP and ANP in 33 patients with unstable angina, 20 patients with stable exertional angina, and 20 control subjects. The plasma levels of BNP were significantly increased in patients with unstable angina compared with those in patients with stable exertional angina and control subjects, respectively (39.5 +/- 29.4 pg/ml vs 15.1 +/- 8.0 pg/ml; p < 0.01 and 39.5 +/- 29.4 pg/ml vs 10.3 +/- 6.4 pg/ml; p < 0.01, respectively). On the other hand, there was no significant difference in the plasma levels of ANP among the three groups. Furthermore, in patients with unstable angina, the plasma levels of BNP decreased significantly after the medical treatment (from 39.5 +/- 29.4 pg/ml to 15.8 +/- 11.0 pg/ ml; p < 0.01), whereas the plasma levels of ANP did not change. We conclude that the plasma levels of BNP are increased in the majority of patients with unstable angina and that the increased levels decrease toward normal after treatment.
Adult↗
Role of adenosine in pathogenesis of syndrome X: assessment with coronary hemodynamic measurements and thallium-201 myocardial single-photon emission computed tomography.
OBJECTIVES: This study was performed 1) to examine the role of adenosine in the pathogenesis of syndrome X in patients with this syndrome and abnormal results on myocardial scintigrams during exercise, and 2) to determine the susceptibility to myocardial ischemia in this subset of patients with syndrome X. BACKGROUND: A role for adenosine in the pathogenesis of syndrome X has recently been postulated, but there are few clinical data supporting this hypothesis. METHODS: Exercise thallium-201 myocardial scintigraphy after intravenous administration of aminophylline, an adenosine receptor blocking agent, or saline solution and adenosine thallium-201 scintigraphy were performed in 26 patients with syndrome X. Hemodynamic variables during exercise and perfusion defect size after aminophylline and saline infusions were compared. At cardiac catheterization, coronary hemodynamic variables during separate infusions of adenosine and doubutamine were also examined and were compared among patients with abnormal or normal scintigrams and 10 control subjects. RESULTS: Perfusion abnormalities on exercise-thallium-201 scintigraphy occurred in 14 of 26 patients with syndrome X. Intravenous infusion of aminophylline suppressed the scintigraphic perfusion defect and prolonged the time to 1-mm ST segment depression in patients with syndrome X with abnormal exercise scintigrams. Intravenous infusion of adenosine induced a perfusion defect in the same myocardial area where the perfusion defect was observed at exercise in 7 of the 14 patients with syndrome X. At cardiac catheterization, patients with syndrome X with abnormal exercise scintigrams had lower coronary flow reserve and a greater frequency of myocardial lactate production and ST segment depression in response to the infusions of adenosine and doubtamine than did the other two groups. During adenosine infusion, great cardiac vein blood flow and oxygen content were significantly increased and myocardial oxygen consumption and lactate extraction were significantly reduced from baseline without a significant increase in rate-pressure product in this subset of patients with syndrome X. CONCLUSIONS: Patients with syndrome X with abnormal exercise scintigrams have high susceptibility to myocardial ischemia during exercise or pharmacologic stress tests, probably owing to reduced coronary flow reserve. A heterogeneous response to endogenous adenosine may contribute to scintigraphic perfusion abnormalities and myocardial ischemia during exercise in this subset of patients with syndrome X.
Adenosine↗
Natriuretic peptides in the treatment of heart failure.
BACKGROUND: This study was designed to examine the hemodynamic, renal, and hormonal effects of infusion of A-type natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in patients with congestive heart failure (CHF). METHODS AND RESULTS: We infused synthetic human ANP or BNP at a rate of 0.1 microgram/kg/ min in patients with CHF and control subjects. ANP and BNP infusion decreased pulmonary capillary wedge pressure (ANP: from 24 +/- 1 to 12 +/- 2 mmHg; BNP: from 21 +/- 3 to 14 +/- 4 mmHg, P < .01, respectively) and systemic vascular resistance (ANP: from 2,129 +/- 293 to 1,737 +/- 293 dyne.sec.cm-5; BNP: from 2,485 +/- 379 to 1,771 +/- 195 dyne.sec.cm-5, P < .01, respectively), and increased stroke volume index (ANP: from 26 +/- 4 to 32 +/- 4 mL/m2; BNP: from 26 +/- 4 to 32 +/- 4 mL/m2, P < .01, respectively) in patients with CHF. ANP and BNP infusion increased urine volume (ANP: from 0.7 +/- 0.3 to 4.5 +/- 3.3 mL/min, BNP; 0.8 +/- 0.2 to 5.3 +/- 1.0 mL/min, P < .01, respectively). excretion of sodium (ANP: from 53 +/- 26 to 478 +/- 389 microEq/min, P = NS; BNP: from 77 +/- 21 to 754 +/- 108 microEq/min, P < .01) and chloride (ANP: from 61 +/- 31 to 470 +/- 369 microEq/min, P = NS, BNP; from 74 +/- 20 to 709 +/- 103 microEq/min, P < .01) in patients with CHF. In the hormonal analysis, ANP and BNP infusion had inhibitory effects on reninangiotensin aldosterone system and the sympathetic nervous system. CONCLUSION: We conclude that ANP and BNP infusion improves left ventricular function in patients with CHF by vasodilation and prominent natriuretic action.
Aged↗