Search PubMed⌕ Search

Biomedical subjects

H Inoue

Publications and source records attributed to H Inoue.

At least 145 records · Page 8Linked to original sources

Identification of a protein phosphorylated by cAMP-dependent protein kinase in drosophila brain.

In the present study, we examined the effects of reagents that elevate cAMP concentration on protein phosphorylation in Drosophila brain cells. Application of forskolin or dopamine to brain cells that were prelabeled with (32)Pi enhanced phosphorylation of a 25-kDa protein (p25a). To identify p25a, we isolated the protein, and partial amino acid sequences were analyzed. Database searches showed that p25a is a J-domain protein, dJDP that contains the J-domain found in the DnaJ (heat shock protein 40) family of molecular chaperones.

Animals↗

Effect of dimethylthiourea, a hydroxyl radical scavenger, on cigarette smoke-induced bronchoconstriction in guinea pigs.

Cigarette smoke exposure causes bronchoconstriction in guinea pigs by stimulating cholinergic and excitatory nonadrenergic, noncholinergic (eNANC)-nerves in vagus system. The aim of this study is to elucidate the role of hydroxyl radical (OH(-)), contained in cigarette smoke, in bronchoconstriction. Anaesthetized animals were exposed to 80 puffs of smoke for 4 min. Pretreatment with dimethylthiourea, a OH(-) scavenger, significantly inhibited cigarette smoke-induced bronchoconstriction. To investigate its site of action, effects of dimethylthiourea were examined on vagally mediated bronchcoconstriction by electrical stimulation and on the bronchoconstriction by intravenous acetylcholine and neurokinin-A. Dimethylthiourea did not inhibit bronchoconstriction evoked by vagal stimulation, acetylcholine or neurokinin-A. These results suggest that dimethylthiourea inhibits cigarette smoke-induced bronchoconstriction by scavenging the smoke-derived OH(-), but not by inhibiting airway nerve function.

Acetylcholine↗

Analysis of citrulline in rat brain tissue after perfusion with haloperidol by liquid chromatography-mass spectrometry.

We have investigated the potential of high-performance liquid chromatography (HPLC) coupled to mass spectrometry (MS) to determine enrichments of citrulline as a marker for in vivo nitric oxide (NO) production in brain tissue. The analysis of citrulline as the butyl ester derivative was evaluated using two types of ionization: electron spray ionization (ESI) and atmospheric pressure chemical ionization (APCI). APCI-MS appeared to be more suitable for determination of citrulline than ESI-MS, because the ion intensity of the protonated molecule ion [M+H]+, m/z 232, of citrulline in the former was about twelve times higher than in the latter. The chromatography was carried out on a reversed C8 column with the mobile phase consisting of 15% acetonitrile: 85% H2O: 0.2% acetic acid (v/v). The calibration curve had good linearity within the concentration range investigated (5 ng to 500 ng/ml). The limit of determination was estimated to be ca. 1 ng/ml of standard solution. The method was applied to the analysis of citrulline in the brain dialysate obtained from rat after perfusion of the striatum with haloperidol (HP, 0.1 mM). It is concluded that APCI-MS in combination with HPLC can be successfully applied to determination of citrulline in brain tissue, thus providing a useful tool for assessment of in vivo NO production.

Animals↗

Identification of a glutamic acid and an aspartic acid residue essential for catalytic activity of aspergillopepsin II, a non-pepsin type acid proteinase.

Aspergillopepsin II from Aspergillus niger var. macrosporus is a non-pepsin type or pepstatin-insensitive acid proteinase. To identify the catalytic residues of the enzyme, all acidic residues that are conserved in the homologous proteinases of family A4 were replaced with Asn, Gln, or Ala using site-directed mutagenesis. The wild-type and mutant pro-enzymes were heterologously expressed in Escherichia coli and refolded in vitro. The wild-type pro-enzyme was shown to be processed into a two-chain active enzyme under acidic conditions. Most of the recombinant mutant pro-enzymes showed significant activity under acidic conditions because of autocatalytic activation except for the D123N, D123A, E219Q, and E219A mutants. The D123A, E219Q, and E219A mutants showed neither enzymatic activity nor autoprocessing activity under acidic conditions. The circular dichroism spectra of the mutant pro- and mature enzymes were essentially the same as those of the wild-type pro- and mature enzyme, respectively, indicating that the mutant pro-enzymes were correctly folded. In addition, two single and one double mutant pro-enzyme, D123E, E219D, and D123E/E219D, did not show enzymatic activity under acidic conditions. Taken together, Glu-219 and Asp-123 are deduced to be the catalytic residues of aspergillopepsin II.

Amino Acid Sequence↗

Activation of serum response factor in the depolarization induction of Egr-1 transcription in pancreatic islet beta-cells.

The results of the current studies define the major elements whereby glucose metabolism in islet beta-cells leads to transcriptional activation of an early response gene in insulinoma cell lines and in rat islets. Glucose stimulation (2-20 mm) resulted in a 4-fold increase in Egr-1 mRNA at 30 min, as did the depolarizing agents KCl and tolbutamide. This response was inhibited by diazoxide and EGTA, indicating that beta-cell depolarization and Ca(2+) influx, respectively, are essential. Pharmacological inhibition of the Egr-1 induction by H89 (48%) and calmidazolium (35%), but not by mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 and 2 or phosphatidylinositol 3-kinase inhibitors, implied that protein kinase A and Ca(2+)/calmodulin pathways are involved. Deletion mapping of the Egr-1 promoter revealed that the proximal -198 base pairs containing two serum response elements (SREs) and one cAMP-response element retained the depolarization response. Depolarization resulted in phosphorylation of cAMP-response element-binding protein, yet partial inhibition by a dominant negative cAMP-response element-binding protein, along with a robust response of a cAMP-response element-mutated Egr-1 promoter suggested the presence of a second Ca(2+)-responsive element. Depolarization activation of 5XSRE-LUC and serum response factor (SRF)-GAL4 constructs, along with activation of SRF-GAL4 by co-transfection with constitutively active calmodulin kinase IV and protein kinase A, and binding of Ser(103)-phosphorylated SRF in nuclear extracts, indicated that the SRE.SRF complexes contribute to the Ca(2+)-mediated transcriptional regulation of Egr-1. The results of the current experiments demonstrate for the first time SRE-dependent transcription and the role of SRF, a transcription factor known to be a major component of growth responses, in glucose-mediated transcriptional regulation in insulinoma cells.

Animals↗

Ru(II)- and Pt(II)-catalyzed cycloisomerization of omega-aryl-1-alkynes. Generation Of carbocationic species from alkynes and transition metal halides and its interception by an aromatic ring

The treatment of aryl-1-alkynes, such as 4-aryl-1-butyne, 5-aryl-1-pentyne, and 6-aryl-1-hexyne, with catalytic amounts of transition metal chlorides, such as PtCl(2) and [RuCl(2)(CO)(3)](2), at 80 degrees C in toluene results in cycloisomerization to give dihydronaphthalenes or dihydrobenzocycloheptenes, in which the cyclization mode is dependent on the length of the tethers. The reaction is limited to substrates containing terminal alkynes. A key step of the reaction is the intramolecular interception by an aromatic ring of the vinylmetal complex 2, which contains a cation center at the beta-position, generated from the electrophilic addition of transition metal halides toward an alkyne. The more electron-rich aryl systems are more reactive.

Journal Article↗

Noncompetitive, reversible inhibition of aminoacylase-1 by a series of L-alpha-hydroxyl and L-alpha-fluoro fatty acids: ligand specificity of aspergillus oryzae and porcine kidney enzymes.

L-lactate and L-beta-phenyllactate have been identified in the culture broth of Streptomyces sp. KY-11 as reversible noncompetitive inhibitors of Aspergillus oryzae aminoacylase-1 and porcine kidney aminoacylase I. A series of alpha-hydroxyl acids (DL-R-CH(OH)-COOH, R = Et, n-pro, n-butyl, n-pentyl, n-hexyl) also inhibited the two enzymes in reversible noncompetitive kinetics, and the inhibition potency (-log K(i)) increased with the increased hydrophobicity of the R group. The two eukaryotic enzymes showed distinct preferences to the ligand alpha-alkyl group, and the fungus enzyme was inhibited by L-beta-phenyllactate (R = benzyl) 10(3)-fold more potently than the mammalian enzyme. L-alpha-Fluoro-beta-phenyl-propionate and its D-isomer were used to show that the L-configuration of the alpha-substituent was important for potent inhibition of both the enzymes. The fungus aminoacylase-1 steeply decreased the affinity to alpha-fluoro- and alpha-hydroxy-n-caproate as pH was raised from 7 to 11, whereas the mammalian enzyme retained the affinity to these ligands under alkaline conditions. These results suggest that A. oryzae aminoacylase-1 has an acidic residue that interacts with -OH or -F, while the mammalian enzyme would have a basic residue that recognizes the alpha-substituents.

Alkylation↗

Cigarette smoking, CYP1A1 MspI and GSTM1 genotypes, and colorectal adenomas.

Cigarette smoking has been related to increased risk of colorectal adenomas, but the underlying mechanisms are unknown. Genetic polymorphisms are known for enzymes involved in the activation of polycyclic aromatic hydrocarbons and other tobacco-related carcinogens. Polycyclic aromatic hydrocarbons are activated by cytochrome P4501A1 (CYP1A1) and detoxified by glutathione S-transferases. We investigated the relation of CYP1A1 MspI and GSTM1 genotypes to the risk of colorectal adenomas with special reference to interaction with cigarette smoking among 205 cases of colorectal adenomas and 220 controls with normal total colonoscopy in a male Japanese population. Cigarette smoking was strongly associated with increased risk of colorectal adenomas. Overall, neither the CYP1A1 MspI genotype nor the GSTM1 genotype was related to colorectal adenomas. A significant trend for increased risk of colorectal adenomas associated with smoking was observed for each of the CYP1A1 MspI genotypes, and the increasing trends did not differ by MspI genotype. The positive association between smoking and colorectal adenomas did not vary much with GSTM1 genotypes. Among former and current smokers, adenoma risk did not differ according to the combination of CYP1A1 MspI and GSTM1 genotypes. CYP1A1 MspI and GSTM1 genotypes do not seem to modify the risk of colorectal adenomas associated with cigarette smoking.

Adenoma↗

Dysfunction of human Rad18 results in defective postreplication repair and hypersensitivity to multiple mutagens.

Postreplication repair functions in gap-filling of a daughter strand on replication of damaged DNA. The yeast Saccharomyces cerevisiae Rad18 protein plays a pivotal role in the process together with the Rad6 protein. Here, we have cloned a human homologue of RAD18, hRAD18. It maps on chromosome 3p24-25, where deletions are often found in lung, breast, ovary, and testis cancers. In vivo, hRad18 protein binds to hHR6 protein through a conserved ring-finger motif. Stable transformants with hRad18 mutated in this motif become sensitive to UV, methyl methanesulfonate, and mitomycin C, and are defective in the replication of UV-damaged DNA. Thus, hRAD18 is a functional homologue of RAD18.

Amino Acid Sequence↗

Down-regulation of drs mRNA in human colon adenocarcinomas.

We have previously reported that the drs gene, whose mRNA expression is down-regulated by retroviral oncogenes such as v-src and v-K-ras, has the ability to suppress transformation by v-src and v-K-ras in the rat cell line F2408. We have also isolated a human homolog of this gene (h-drs) and shown that expression of h-drs mRNA is markedly reduced in a variety of human cancer cell lines, including those of carcinomas of the colon, bladder, and ovary, suggesting that down-regulation of drs mRNA is correlated with the development of human cancers. To clarify the correlation between down-regulation of the drs gene and malignant tumor formation in human cancer tissues, we examined expression of drs mRNA in human normal tissues, colon adenoma, and adenocarcinoma tissues by in situ hybridization. Expression of drs mRNA was detected in most normal tissues tested, including those of the colon, bladder, and ovary. However, drs mRNA was hardly expressed in any of the colon adenocarcinoma tissues examined. Northern blot analyses confirmed these results. Neither gross deletion nor re-arrangement of the drs genome was detected by Southern blot hybridization in these adenocarcinoma tissues. drs mRNA was significantly expressed in colon adenoma with mild atypia but down-regulated in adenomas with moderate atypia and focal carcinoma. Our results indicate that down-regulation of drs mRNA is closely correlated with development of colon adenocarcinoma, suggesting a tumor-suppressor function of the drs gene in human cancers.

Adenocarcinoma↗

Exercise-induced negative U waves in precordial leads as a marker of viable myocardium in patients with recent anterior myocardial infarction.

Patients with recent anterior myocardial infarction and a significant stenosis in the left anterior descending coronary artery were divided into two groups according to the presence (Group A, n=24) or absence (Group B, n=77) of negative U waves in the precordial leads during exercise stress test to compare the coronary arteriographic findings. Both total occlusion of the left anterior descending coronary artery (79% vs. 31%, P<0.01)) and good (index=2, 3) collateral circulation to the territory of this artery (92% vs. 36%, P<0.01) were observed more often in group A than in group B. In order to determine whether detection of exercise-induced negative U waves in precordial leads can predict the presence of viable myocardium, the 56 patients (20 of group A and 36 of group B) with total or subtotal occlusion of the left anterior descending coronary artery were studied further. The coronary arteriographic and exercise 201Tl scintigraphic findings were compared between the groups. Good collateral circulation to the territory of this artery was observed significantly (P<0.05) more often in group A (100%) than in group B (61%). Patients with multivessel disease were significantly (P<0.05) more prevalent in group A (70%) than in group B (33%). The incidence of a significant partial redistribution in the anteroseptal area in the 20Tl images 4 h after exercise was significantly (P<0.01) higher in group A (85%) than in group B (39%). In 29 patients with anterior Q-wave myocardial infarction and exercise-induced ST elevation in precordial leads, a significant 201Tl redistribution in the anteroseptal area was observed in 8 (80%) of 10 patients of group A in contrast to only 4 (21%, P<0.05) of 19 in group B. In the diagnosis of the viability associated with 201Tl redistribution in the anteroseptal area by the finding of exercise-induced negative U waves, the sensitivity was 67% and the specificity was 88% in these patients. We conclude that exercise-induced negative U waves in precordial leads are a convenient and specific marker for the presence of viable myocardium in patients with recent anterior myocardial infarction.

Collateral Circulation↗

Fractalkine-mediated endothelial cell injury by NK cells.

Endothelial cells (ECs) are primary targets of immunological attack, and their injury can lead to vasculopathy and organ dysfunction in vascular leak syndrome and in rejection of allografts or xenografts. A newly identified CX3C-chemokine, fractalkine, expressed on activated ECs plays an important role in leukocyte adhesion and migration. In this study we examined the functional roles of fractalkine on NK cell activity and NK cell-mediated endothelial cell injury. Freshly separated NK cells expressed the fractalkine receptor (CX3CR1) determined by FACS analysis and efficiently adhered to immobilized full-length fractalkine, but not to the truncated forms of the chemokine domain or mucin domain, suggesting that fractalkine functions as an adhesion molecule on the interaction between NK cells and ECs. Soluble fractalkine enhanced NK cell cytolytic activity against K562 target cells in a dose- and time-dependent manner. This enhancement correlated well with increased granular exocytosis from NK cells, which was completely inhibited by the G protein inhibitor, pertussis toxin. Transfection of fractalkine cDNA into ECV304 cells or HUVECs resulted in increased adhesion of NK cells and susceptibility to NK cell-mediated cytolysis compared with control transfection. Moreover, both enhanced adhesion and susceptibility of fractalkine-transfected cells were markedly suppressed by soluble fractalkine or anti-CX3CR1 Ab. Our results suggest that fractalkine plays an important role not only in the binding of NK cells to endothelial cells, but also in NK cell-mediated endothelium damage, which may result in vascular injury.

Adjuvants, Immunologic↗

CX3C-chemokine, fractalkine-enhanced adhesion of THP-1 cells to endothelial cells through integrin-dependent and -independent mechanisms.

Leukocyte adhesion and trafficking at the endothelium requires both cellular adhesion molecules and chemotactic factors. A newly identified CX3C chemokine, fractalkine, expressed on activated endothelial cells, plays an important role in leukocyte adhesion and migration. We examined the functional effects of fractalkine on beta1 and beta2 integrin-mediated adhesion using a macrophage-like cell line, THP-1 cells. In this study, we report that THP-1 cells express mRNA encoding a receptor for fractalkine, CX3CR1, determined by Northern blotting. Scatchard analysis using fractalkine-SEAP (secreted form of placental alkaline phosphatase) chimeric proteins revealed that THP-1 cells express a single class of CX3CR1 with a dissociation constant of 30 pM and a mean expression of 440 sites per cell. THP-1 cells efficiently adhered, in a fractalkine-dependent manner, to full-length of fractalkine immobilized onto plastic and to the membrane-bound form of fractalkine expressed on ECV304 cells or TNF-alpha-activated HUVECs. Moreover, soluble-fractalkine enhanced adhesion of THP-1 cells to fibronectin and ICAM-1 in a dose-dependent manner. Pertussis toxin, an inhibitor of Gi, inhibited the fractalkine-mediated enhancement of THP-1 cell adhesion to fibronectin and ICAM-1. Finally, we found that soluble-fractalkine also enhanced adhesion of freshly separated monocytes to fibronectin and ICAM-1. These results indicate that fractalkine may induce firm adhesion between monocytes and endothelial cells not only through an intrinsic adhesion function itself, but also through activation of integrin avidity for their ligands.

Adjuvants, Immunologic↗

Methylenetetrahydrofolate reductase polymorphism and risk of colorectal adenomas.

A homozygous mutation at bp 677 in the gene for the methylenetetrahydrofolate reductase (MTHFR) was previously shown to be associated with a decreased risk of colorectal cancer. We examined the relation between the MTHFR genetic polymorphism and risk of colorectal adenoma in Japanese men using 205 cases of colorectal adenomas and 220 controls of normal total colonoscopy. The homozygous mutation was not measurably associated with colorectal adenomas. The findings corroborate the lack of an association between the MTHFR genotype and colorectal adenomas, but do not deny the possibility that the genotype may be involved in the late stage of colorectal carcinogenesis.

Adenoma↗

2-Methoxy-4-(2-phthalimidinyl)phenylsulfonyl chloride as a fluorescent labeling reagent for determination of phenols in high-performance liquid chromatography and application for determination of urinary phenol and p-cresol.

Highly sensitive fluorescent labeling reagents, 2-(alkyloxy)-4-(2-phthalimidinyl)phenylsulfonyl chlorides (alkyloxy = methoxy, ethoxy, and propoxy; MPS-Cl, EPS-Cl, and PPS-Cl, respectively), for determination of phenols by high-performance liquid chromatography (HPLC) have been developed. These reagents react with phenols in basic medium to produce the corresponding fluorescent sulfonyl esters. The maximum fluorescence wavelengths of the derivatives were 308 nm for excitation and 410 nm for emission. The peaks due to phenol labeled with MPS-Cl, EPS-Cl, and PPS-Cl eluted at 6.3, 8.8, and 12.8 min, respectively, on a reversed-phase column with isocratic elution of methanol/water (2:1, v/v), and the detection limits (signal-to-noise = 3) of the derivatives were 10, 12, and 17 fmol per injection, respectively. Among these reagents, MPS-Cl was advantageous because its derivatives had shorter retention times and higher sensitivities in HPLC. The efficiency of converting phenol to the fluorescent derivative by MPS-Cl was about 100%. When MPS-Cl was applied to the determination of urinary phenol and p-cresol by HPLC using p-ethylphenol as an internal standard, the derivatives were separated at retention times of 6.3, 8.7, and 12.3 min, respectively, under the HPLC conditions described above. The concentrations of phenol and p-cresol in normal human urine were 11.9-293.5 and 8.2-346.1 nmol/mg creatinine, respectively.

Chromatography, High Pressure Liquid↗

Transcatheter arterial chemoembolization therapy using iodized oil for patients with unresectable hepatocellular carcinoma: evaluation of three kinds of regimens and analysis of prognostic factors.

BACKGROUND: The current study was conducted to evaluate retrospectively the effects of three kinds of regimens used in transcatheter arterial chemoembolization (TACE) in patients with unresectable hepatocellular carcinoma (HCC) and patients' prognosis, and to analyze their prognostic factors. METHODS: The study population was comprised of 152 patients who were treated by TACE alone. Three kinds of regimens were used successively: doxorubicin hydrochloride (ADM) and mitomycin C mixed with iodized oil in 26 patients (ADMOS group), a combination of cisplatin (CDDP) solution and ADMOS in 70 patients (CDDP-ADMOS group), and CDDP powder and pirarubicin hydrochloride mixed with iodized oil in 56 patients (CTLS group). The CTLS group was comprised of patients with significantly worse background factors than the other two groups. RESULTS: The initial tumor response rate with a > 50% reduction was 12%, 23%, and 30%, respectively, in the ADMOS, CDDP-ADMOS, and CTLS groups. CTLS was significantly more effective than ADMOS (P < 0.05), and slightly but not significantly better than CDDP-ADMOS (P <0.1). The cumulative survival rates for the ADMOS, CDDP-ADMOS, and CTLS groups were 59.0%, 70.1%, and 72.0%, respectively, at 1 year; 0%, 16. 3%, and 29.8%, respectively, at 3 years; and 0%, 4.1%, and 16.8%, respectively, at 5 years, with median survival times of 448 days, 574 days, and 758 days, respectively. The CTLS group showed a slightly but not significantly better survival than the ADMOS and CDDP-ADMOS groups (P <0.1). Multivariate analysis indicated that the significantly important prognostic factors (in order) were extrahepatic metastasis followed by the TACE regimen, serum alpha-fetoprotein levels, and portal vein involvement and that CTLS was the best of the three regimens. CONCLUSIONS: Although TACE, using an effective regimen, improves clinical results, tumor factors appear to be more important when determining prognosis.

Adult↗

Radiographic analysis of lumbar motion in relation to lumbosacral stability. Investigation of moderate and maximum motion.

STUDY DESIGN: This in vivo study was performed to examine active lumbar motion without any support. OBJECTIVES: To establish the behavior of segmental flexibility according to the degree of whole lumbar motion and to clarify the correlation between bony characteristics of the lumbosacral junction and stability in the segment. SUMMARY OF BACKGROUND DATA: In previous studies, the full mobility of the lumbar segments has been investigated. The details of motion commonly seen with the activities of daily living have not been clarified. It has been reported that the iliolumbar ligaments have an influence on lumbosacral stability and that the relative thickness of the transverse process of L5 could indicate the functional strength of the iliolumbar ligaments. However, the effects of the iliolumbar ligaments on the lumbosacral range of motion have not been studied in vivo. METHODS: Ninety adults, aged 20-39 years, were requested to perform motion commonly associated with activities of daily living, defined as moderate motions of the lumbar spine. The subjects then were asked to perform maximal motion of the lumbar spine. The segmental ranges of motion, segmental flexion, and extension at every level of the lumbar spine were calculated by using functional radiographs. The correlation between the relative thickness of the transverse process of L5 and the motion seen at the lumbosacral junction was also determined. RESULTS: The greatest segmental range of motion was found at L2-L3 in moderate motion and at L4-L5 in maximal motion. It shifted gradually from the upper to lower lumbar levels with the increase in total lumbar motion. With an increase in lumbar spine motion, maximum segmental flexion shifted from L2-L3 to L3-L4, then to L4-L5. Segmental extension changed only at L5-S1, increasing with total lumbar spine motion. There was an inverse statistical correlation between lumbosacral motion and relative thickness of the L5 transverse process. CONCLUSIONS: The greatest segmental flexibility induced by the moderate lumbar motion, usually seen with the activities of daily living, occurred more in the upper segments of the lumbar spine, especially in flexion. Further, the iliolumbar ligaments regulate lumbosacral motion especially flexion.

Activities of Daily Living↗

Exercise-induced U-wave alterations as a marker of well-developed and well-functioning collateral vessels in patients with effort angina.

OBJECTIVES: We sought to determine whether exercise-induced U-wave alterations are observed in association with well-developed and well-functioning collateral vessels. BACKGROUND: Although exercise-induced electrocardiographic (ECG) U-wave alterations including negative and prominent U waves have been established as a marker of significant or critical narrowing of a major coronary artery, the relation between this finding and the degree of collateral development has not yet been determined. METHODS: Patients with stable effort angina were divided into two groups according to the presence (group A, n = 46) or absence (group B, n = 79) of exercise-induced either negative or prominent U waves in the precordial leads; the clinical profiles, coronary angiographic findings and also ischemic status during 60 s of coronary balloon occlusion were compared between the two groups. RESULTS: The incidence of severe angina (CCS [Canadian Cardiovascular Society] class III or IV) was higher (p < 0.05) in group A (52%) than in group B (32%) patients. Good collateral vessels (Rentrop grade 2 or 3) into the perfusion territory of the culprit vessel were observed more frequently (p < 0.05) in group A (70%) than in group B (43%) patients. Coronary balloon angioplasty was carried out in 23 patients of group A and 40 patients of group B. Both ischemic ST changes (52% vs. 85%) and angina (57% vs. 80%) during balloon inflation were less (p < 0.05) frequently observed in group A than in group B. The incidence of no apparent myocardial ischemia with ST deviation or angina during the balloon inflation was higher (p < 0.05) in group A (39%) than in group B (10%) patients. In the prediction of the absence of myocardial ischemia during balloon inflation by the presence of exercise-induced U-wave alterations, the sensitivity was 69% (9/13) and the specificity was 72% (36/50) in the study patients. CONCLUSIONS: Exercise-induced U-wave alterations are a marker for well-developed collateral circulation in patients with stable but severe effort angina. This finding is also highly predictive of the absence of myocardial ischemia during transient coronary balloon occlusion and possibly of low-risk for development of acute myocardial infarction or hemodynamic instability upon abrupt closure of the culprit coronary artery.

Angina Pectoris↗