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Biomedical subjects

H Tsutsui

Publications and source records attributed to H Tsutsui.

At least 73 records · Page 4Linked to original sources
PubMed1999

Sarcoplasmic reticulum Ca2+ regulatory protein gene expression in human right atrium under hemodynamic overload.

Sarcoplasmic reticulum (SR) Ca2+-adenosine triphosphatase (ATPase) mRNA expression is reduced in the failing human myocardium. However, it is not known whether SR Ca2+-regulatory protein gene expression is altered in human myocardial tissue subjected to pressure overload or volume overload. We sought to determine whether SR Ca2+-regulatory protein gene expression is altered in human atrial tissue subjected to mechanical overload. We obtained right atrial myocardial tissue (about 250mg) at open-heart surgery from three groups of patients: no hemodynamic overload to the right atrium (control group; 12 patients), atrial septal defect (ASD group; 8 patients), and tricuspid regurgitation (TR group; 7 patients). We measured the myocyte size, the area of interstitial fibrosis, SR Ca2+,-ATPase, and ryanodine receptor mRNA abundance. The isolated cardiocyte area and the percent area of interstitial fibrosis were in the order TR > ASD > control (P < 0.05). The SR Ca2+-ATPase mRNA level in TR was significantly decreased (P = 0.004) compared with the control, whereas in the ASD group it did not differ significantly from control. There were no significant differences in ryanodine receptor mRNA levels among the three groups. SR Ca2+-ATPase gene expression was downregulated in human atrial tissue with TR but not in ASD, which might have resulted from the differences in the degree and/or the type of hemodynamic overload to the myocardium.

Adolescent↗
PubMed1999

Endocardial versus epicardial differences of sarcoplasmic reticulum Ca2+-ATPase gene expression in the canine failing myocardium.

It is unknown whether the transmural heterogeneity of sarcoplasmic reticulum (SR) Ca2+-ATPase gene expression is present within the left ventricular (LV) wall. Moreover, the changes of transmural distribution have not been examined in the failing hearts. We thus quantified steady-state mRNA abundance of SR Ca2+ regulatory proteins by Northern blot analysis in both subendocardial and subepicardial LV layers from normal and rapid pacing-induced heart failure (HF) dog hearts. For normal LV, Ca2+-ATPase mRNA abundance (normalized to glyceraldehyde-3-phosphate dehydrogenase [GAPDH] mRNA) was significantly reduced in the subendocardium, whereas calsequestrin mRNA abundance was comparable between the two layers. For HF LV, Ca2+-ATPase mRNA abundance in the subendocardium was also reduced compared to the subepicardium. However, the endocardium to epicardium ratio was comparable between control and HF (0.62 +/- 0.08 vs. 0.65 +/- 0.07; p = NS). Therefore, the transmural gradient of this gene was constant in both control and HF. Even though the data on the transmural heterogeneity of protein level is not available, the subendocardium contained significantly less Ca2+-ATPase mRNA, which might contribute, at least in part, to the transmural gradients of biochemical and mechanical function.

Animals↗
PubMed1999

Adrenoceptor-mediated regulation of myofibrillar Ca2+ sensitivity through the GTP-binding protein-related mechanisms: tension recording in beta-escin-skinned single rat cardiac cells with preserved receptor functions.

To investigate the mechanisms of receptor-mediated regulation of heart muscle contraction, we developed a tension-recording system using beta-escin-skinned single cardiac cells of rats and studied the effects of agonists on myofibrillar Ca2+ sensitivity and Ca2+ release from the sarcoplasmic reticulum (SR). In pCa/tension relations, 1 microM isoproterenol plus 100 microM guanosine 5'-triphosphate (GTP) decreased the myofibrillar Ca2+ sensitivity (pCa50, the [Ca2+] required for half-maximal tension, as an indicator of the sensitivity; from 6.07 to 5.92); this effect was blocked by 1 microM metoprolol or 1 mM guanosine 5'-O-(2-thiodiphosphate) (GDPbetaS). Phenylephrine (10 microM) plus 100 microM GTP increased the Ca2+ sensitivity (pCa50; from 6.12 to 6. 28), and this effect was blocked by 1 microM phentolamine or 1 mM GDPbetaS. After Ca2+ loading into the SR, 10 microM phenylephrine plus 100 microM GTP in a low-ethylene- glycol-bis(beta-aminoethylether)-N,N,N',N'-tetraacetic acid (EGTA, 0. 1 mM) relaxing solution induced oscillatory contractions that were attenuated by either 1 microM phentolamine or pre-treatment with 10 microM inositol 1,4,5-trisphosphate. Our results demonstrate that beta1-adrenergic stimulation decreases myofibrillar Ca2+ sensitivity and that alpha1-adrenergic stimulation both increases the Ca2+ sensitivity and activates Ca2+ release from the agonist-sensitive SR through GTP-binding protein-related mechanisms.

Adrenergic Agonists↗
PubMed1999

Positive inotropic effect of insulin-like growth factor-1 on normal and failing cardiac myocytes.

OBJECTIVE: The acute administration of growth hormone (GH) or insulin-like growth factor-1 (IGF-1) improves cardiac performance, possibly contributing to the beneficial effects of GH therapy on heart failure (HF). GH can induce the production of IGF-1 and thus the actions of GH may be mediated through its IGF-1 induction. However, these effects have not yet been demonstrated in failing hearts and the cellular basis of GH or IGF-1-induced inotropic effects remains unknown. We examined the direct effects of GH and IGF-1 on the contractile function and intracellular calcium ([Ca2+]i) homeostasis in normal and failing myocytes. METHODS: To determine whether GH and IGF-1 have a direct effect on myocardial contractility and whether the GH/IGF-1-induced effect was the results of changes in Ca2+ activation, cell shortening and [Ca2+]i transient were simultaneously measured in the left ventricular myocyte preparations, isolated from normal and rapid pacing-induced HF dogs. RESULTS: Basal shortening of HF myocytes was reduced by 64% (p < 0.01). In normal and HF myocytes, GH (0.4-40 x 10(-3) IU/ml) had no effect on either cell shortening or [Ca2+]i transients. In normal myocytes, IGF-1 exerted a positive inotropic effect in a time- and dose-dependent manner (25-500 ng/ml), associated with a parallel increase of [Ca2+]i transient amplitude. IGF-1 increased the shortening magnitude in normal (121 +/- 5% increase from baseline, p < 0.05) and HF (118 +/- 4% increase from baseline, p < 0.05) myocytes. It also increased [Ca2+]i transient amplitude in normal and HF cells by 124 +/- 4 and 125 +/- 7%, respectively. The percent increase of cell shortening and [Ca2+]i transient amplitude was comparable between normal and HF myocytes. Furthermore, IGF-1 did not shift the trajectory of the relaxation phase in the phase-plane plots of cell length vs. [Ca2+]i, indicating that it did not change myofilament Ca2+ sensitivity. CONCLUSIONS: In both normal and HF conditions, IGF-1 exerted an acute direct positive inotropic effect in adult cardiac myocytes by increasing the availability of [Ca2+]i to the myofilaments, possibly explaining the beneficial effect of GH on HF.

Actin Cytoskeleton↗
PubMed1999

Role of Ca2+ availability to myofilaments and their sensitivity to Ca2+ in myocyte contractile dysfunction in heart failure.

OBJECTIVE: Contractile function is depressed at the isolated myocyte level in heart failure (HF), which could result from the decreased availability of intracellular calcium ([Ca2+]i) to the myofibrils and/or the depressed sensitivity of myofilaments to [Ca2+]i. However, the cellular basis of contractile dysfunction remains unestablished. METHODS: We isolated left ventricular myocytes from dogs with rapid pacing-induced HF. Cell shortening and [Ca2+]i transients were measured by indo-1 fluorescence and the myofilament Ca2+ sensitivity was analyzed by the shortening-[Ca2+]i relation in intact myocytes as well as by the pCa tension relation in skinned cells. RESULTS: Peak cell shortening magnitude was depressed in HF, associated with a parallel decrease of [Ca2+]i transient amplitude. There was a significant positive correlation between these two variables (r = 0.71, P < 0.01). In contrast, myofibrillar sensitivity to Ca2+, determined by both intact and skinned myocytes, was comparable between control and HF. Further, there was no significant difference in Ca2+ sensitivity between control and HF even at shorter (1.8 microns) or longer (2.2 microns) sarcomere length. CONCLUSIONS: Using both intact and skinned cellular preparations, a potential defect in myocyte contractile function in HF was a reduction in Ca2+ availability to the myofilaments, rather than the inherent defects in myofilament sensitivity to Ca2+.

Actin Cytoskeleton↗
PubMed1999

Caspase-1-independent, Fas/Fas ligand-mediated IL-18 secretion from macrophages causes acute liver injury in mice.

IL-18, produced as a biologically inactive precursor, is processed by caspase-1 in LPS-activated macrophages. Here, we investigated caspase-1-independent processing of IL-18 in Fas ligand (FasL)-stimulated macrophages and its involvement in liver injury. Administration of Propionibacterium acnes (P. acnes) upregulated functional Fas expression on macrophages in an IFNgamma-dependent manner, and these macrophages became competent to secrete mature IL-18 upon stimulation with FasL. This was also the case for caspase-1-deficient mice. Administration of recombinant soluble FasL (rFasL) after P. acnes priming induced comparable elevation of serum IL-18 in parallel with elevated serum liver enzyme levels. However, liver injury was not induced in IL-18-deficient mice after rFasL administration. These results indicate a caspase-1-independent pathway of IL-18 secretion from FasL-stimulated macrophages and its critical involvement in FasL-induced liver injury.

Amino Acid Chloromethyl Ketones↗
PubMed1999

Hepatocyte growth factor gene therapy of liver cirrhosis in rats.

Liver cirrhosis is the irreversible end result of fibrous scarring and hepatocellular regeneration, characterized by diffuse disorganization of the normal hepatic structure of regenerative nodules and fibrotic tissue. It is associated with prominent morbidity and mortality, and is induced by many factors, including chronic hepatitis virus infections, alcohol drinking and drug abuse. Hepatocyte growth factor (HGF), originally identified and cloned as a potent mitogen for hepatocytes, shows mitogenic, motogenic and morphogenic activities for a wide variety of cells. Moreover, HGF plays an essential part in the development and regeneration of the liver, and shows anti-apoptotic activity in hepatocytes. In a rat model of lethal liver cirrhosis produced by dimethylnitrosamine administrations, repeated transfections of the human HGF gene into skeletal muscles induced a high plasma level of human as well as enodogenous rat HGF, and tyrosine phosphorylation of the c-Met/HGF receptor. Transduction with the HGF gene also suppressed the increase of transforming growth factor-beta1 (TGF-beta1), which plays an essential part in the progression of liver cirrhosis, inhibited fibrogenesis and hepatocyte apoptosis, and produced the complete resolution of fibrosis in the cirrhotic liver, thereby improving the survival rate of rats with this severe illness. Thus, HGF gene therapy may be potentially useful for the treatment of patients with liver cirrhosis, which is otherwise fatal and untreatable by conventional therapy.

Animals↗
PubMed1999

Structural organization and expression of the mouse gene for Pur-1, a highly conserved homolog of the human MAZ gene.

We have characterized the genomic structure and expression of the mouse gene for Pur-1. The cloned Pur-1 gene spans a 5-kb region encompassing the promoter, five exons, four introns and the 3'-untranslated region. All exon-intron junction sequences conform to the GT/AG rule. The promoter region has typical features of a housekeeping gene: a high G + C content (77.5%); a high frequency of CpG dinucleotides, in particular within the region 0.5 kb upstream of the site of initiation of translation; and the absence of canonical TATA and CAAT boxes. S1 nuclease protection assay demonstrated the presence of multiple sites for initiation of transcription around a site 108 nucleotides upstream of the ATG codon. Comparison of Pur-1 with the human gene for MAZ (Myc-associated zinc finger protein) revealed a striking homology of both their nucleotide and deduced protein sequences, an identical genomic organization and high similarity in promoter architecture and mRNA expression pattern. Sequence analysis of the 5'-flanking region of Pur-1 revealed numerous potential binding sites for transcription factors Sp1, AP-2 and Pur-1/MAZ itself. An element required for basal Pur-1 expression was mapped from nucleotide -258 to +43. This region also mediated stimulation of basal transcription by ectopically expressed MAZ protein. We conclude that the Pur-1 gene is the murine homolog of human MAZ and, like it, belongs to the family of housekeeping genes.

Animals↗
PubMed1999

IL-18-deficient mice are resistant to endotoxin-induced liver injury but highly susceptible to endotoxin shock.

IL-18 is an IL-1-related cytokine which shares biological functions with IL-12. These include the activation of NK cells, induction of IFN-gamma production and Th1 cell differentiation. In this study we analyzed the effect of IL-18 deficiency on lipopolysaccharide (LPS)-induced liver injury and endotoxin shock in Propionibacterium acnes-primed mice. P. acnes-primed IL-18-deficient (IL-18KO) mice showed resistance to LPS-induced liver injury. Unexpectedly, P. acnes-primed IL-18KO mice were highly susceptible to LPS-induced endotoxin shock. Serum level of tumor necrosis factor (TNF)-alpha were markedly elevated (approximately 10-fold higher) within 1.5 h after LPS challenge in IL-18KO mice as compared with wild-type mice. Anti-TNF-alpha antibody administration to IL-18KO mice was significantly protective against endotoxin-induced lethality. P. acnes-primed IL-18KO macrophages produced approximately 6-fold more TNF-alpha protein than did P. acnes-primed wild-type control macrophages. Taken together, these findings demonstrate that IL-18 is responsible for the progression of endotoxin-induced liver injury as well as down-regulation of endotoxin-induced TNF-alpha production in P. acnes-primed mice.

Animals↗
PubMed1999

High IL-18 (interferon-gamma inducing factor) concentration in a purine nucleoside phosphorylase deficient patient.

The plasma concentration of IL-18 (interferon-gamma inducing factor) was severely increased in a 3 year old boy with purine nucleoside phosphorylase (PNP) deficiency. The presence and activity of IL-18 were confirmed by immunoblotting and bioassay, respectively. These results suggest that IL-18 may be abundantly produced and secreted into plasma by PNP deficient macrophages in PNP deficiency.

Biomarkers↗
PubMed1998

Genomic organization and expression of a human gene for Myc-associated zinc finger protein (MAZ).

We have cloned and characterized the genomic structure of the human gene for Myc-associated zinc finger protein (MAZ), which is located on chromosome 16p11.2. This gene is transcribed as an mRNA of 2.7 kilobases (kb) that encodes a 60-kDa MAZ protein. A 40-kb cosmid clone was isolated that includes the promoter, five exons, four introns, and one 3'-untranslated region. All exon-intron junction sequences conform to the GT/AG rule. The promoter region has features typical of a housekeeping gene: a high G + C content (88. 4%); a high frequency of CpG dinucleotides, in particular within the region 0.5 kb upstream of the site of initiation of translation; and the absence of canonical TATA and CAAT boxes. An S1 nuclease protection assay demonstrated the presence of multiple sites for initiation of transcription around a site 174 nucleotides (nt) upstream of the ATG codon and such expression was reflected by the promoter activity of a MAZ promoter/CAT (chloramphenicol acetyltransferase) reporter gene. Cis-acting positive and negative elements controlling basal transcription of the human MAZ gene were found from nucleotides (nt) -383 to -248 and nt -2500 to -948. Moreover, positive and negative autoregulatory elements were also identified in the regions from nt -248 to -189 and from nt -383 to -248 after co-transfection of HeLa cells with plasmids that carried the MAZ promoter/CAT construct and the MAZ-expression vector. Our results indicate that the 5'-end flanking sequences are responsible for the promoter activities of the MAZ gene.

Amino Acid Sequence↗
PubMed1998

Intravascular ultrasound evaluation of plaque distribution at curved coronary segments.

Although the distribution of atherosclerosis at the curved coronary segments has implications for atherogenesis and interventional procedures, few data exist regarding the plaque distribution in these sites. Therefore, we prospectively analyzed the intravascular ultrasound images of 55 coronary sites from 37 patients where the atherosclerotic plaque and pericardium were simultaneously demonstrated by intravascular ultrasound. The pericardial images were defined as a high-intensity linear echo image moving during cardiac cycles outside the vessel wall. By the line that was parallel to the pericardial image, the vessel area was divided into 2 semicircles with the same area, namely myocardial and pericardial sides. In each side, the maximal thickness, area, and percent area of plaque were measured. The plaque thickness and area of the myocardial side were significantly greater (1.5 +/- 0.5 mm, 4.9 +/- 2.1 mm or 66%, mean +/- SD) than those of the pericardial side (1.1 +/- 0.4 mm, 3.5 +/- 2.1 mm2 or 45%, p < 0.01). The maximal plaque thickness was positioned at the point with a mean angle of 139 +/- 37 degrees from the point just facing the pericardial image, indicating that atherosclerosis was eccentrically located on the opposite side of the pericardium in these coronary segments, and suggesting that the side of the pericardial image represents the outer curvature of the coronary artery. These results indicate that the pericardial images can be seen by intravascular ultrasound, facilitating the recognition of the disease distribution in situ. The eccentric plaque located on the inner wall at the curved coronary segments, probably due to uneven local shear stress, may have implications for the interventional procedures for these segments.

Aged↗
PubMed1998

Involvement of intrasinusoidal hemostasis in the development of concanavalin A-induced hepatic injury in mice.

Concanavalin A (Con A) stimulation induces T-cell activation-associated hepatic injury. This study is designed to show the involvement of microcirculatory disturbance in the pathogenesis. Con A administration led to prominent intrasinusoidal hemostasis, which consisted of erythrocyte agglutination, lymphocyte/neutrophil sticking to endothelial cells, and platelet aggregation and degranulation, resulting in a marked decrease in the intrahepatic blood flow and elevation of portal perfusion pressure. After hemostasis, confluent hepatic necrosis occurred within the congested area of liver parenchyma. Reduction in the extent of hemostasis by the treatment with heparin (thrombin inhibitor) or cyproheptadine (serotonin inhibitor) decreased hepatic injury. Pretreatment with either anti-tumor necrosis factor alfa (TNF-alpha) or anti-interferon gamma (IFN-gamma) monoclonal antibody (MAb) moderately decreased hemostasis and hepatic injury, whereas combined use of two MAbs almost perfectly protected mice from these disorders. Complete obliteration of hemostasis and hepatic injury was also accomplished by the pretreatment with FK506 which suppressed TNF-alpha and IFN-gamma production. Intrasinusoidal accumulation of leukocytes and platelets was, however, not blocked by FK506, indicating that Con A activities other than the stimulation of cytokine production are responsible for this event. The administration of anti-CD3 MAb, a T-cell stimulant without agglutination activities, which elevated plasma cytokine levels in a comparable degree without inducing prominent leukocyte infiltration, did not induce hepatic congestion and injury. These findings indicate that the agglutination activities of Con A and T-cell activation mediated TNF-alpha/IFN-gamma production are both required for the induction of intrasinusoidal hemostasis, which is indispensable for the development of hepatic injury.

Animals↗
PubMed1998

GnRH-immunoreactive neuronal system in the presumptive ancestral chordate, Ciona intestinalis (Ascidian).

Gonadotropin-releasing hormone (GnRH) of the vertebrate brain, which has originally been identified as a peptidergic hypophysiotropic hormone, is now believed to act also as a neuromodulator. It has recently been shown that a vertebrate-like GnRH-gonadotropin system occurs in the urochordates, which are considered to be the presumptive ancestral chordate. In this paper, we examined the morphology of the GnRH neuronal system of ascidian, Ciona intestinalis, by immunocytochemistry and found many GnRH-immunoreactive neuronal cells and fibers in a specific surface area of the cerebral ganglion, along the inner wall of the dorsal blood sinus, as well as on the anterior surface of the ovary.

Animals↗
PubMed1998

Role of microtubules in the contractile dysfunction of myocytes from tachycardia-induced dilated cardiomyopathy.

Microtubules of cardiac myocytes are increased in pressure-overloaded cardiac hypertrophy, which interfere with the actin-myosin crossbridge motion and depress muscle contractility. However, it is unknown whether microtubules are increased in non-hypertrophied, dilated cardiomyopathy and, if so, their increase could contribute to the depressed contractility. We assessed the contractile function of isolated left-ventricular (LV) myocytes and also quantitated tubulin mRNA levels as well as free and polymerized tubulin proteins using the LV myocardium obtained from dogs with rapid pacing (240 beats/min, 4 weeks)-induced dilated failing cardiomyopathy (HF; n = 6) and control dogs (n = 6). Myocyte contractility was significantly depressed in HF compared to control. Northern blot analysis indicated that tubulin mRNA levels (normalized to GAPDH mRNA) in HF dogs were upregulated (0.43 +/- 0.04 v 0.13 +/- 0.02; P < 0.01). In contrast, the amount of total tubulins (633 +/- 52 v 697 +/- 42 micrograms/g wet weight; P = N.S.) and the ratio of polymerized tubulin fraction-to-total tubulin (0.44 +/- 0.02 v 0.44 +/- 0.01; P = N.S.) did not differ between the two groups. Immunohistochemical studies showed no apparent differences in the distribution or density of intracellular microtubule network. Further, the exposure of myocytes to colchicine (1 mumol/l, 30 min), which depolymerizes microtubules, did not promote any improvement of the depressed myocyte contraction. Pacing-induced tachycardia increased myocardial tubulin mRNA, but the amount of total and polymerized tubulins were not increased, indicating that alterations in myocyte microtubules do not contribute to the contractile abnormalities in this model of HF.

Animals↗
PubMed1998

Role of microtubules in the viscoelastic properties of isolated cardiac muscle.

Myocardial viscoelastic properties are determined by both interstitial collagens and intramocyte structures, including sarcolemma, contractile proteins and the cytoskeleton. It is not known whether myocyte microtubules are significant constituents that contribute to the viscoelastic properties of cardiac muscle. We examined the passive properties of isolated right-ventricular papillary muscles before and after altering the polymerization states of microtubules. The muscles were subjected to sinusoidal changes in length (strain) and the resultant changes in resting tension (stress) were measured. The elastic constant was determined by the slope of the stress-strain relation during the slow increase in muscle length (duration 60 s). The viscous constant was determined by the loop area between the stress-strain relation obtained during the rapid increase and decrease in muscle length (duration 1 s). Colchicine (1 micromol/l, 1 h), which depolymerized microtubules, had little effect on either the elastic constant or viscous constant. In contrast, taxol (10 micromol/l), which hyperpolymerized and stabilized microtubules, exerted a time-dependent increase in the viscous constant (133+/-9% of control; n=9, P<0.05), but did not affect the elastic constant (18. 9+/-2.2 to 17.7+/-2.1; n=7, P=n.s.). The increase of viscosity by taxol closely paralleled the increase in the strain rate. The specificity of each pharmacological intervention for the microtubule polymerization state was confirmed by both a Western blot analysis and the immunofluorescence micrographs of myocyte tubulin. Like other cytoskeleton and extracellular collagens, the increase in the myocyte microtubule density was able to modify the viscous component of the passive properties of the isolated cardiac muscle.

Animals↗
PubMed1998

Comparative usefulness of myocardial velocity gradient in detecting ischemic myocardium by a dobutamine challenge.

OBJECTIVES: We tested the hypothesis that ischemic myocardium can be sensitively detected using tissue Doppler-derived myocardial velocity gradient (MVG) by a dobutamine challenge. BACKGROUND: Although tissue Doppler imaging (TDI) has recently emerged to quantify regional myocardial contraction, increased translational motion during a dobutamine challenge may affect the measurements. MVG is an indicator of regional myocardial contraction independent of the translational motion. METHODS: We studied 19 patients with (n = 13) and without (n = 6) confirmed single-vessel coronary artery disease. Left ventricular short-axis tissue Doppler images were obtained along with conventional echocardiograms during a submaximal two-step dobutamine challenge (10 and 30 microg/kg body weight per min). Endocardial velocity as well as MVG were derived from TDI using computer analysis in the anteroseptal and posterior segments and were compared with visual interpretation. RESULTS: MVG demonstrated a significant dose-responsive increase in the nonischemic segments (anteroseptal: 2.6 +/- 0.8/s to 6.0 +/- 1.0/s [mean +/- SD], p < 0.05; posterior: 3.9 +/- 0.7/s to 7.6 +/- 1.8/s, p < 0.05) but remained unchanged in the ischemic segments (anteroseptal: 2.5 +/- 0.8/s to 2.7 +/- 0.7/s, p = NS; posterior: 3.4 +/- 1.0/s to 4.1 +/- 0.9/s, p = NS). Endocardial velocity failed to clearly demonstrate the differing responses between the nonischemic (anteroseptal: -2.3 +/- 1.2 to -2.7 +/- 1.6 cm/s, p = NS; posterior: 3.8 +/- 1.1 to 73 +/- 2.7 cm/s, p < 0.05) and ischemic segments (anteroseptal: -2.1 +/- 0.5 to -2.8 +/- 0.8 cm/s, p = NS; posterior: 4.2 +/- 0.8 to 6.5 +/- 2.6 cm/s, p = NS). Wall motion abnormality was hardly detectable with visual interpretation (wall motion score range 1.00 to 1.33). CONCLUSIONS: Abnormal segments could be sensitively detected by using MVG in a submaximal dobutamine challenge, even where conventional methods failed to detect the abnormality.

Aged↗