[Coronary spastic myocardial infarction].
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Coronary Angiography↗
Biomedical subjects
H Yasue
Publications and source records attributed to H Yasue.
[Blood coagulation and fibrinolysis in patients with acute coronary syndrome].
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Acute Disease↗
Soluble P-selectin is released into the coronary circulation after coronary spasm.
BACKGROUND: The glycoprotein P-selectin is an adhesion molecule involved in the property change of leukocytes at the initiation of the inflammatory process. The purpose of the present study was to determine whether acute myocardial ischemia induced by coronary spasm causes an acute inflammatory response in the coronary circulation. METHODS AND RESULTS: We examined plasma soluble P-selectin levels in the coronary sinus and the aortic root simultaneously in 16 patients with coronary spastic angina before and after left coronary artery spasm induced by intracoronary injection of acetylcholine and in 15 patients with stable exertional angina before and after acute myocardial ischemia induced by rapid atrial pacing. Ten control patients with chest pain but normal coronary arteries and no coronary spasm also received intracoronary acetylcholine. Plasma soluble P-selectin levels were increased significantly in the coronary sinus (32.8 +/- 3.6 to 52.8 +/- 5.9 ng/mL, P < .001) and in the aortic root (34.6 +/- 3.7 to 41.9 +/- 4.4 ng/mL, P < .05) after the attacks in the coronary spastic angina group but remained unchanged in the stable exertional angina group after the attacks and in the control group after the administration of acetylcholine. Furthermore, the coronary sinus-arterial difference of soluble P-selectin increased significantly after the attacks in the coronary spastic angina group (-1.8 +/- 2.2 to 10.9 +/- 2.7 ng/mL, P < .001). CONCLUSIONS: Our data indicate that soluble P-selectin is released into the coronary circulation after coronary artery spasm. We conclude that coronary artery spasm may induce the leukocyte adhesion in the coronary circulation and may lead to myocardial damage.
Acetylcholine↗
[Clinical study and physiopathology of coronary vasospasm].
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Acetylcholine↗
Linear ablation of the isthmus between the inferior vena cava and tricuspid annulus for the treatment of atrial flutter. A study in the canine atrial flutter model.
BACKGROUND: The isthmus between the inferior vena cava and the tricuspid annulus has been shown to be involved in the reentry circuit of common atrial flutter. The effects of radio-frequency catheter ablation of this isthmus were examined in the canine model of atrial flutter due to reentry around the tricuspid annulus. METHODS AND RESULTS: A model of atrial flutter was prepared in 11 of 14 dogs by creating intercaval and connected transverse lesions (Y-shaped lesion). Bipolar electrodes were attached at 24 atrial sites, and computer-assisted mapping was performed. Stable atrial flutter with a cycle length of 133 +/- 11 ms was repeatedly induced by rapid atrial pacing in all dogs, and atrial mapping revealed reentry around the tricuspid annulus including the isthmus. In 6 dogs, the isthmus was ligated during atrial flutter (mechanical ablation). In the other 5 dogs, a 7F large-tip electrode catheter was placed at the isthmus under a fluoroscopic control. Radiofrequency energy (25 W for 30 s) was delivered to three sequential sites from the tricuspid annulus to the inferior vena cava to ablate the isthmus linearly. Atrial flutter was terminated in all dogs after mechanical and radio-frequency ablation of the isthmus and was not induced again. Atrial pacing from the posterior left atrium during sinus rhythm demonstrated intra-atrial conduction block at the isthmus after ablation. Pathological examination of the isthmus showed transmural myocardial damage. CONCLUSIONS: Linear radiofrequency ablation of the isthmus can induce intra-atrial conduction block and is effective as a curative therapy for atrial flutter when the reentry circuit involves the isthmus.
Animals↗
Augmented expression of atrial myosin light chain 1 in ventricular aneurysms of human: enzyme immunoassay for atrial myosin light chain 1.
We established an enzyme immunoassay (EIA) for atrial myosin light chain 1 (ALC1) using monoclonal antibodies KA1 and KB1, which were specific for ALC1 and for both ALC1 and ventricular myosin light chain 1, respectively. The serum ALC1 levels of healthy subjects were 0.28 +/- 0.14 ng/ml (mean +/- SD). The tissue ALC1 levels of normal adult human atria were much higher than those of ventricles (p < 0.01, 2,120 +/- 1,200 in right atria, 2,180 +/- 1,450 in left atria vs. 36.0 +/- 20.2 in right ventricles, 37.7 +/- 15.3 in left ventricles, ng/mg of proteins). The tissue ALC1 levels of ventricular aneurysms were significantly higher than those of normal ventricles (p < 0.01, 206.7 +/- 101.8). These results indicate that ALC1 is augmented in aneurysms and that the EIA provides a useful tool to investigate the roles of ALC1.
Adult↗
A histochemical and electron microscopic study of skeletal and cardiac muscle from a Fabry disease patient and carrier.
Histochemical and electron microscopic studies were performed in an attempt to clarify the muscle pathology in an 18-year-old man with Fabry disease, showing proximal limb muscle atrophy, and his 52-year-old mother, who is a Fabry carrier with hypertrophic cardiomyopathy. Despite the relatively mild myopathic changes revealed by histochemistry, electron microscopy demonstrated the widespread accumulation of abundant lamellated bodies in myofibers, associated with increased glycogen granules and autophagic vacuoles. The cardiac muscle of the proband's mother revealed a mosaic pattern of normal-appearing and hypertrophic myofibers containing a number of ring-like, lamellated bodies. Although further studies are necessary to support our findings, skeletal muscle is apparently involved in patients with Fabry disease, and a mosaic pattern of cardiac muscle involvement possibly reflecting Lyonization, may be one of the characteristic findings of a Fabry disease carrier.
Adolescent↗
Serial changes of plasma plasminogen activator inhibitor activity in acute myocardial infarction: difference between thrombolytic therapy and direct coronary angioplasty.
The fibrinolytic system is impaired in patients with acute myocardial infarction (AMI). The primary regulatory element of fibrinolytic activity is plasminogen activator inhibitor (PAI). There are no reports, however, on the serial changes of PAI activity after thrombolysis or coronary angioplasty in patients with AMI undergoing emergency coronary angiography. This study was designed to examine the difference in the change of fibrinolytic activity between patients with AMI who underwent thrombolytic therapy with recombinant tissue-plasminogen activator (rTPA) and those who underwent direct percutaneous coronary angioplasty (PTCA). We measured the serial changes of PAI activity and tissue plasminogen activator (TPA) antigen after rTPA therapy or direct PTCA. Twenty-two patients received emergency coronary angiography and were treated with rTPA intravenously. Twenty patients underwent direct PTCA. Plasma PAI activity levels were increased on admission and further increased within 24 hours in patients treated with rTPA and in those treated with direct PTCA. In the thrombolysis group, there were two peaks in plasma PAI activity levels (IU/ml) at 4 hours (27.0 +/- 2.9) and at 16 hours (25.6 +/- 2.5) after the initiation of rTPA infusion. However, in the direct PTCA group, there was one peak of PAI activity (IU/ml) at 16 hours (23.9 +/- 2.7) after the initiation of direct PTCA. In conclusion, the PAI activity has two peaks in the thrombolysis group and one peak in the direct PTCA group.
Aged↗
Comparison of efficacy of nisoldipine, metoprolol, and isosorbide dinitrate in patients with stable exertional angina: a randomized, cross-over, placebo-controlled study.
We evaluated the acute antianginal effect of oral nisoldipine (10 mg), metoprolol (40 mg), and long-acting isosorbide dinitrate (20 mg) in 15 patients with stable exertional angina. The patients performed symptom-limited treadmill exercise at 2 h after the administration of placebo (Placebo stages 1 and 2) and each of the active drugs. After Placebo stage 1, the patients were randomized for cross-over evaluation of the acute effect of a single oral dose of placebo (Placebo stage 2), nisoldipine, metoprolol, or long-acting isosorbide dinitrate. All 15 patients developed angina during all of exercise tests and their exercise tests were terminated at the onset of angina. The time until development of 0.1 mV ST segment depression was increased by all three drugs compared to placebo, and it was significantly longer with metoprolol than with isosorbide dinitrate. Similarly, the time to ceasing exercise because of angina was also prolonged by all three drugs. The exercise time was longer with nisoldipine and metoprolol compared to isosorbide dinitrate, but there was no significant difference between nisoldipine and metoprolol. In conclusion, metoprolol and nisoldipine more effectively prolonged exercise compared to long-acting isosorbide dinitrate in patients with stable exertional angina.
Administration, Oral↗
Increased constrictor response to acetylcholine of the isolated coronary arteries from patients with variant angina.
The aim of this study was to determine whether isolated coronary arteries from patients with variant angina show hyperreactivity and/or supersensitivity to acetylcholine in vitro. Coronary arterial rings were obtained at autopsy within 3 h after death from six coronary arteries having spasm in four patients with variant angina and from 22 coronary arteries in 14 control patients with non-cardiac death. The coronary rings were suspended in the organ chamber filled with Krebs Henseleit solution bubbled with 95% O2 + 5% CO2, and their isometric tensions were monitored. Arterial rings isolated from both the patients with variant angina and the controls contracted dose-dependently in response to acetylcholine (10(-9)-10(-5) mol/l). EC50 of acetylcholine (i.e. concentration producing 50% of maximum contraction) was not significantly different between the coronary arteries from patients with variant angina and those from controls, but maximum contraction elicited by acetylcholine (expressed as a percentage of the contraction elicited by 60 mmol/l KCl) was significantly greater in the coronary arteries from patients with variant angina than those from controls. In conclusion, the isolated coronary arteries from patients with variant angina have hypercontractile reactivity to acetylcholine. This intrinsic alteration of the coronary reactivity to acetylcholine may play a role in the genesis of coronary spasm occurring in the situations of enhanced parasympathetic nervous discharge.
Acetylcholine↗
Effects of brain (B-type) natriuretic peptide on coronary artery diameter and coronary hemodynamic variables in humans: comparison with effects on systemic hemodynamic variables.
OBJECTIVES: This study attempted to clarify the effects of human brain (B-type) natriuretic peptide on coronary artery diameter and coronary vascular resistance in humans. BACKGROUND: Brain natriuretic peptide induces vasodilation in systemic circulation by activating particulate guanylate cyclase of the vascular smooth muscle. METHODS: In 13 patients with normal coronary arteries and left ventricular function, brain natriuretic peptide was infused at 0.5 microgram/kg body weight per min for 4 min into the left main coronary artery (six patients, Group A) or into the pulmonary artery (seven patients, Group B). Systemic hemodynamic variables and coronary sinus blood flow were measured before and after the infusion. The lumen diameter of the left coronary artery was quantitatively measured. RESULTS: In both groups, brain natriuretic peptide significantly increased heart rate and decreased mean arterial pressure. Rate-pressure product remained unchanged in both groups. Brain natriuretic peptide decreased systemic vascular resistance index significantly in both groups (both p < 0.01 vs. baseline), and there was no difference in the effect between the groups. Brain natriuretic peptide decreased coronary vascular resistance in Group A (p < 0.01 vs. baseline) but did not affect coronary vascular resistance in Group B (p < 0.01 vs. Group A). The lumen diameters of the proximal and distal segments of the left coronary artery were increased significantly after brain natriuretic peptide in both groups. After infusion of brain natriuretic peptide, mean plasma level of brain natriuretic peptide in the coronary sinus increased from 36 to 130,411 pg/ml in Group A and from 64 to 12,329 pg/ml in Group B. CONCLUSIONS: Brain natriuretic peptide shows a vasodilator effect on the coronary artery system in humans. However, the effect does not appear uniformly but is seen preferentially in the epicardial coronary artery. The sensitivity of the coronary resistance vessels to brain natriuretic peptide is low compared with that of the resistance vessels of the systemic circulation.
Cardiac Catheterization↗
Comparison of secretion pattern between A-type and B-type natriuretic peptides in patients with old myocardial infarction.
OBJECTIVES: The present study was designed to compare the secretion patterns of two cardiac hormones--A-type (atrial) and B-type (brain) natriuretic peptides--from the ventricles in patients with old myocardial infarction. BACKGROUND: Plasma levels of these two natriuretic peptides are increased, and their secretion from the ventricles is augmented, in patients with congestive heart failure. METHODS: We measured the plasma levels of these two types of natriuretic peptides at the aortic root and the anterior interventricular vein in 42 patients with old myocardial infarction (anterior in 22 and inferior in 20) and 18 control subjects. RESULTS: The difference between the plasma levels of both A- and B-type natriuretic peptide in the anterior interventricular vein and aortic root was significantly greater in the groups with anterior and inferior infarction than in the control group (A-type [mean +/- SD] 380 +/- 290 and 247 +/- 205 pg/ml in the infarction groups vs. 11 +/- 14 pg/ml; B-type 497 +/- 445 and 75 +/- 73 pg/ml vs. 23 +/- 16 pg/ml, respectively). The difference between the plasma levels of each peptide at the anterior interventricular vein and aortic root had a significant negative linear correlation with left ventricular ejection fraction in both groups with infarction. The slope of the regression line of the arteriovenous difference of B-type natriuretic peptide at the anterior interventricular vein was significantly steeper in the anterior than in the inferior infarction group (left ventricular ejection fraction -12.801 vs. -1.891, p < 0.01). CONCLUSIONS: These results indicate that 1) the secretion of A- and B-type natriuretic peptide from the left ventricular increases in proportion to the severity of left ventricular dysfunction, and 2) secretion of B-type natriuretic peptide is much greater from the infarct than from the noninfarct region, suggesting that the regional ventricular wall stretch caused by infarction strongly stimulates secretion of B-type natriuretic peptide.
Atrial Natriuretic Factor↗
Survey on swine SINEs (PRE-1) as candidates for SSCP markers in genetic linkage analysis.
Of 310 random cosmid clones, 216 were positive for PRE-1 sequences by Southern hybridization. Thirty nine sub-fragments positive for the PRE-1 sequences were cloned from independent cosmid clones, and sequenced, with 17 complete PRE-1 elements found. Seven PRE-1 loci were amplified by polymerase chain reaction using genomic DNA of 12 unrelated pigs as template. The amplified fragments were then subjected to an analysis of single strand conformation polymorphism, with all the loci being polymorphic.
Animals↗
Assignment of the tenascin gene (HXB) to swine chromosome 1q21.1-->q21.3 by fluorescence in situ hybridization.
The chromosomal location of the swine tenascin gene (HXB) was determined by fluorescence in situ hybridization and simultaneous R-banding. Swine tenascin cDNA was labeled with biotin, and used as a probe. Hybridization was detected by the FITC-labeled streptavidin/biotinylated antistreptavidin antibody system. The signals revealed that the tenascin gene is localized on swine chromosome 1q21.1-->q21.3.
Animals↗
Assignment of alpha 1-acid glycoprotein gene (ORM1) to swine chromosome region 1q210-->q212 by fluorescence in situ hybridization.
The porcine gene for alpha 1-acid glycoprotein (ORM1) was localized to chromosome region 1q210-->q212 by fluorescence in situ hybridization. From this result and published gene mapping data, it was concluded that the syntenic group comprised of ORM1, IFNA1, and GRP78 in the human genome is also conserved in the pig.
Animals↗
Assignment of the uteroferrin gene (ACP5) to swine chromosome 2q12-->q21 by fluorescence in situ hybridization.
A cosmid clone containing the uteroferrin gene (ACP5) was selected from a cosmid library of swine genomic fragments by colony hybridization using uteroferrin cDNA as a probe. The genomic fragment thus cloned was examined by Southern blot and sequence analysis which demonstrated that it contained at least a part of the uteroferrin gene. The cosmid clone DNA was labeled with biotin, and used a probe for in situ hybridization to swine chromosomes. Hybridization was visualized by the FITC-labeled streptavidin/biotinylated antistreptavidin system together with R-banding of chromosomes. The hybridization signals revealed that the uteroferrin gene (ACP5) is located on swine chromosome 2q12-->q21.
Acid Phosphatase↗
Assignment of the glucose transporter 1 gene (SLC2A1) to swine chromosome 6q34-->qter.
A cosmid clone containing the glucose transporter gene (SLC2A1) was selected from a cosmid library of swine genomic fragments by colony hybridization using the cDNA of swine glucose transporter as a probe. The genomic fragment thus cloned was partially sequenced, and the sequence was compared first with the sequence of the cDNA and then with the reported rat genomic sequence. The sequence homology and exon/intron structure indicated that the genomic fragment contained at least part of SLC2A1. The fragment, together with vector DNA, was then labeled by biotin and used as a probe for in situ hybridization on swine chromosome spreads. Hybridization was visualized by the FITC-labeled streptavidin/biotinylated anti-streptavidin system together with the R-band pattern of chromosomes. The fluorescence signals revealed that SLC2A1 is localized on swine chromosome 6q34-->qter.
Animals↗
Lipoproteins regulate C-type natriuretic peptide secretion from cultured vascular endothelial cells.
We have shown that oxidized low-density lipoprotein (Ox-LDL) modulates various endothelial cell (EC) functions. C-type natriuretic peptide (CNP), the third member of the natriuretic peptide family to be discovered, is secreted from peripheral vascular ECs and regulates body fluid homeostasis, vascular tone, and vascular growth. This study was designed to investigate the effects of lipoproteins on CNP secretion from cultured ECs. Treatment of bovine carotid ECs with OX-LDL and its extracted lipids resulted in a concentration-dependent suppression of the spontaneous and transforming growth factor-beta 1-stimulated secretion CNP. Native LDL, its extracted lipids, and acetylated LDL were inactive. OX-LDL depleted of its amphiphilic lipids, which was prepared by incubation with defatted albumin, lost its suppressive effect on CNP secretion. 7-Ketocholesterol, one of the amphiphilic lipids in OX-LDL that is transferable from OX-LDL to defatted albumin, suppressed CNP secretion by ECs, thus mimicking the effect of OX-LDL. Coincubation with high-density lipoprotein (HDL), which alone had no effect on CNP release, significantly prevented OX-LDL-induced inhibition of CNP secretion by ECs. Analysis by thin-layer chromatography demonstrated that oxysterols, including 7-ketocholesterol, in OX-LDL were transferred from OX-LDL to HDL during coincubation of these two lipoproteins. These results indicate that OX-LDL suppresses CNP secretion from ECs by 7-ketocholesterol or other transferable hydrophilic lipids in OX-LDL, and the suppressive effect of OX-LDL is reversed by HDL. Lipoproteins thus may regulate CNP secretion from the endothelium of atherosclerotic arteries.
Animals↗