Biomedical subjects

Nahoko Ikeda

Publications and source records attributed to Nahoko Ikeda.

14 recordsLinked to original sources

PubMed2005

Relation of atherothrombosis burden and volume detected by intravascular ultrasound to angiographic no-reflow phenomenon during stent implantation in patients with acute myocardial infarction.

This study investigated the mechanism of occurrence of the no-reflow phenomenon during stent implantation in patients with acute myocardial infarction (AMI) using intravascular ultrasound (IVUS) with volumetric analysis. Of 70 patients with AMI who underwent IVUS-guided stent implantation within 24 hours of symptom onset, 12 developed decreased Thrombolysis In Myocardial Infarction flow grade during stent implantation and without subsequent restoration to Thrombolysis In Myocardial Infarction flow grade before stenting. External elastic membrane cross-sectional area and maximum diameter at the culprit lesion as measured by IVUS before stent implantation were significantly larger in the no-reflow group (n = 12) than in the normal reflow group (n = 58; 20.1 +/- 6.5 vs 16.4 +/- 4.3 mm2, p = 0.015 for cross-sectional area and 5.2 +/- 0.9 vs 4.8 +/- 0.6 mm, p = 0.049 for maximum diameter). Plaque volume, volumetric plaque burden (plaque volume/external elastic membrane volume), and change in plaque volume during stent implantation (plaque volume after vs before) were significantly greater in the no-reflow group than in the normal reflow group (239 +/- 142 vs 178 +/- 72 mm3, p = 0.030; 0.76 +/- 0.07 vs 0.71 +/- 0.06, p = 0.010; and -46 +/- 63 vs -11 +/- 37 mm3, p = 0.013, respectively). In conclusion, high atherothrombotic burden and decreased plaque volume as detected by IVUS may be risk factors for development of the no-reflow phenomenon during stent implantation in patients with AMI.

Aged↗

PubMed2005

Up-regulated synthesis of mature-type adrenomedullin in coronary circulation immediately after reperfusion in patients with anterior acute myocardial infarction.

OBJECTIVE: Levels of adrenomedullin (AM), a potent vasodilatory peptide, have been shown to increase in the early stage of acute myocardial infarction (AMI). The purpose of this study was to determine whether coronary sinus-aortic step-up of mature forms of AM is accelerated in patients with AMI after reperfusion. METHODS: The subjects were 29 consecutive patients with a first episode of anterior AMI and 10 normal controls. All patients with AMI underwent balloon reperfusion therapy within 24 h after symptom onset. Plasma levels of two molecular forms of AM (an active, mature form [AM-m] and an intermediate, inactive glycine-extended form [AM-Gly]) in the aorta and coronary sinus (CS) were measured by specific immunoradiometric assay after reperfusion. RESULTS: Plasma levels of AM-m and AM-Gly in the aorta and CS were higher in AMI patients than in controls. CS-aortic step-up of AM-m, which is an index of myocardial production of AM-m, was significantly greater in AMI patients than in controls (1.7 +/- 1.4 vs. 0.4 +/- 0.3 pmol/L, P < 0.01). However, there was no significant difference in CS-aortic step-up of AM-Gly (P = 0.30). AMI patients with left ventricular dysfunction (n = 10) had a significantly higher CS-aortic AM-m step-up than AMI patients without left ventricular dysfunction (n = 19). AM-m in the aorta and CS negatively correlated with the left ventricular ejection fraction (r = -0.50, r = -0.48, P < 0.01). CONCLUSIONS: Myocardial synthesis of AM-m is accelerated in patients with reperfused AMI, especially in patients with critical left ventricular dysfunction. Increased myocardial synthesis of active AM may protect against cardiac dysfunction, myocardial remodeling, or both after the onset of AMI.

Adrenomedullin↗

PubMed2005

Three episodes of inferior acute myocardial infarction due to thrombotic occlusion of the right coronary artery: a case report.

A 77-year-old female with two previous inferior myocardial infarctions was transferred to our medical center with a third inferior acute myocardial infarction. Coronary angiography revealed 99% stenosis with rich thrombus in the distal right coronary artery [Thrombolysis in Myocardial Infarction (TIMI) grade 2 flow]. The angiographic appearance of the right coronary artery was similar to the two previous myocardial infarctions. Coronary aspiration was performed and TIMI grade 3 flow was established. To confirm the presence of thrombus, intravascular ultrasound (IVUS) and coronary angioscopy were performed at pre-discharge. IVUS showed a thrombus-like low-density area at the mid right coronary artery. Red thrombi were observed in the same area using coronary angioscopy. Although warfarin had been prescribed for secondary prevention since the first acute myocardial infarction, both the second and third acute myocardial infarction occurred after cessation of warfarin. Patients with acute myocardial infarction due to thrombotic occlusion, confirmed by IVUS or angioscopy, might be good candidates for permanent warfarin therapy.

Aged↗

PubMed2005

Recurrent cardiogenic shock caused by dynamic mitral regurgitation in a patient with hypertrophic obstructive cardiomyopathy: a case report.

A 68-year-old man with hypertrophic obstructive cardiomyopathy developed recurrent cardiogenic shock due to dynamic mitral regurgitation. The pressure gradient in the left ventricular outflow tract under medication was 30 mmHg, and he complained of no symptom. He developed shock with dyspnea suddenly after bathing and defecation. Echocardiography and left ventriculography revealed massive mitral regurgitation and mild increment of pressure gradient in the left ventricular outflow tract (50 mmHg). He underwent successful mitral valve replacement following treatment with beta-blocker under intraaortic balloon pumping support. This case illustrates that exacerbation of the systolic anterior motion of the mitral anterior leaflet can cause dynamic severe mitral regurgitation with 'mild' increment of pressure gradient in the left ventricular outflow tract, resulting in cardiogenic shock with severe lung edema.

Adrenergic beta-Antagonists↗

PubMed2004

Contribution of fluid shear response in leukocytes to hemodynamic resistance in the spontaneously hypertensive rat.

The mechanisms for elevation of peripheral vascular resistance in spontaneously hypertensive rats (SHR), a glucocorticoid-dependent form of hypertension, are unresolved. An increase in hemodynamic resistance caused by circulating blood may be a factor. Physiological fluid shear stress induces a variety of responses in circulating leukocytes, including pseudopod retraction. Due to high rigidity, leukocytes with pseudopods have greater difficulty to pass through capillaries. Because SHR have more circulating leukocytes with pseudopods, we hypothesize that inhibition of the leukocyte shear response by glucocorticoids in SHR impairs normal leukocyte passage through capillaries and causes enhanced resistance in capillary channels. Fluid shear leads to retraction of pseudopods in normal leukocytes, whereas shear induces pseudopod projection in SHR and dexamethasone-treated Wistar rats. The high incidence of circulating leukocytes with pseudopods results in slower cell passage through capillaries under normal blood flow and during reduced flow enhanced capillary plugging both in vivo and in vitro. SHR blood requires higher pressure (90.0+/-8.2 mm Hg) than Wistar Kyoto rat (WKY, 69.6+/-6.5 mm Hg; P<0.0001) or adrenalectomized SHR (73.5+/-2.1 mm Hg; P=0.0009) at the same flow rate in the resting hemodynamically isolated skeletal muscle microcirculation. Intravenous injection of blood from SHR, but not WKY, causes blood pressure increase in normal rats, which depends on pseudopod formation. We conclude that in addition to enhanced vascular tone, pseudopod formation with lack of normal fluid shear response may serve as mechanisms for an elevated hemodynamic resistance in SHR.

Animals↗

PubMed2004

Effect of atrial septal aneurysm on risk of cerebrovascular events in Japanese patients.

BACKGROUND: The aim of the present study was to determine whether atrial septal aneurysm (ASA) detected by transthoracic echocardiography (TTE) is an independent risk factor of cerebrovascular events for Japanese people. METHODS: A control study was conducted with 178 patients with ASA (follow-up rate, 96.7%; median follow-up period, 5.6 years) and 176 control patients (follow-up rate, 97.8%; median follow-up period, 5.4 years), selected from 42,528 consecutive patients who underwent TTE in the Omiya Medical Center, Jichi Medical School, from April 1991 to March 2001. Data were collected by structured review of patient charts and a subsequent telephone survey. Long-term cerebrovascular risk factors were evaluated by logistic regression analysis. RESULTS: A previous episode of cerebral infarction had occurred in nine ASA patients (5.1%) and 11 control patients (6.3%). During the follow-up period, new cerebral infarction occurred in 12 ASA patients (6.7%) and six control patients (3.4%). Only atrial fibrillation was found to be an independent risk factor of new cerebral infarction (OR, 5.06; 95% CI, 1.32-19.46; P=0.04). CONCLUSIONS: ASA is not an independent risk factor of cerebrovascular events for Japanese patients. Thus, aggressive strategies such as anticoagulation are not essential for ASA patients without embolic episodes.

Aged↗

PubMed2004

Effect of reperfusion therapy on cardiac rupture after myocardial infarction in Japanese.

BACKGROUND: Cardiac rupture after acute myocardial infarction (AMI) is unpredictable and almost always fatal, so the present study reviewed all the clinical characteristics of patients with cardiac rupture to determine if its occurrence can be predicted. METHODS AND RESULTS: The clinical characteristics of 1,296 consecutive AMI patients from January 1992 to February 2002 were retrospectively evaluated using multi-logistic analysis. Cardiac rupture occurred in 45 patients (3.5%), comprising left ventricular free wall rupture (n=23), ventricular septal perforation (n=20) and papillary muscle rupture (n=2). Early-phase rupture (within 72 h after AMI onset) was associated with anterior infarction. Of the 45 patients who experienced ruptures, 24 (53.3%) survived to discharge; 21 (46.6%) of the 45 ruptures occurred after admission. Successful reperfusion therapy was performed within 24 h for 840 patients. The incidence of rupture was significantly lower for reperfused patients than for non-reperfused patients (0.6% vs 3.5%, respectively; p<0.01). Peak C-reactive protein concentration was a reliable predictor of late-phase rupture (p=0.01), but not of early-phase rupture. CONCLUSIONS: Reperfusion therapy appears to aid in the prevention of cardiac rupture, especially late-phase rupture.

Aged↗

PubMed2004

Effects of a distal protection device during primary stenting in patients with acute anterior myocardial infarction.

BACKGROUND: The angiographic no-reflow phenomenon is an adverse prognostic factor in patients with acute myocardial infarction (AMI). The aim of the present study was to evaluate the effects of an occlusive balloon type distal protection device (PercuSurge GuardWire: GW) during primary stenting in patients with anterior AMI. METHODS AND RESULTS: The GW group included 42 patients treated by primary stenting with GW protection and the control group included 30 patients treated by primary stenting after thrombectomy without distal protection. Left ventricular (LV) function was measured and compared by left ventriculography obtained soon after percutaneous coronary intervention (PCI) and 3 weeks after onset. The corrected TIMI frame count values were lower in the GW group than in the control group (27.5+/-2.3 vs 35.1 +/-2.5, p=0.030). The number of patients with myocardial blush grade 3 after PCI was higher in the GW group than in the control group (45.7 vs 20.0%, p=0.029). Peak concentration of creatine kinase myocardial fraction was lower in the GW group than in the control group (326.6+/-41.5 vs 454.9+/-46.2 mg/dl, p=0.043). GW patients showed greater improvement at 3 weeks after PCI in terms of LV ejection fraction (+4.6+/-1.2 vs -1.1+/-1.5, p=0.004), LV end-systolic volume index (+0.5+/-2.4 vs +9.0+/-2.7, p=0.023), and regional wall motion abnormalities (-2.03+/-0.14 vs -2.51+/-0.14, p=0.018). CONCLUSION: Primary stenting with GW protection can restore epicardial coronary flow and myocardial perfusion, and also preserve LV function in anterior AMI.

Blood Flow Velocity↗

PubMed2004

Long-term prognosis of fulminant myocarditis rescued by percutaneous cardiopulmonary support device.

BACKGROUND: The long-term prognosis and cardiac function of fulminant myocarditis treated with percutaneous cardiopulmonary support (PCPS) was compared with the outcome of those not treated with PCPS. METHODS AND RESULTS: From 1991 to 2000, 14 patients with fulminant myocarditis (left ventricle ejection fraction (LVEF) < or =40%) were admitted to hospital. PCPS was necessary for treatment of shock in 8 (PCPS group), but not for the remaining 6 patients (non-PCPS group). In the PCPS group, 6 patients (75%) survived the critical phase and did not have any cardiac problems after discharge (range of follow-up period, 1.4-6.0 years). All patients in the non-PCPS group survived the acute phase; 1 patient had congestive heart failure 1.5 years after discharge, and another died from malignancy (follow-up period range, 2.2-9.4 years). Although the left ventricular ejection fraction (LVEF) of the PCPS group was significantly lower than that of the non-PCPS group in the acute phase, there was no significant difference in LVEF between the 2 groups in the chronic phase. CONCLUSION: Patients who survive the acute phase crisis of acute myocarditis have a favorable long-term survival rate, whether or not mechanical support is used.

Adult↗

PubMed2004

[Prospective randomized study of argatroban versus heparin anticoagulation therapy after percutaneous coronary intervention for acute myocardial infarction].

OBJECTIVES: Argatroban, a selective thrombin inhibitor, is expected to decrease acute coronary re-occlusion and restenosis via direct suppression of thrombin generation after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction. This study evaluated the effect of argatroban compared with heparin as an adjunctive anticoagulation therapy after PCI in patients with acute myocardial infarction. METHODS: Fifty-four consecutive patients with acute myocardial infarction underwent PCI within 6 hr from the onset and were randomly allocated to receive argatroban (argatroban group: n = 27) or heparin (heparin group: n = 27) after PCI. Each drug was administered intravenously for 72 hr. Coronary angiography was repeated at 1 and 6 months after the onset of acute myocardial infarction. In-hospital cardiac events, bleeding complications, and long-term outcome were surveyed. RESULTS: Baseline clinical and angiographic variables were similar in the two groups. Acute coronary re-occlusion and major hemorrhagic complications did not occur in either group. Minor bleeding complications, such as hematoma of the puncture sites, occurred significantly less frequently in the argatroban group than in the heparin group (4% vs 30%, p < 0.05). After 6 months, there were no significant differences in restenosis rate and target vessel recanalization rate between the two groups. Subgroup analyses revealed no significant differences in restenosis rate between patients treated with only balloon angioplasty and stent implantation. CONCLUSIONS: Argatroban provides similar prevention of acute thrombotic events and restenosis compared with heparin. However, argatroban might reduce bleeding complications in patients with acute myocardial infarction after PCI.

Angioplasty, Balloon, Coronary↗

PubMed2003

Src family kinases and nitric oxide production are required for hepatocyte growth factor-stimulated endothelial cell growth.

Hepatocyte growth factor (HGF) is a potent mitogen for vascular endothelial cells (EC); however, signal transduction pathways for HGF-stimulated EC growth remain unclear. In the present study we investigated the role of Src family kinases and nitric oxide (NO) in HGF-stimulated EC growth. Human umbilical vein endothelial cells (HUVEC) were stimulated with HGF and NO was measured by an NOx analyzing HPLC system. Activation of ERK1/2 and p38 MAPK was assessed by Western blot. NO production in HUVEC increased 1.8-fold by HGF. A Src family kinases inhibitor PP1 inhibited HGF-stimulated NO production by 71%. HUVEC growth increased 1.9-fold in cell number by HGF. PP1 and Nitro-L-arginine methylester (L-NAME) inhibited HGF-stimulated HUVEC growth by 51 and by 71%. ERK1/2 and p38 MAPK were phosphorylated by HGF and a MEK inhibitor PD98059 and a p38 MAPK inhibitor SB203580 inhibited HGF-stimulated HUVEC growth by 66% and by 58%; however, HGF-induced phosphorylation of ERK1/2 and p38 MAPK was not inhibited by L-NAME, indicating that NO is not an upstream activator of ERK1/2 and p38 MAPK. These findings demonstrated that Src family kinases regulate HGF-stimulated NO production in HUVEC and that HGF stimulates HUVEC growth through NO-dependent and NO-independent pathways.

Analysis of Variance↗

PubMed2003

Exercise training in patients with chronic heart failure improves endothelial function predominantly in the trained extremities.

The present study investigates whether lower-limb dominant exercise training in patients with chronic heart failure (CHF) improves endothelial function primarily in the trained lower extremities or equally in the upper and lower extremities. Twenty-eight patients with CHF were randomized to the exercise or control group. The exercise group underwent cycle ergometer training for 3 months while controls continued an inactive sedentary lifestyle. Exercise capacity (6-min walk test) and flow-mediated vasodilation in the brachial and posterior tibial arteries were evaluated. After 3 months, walking performance increased only in the exercise group (488+/-16 to 501+/-14 m [control]; 497+/-23 to 567+/-39 m [exercise, p<0.05]). The flow-mediated vasodilation in the brachial arteries did not change in either group (4.2+/-0.5 to 4.5+/-0.4% [control]; 4.3+/-0.5 to 4.6+/-0.4% [exercise]), but that in the posterior tibial arteries increased only in the exercise group (4.1+/-0.5 to 4.1+/-0.3% [control]; 3.6+/-0.3 to 6.4+/-0.6% [exercise, p<0.01]). Cycle ergometer training improved flow-mediated vasodilation in the trained lower limbs, but not in the untrained upper limbs. Exercise training appears to correct endothelial dysfunction predominantly by a local effect in the trained extremities.

Arm↗

PubMed2002

Nicorandil and leukocyte activation.

Nicorandil, a hybrid compound of an ATP-sensitive potassium (KATP ) channel opener and a nitric oxide donor, has been reported to preserve microvascular integrity in patients with reperfused myocardial infarction. The aim of the current study was to test the hypothesis that nicorandil suppresses activation of polymorphonuclear leukocytes (PMNLs), resulting in reduction of PMNL migration into tissue upon ischemia/reperfusion. Nicorandil, along with the mitochondrial KATP channel opener diazoxide and the nitric oxide donors nitroglycerin and isosorbide dinitrate, suppressed pseudopod projection in human PMNLs treated with 10(-9)-formyl-methionyl-leucyl-phenylalanine (FMLP) and subjected to shear stress (5 dyn/cm(2)) with a cone-and-plate shear device. Suppression by nicorandil and diazoxide was reversed by KATP channel blockers, 5 hydroxydecanoate and glibenclamide. FMLP-induced increase of [Ca2+] in PMNLs was suppressed by nicorandil and diazoxide, and 5 hydroxy-decanoate and glibenclamide reversed this suppression. Results of reverse transcription polymerase chain reaction with rat PMNL mRNA indicated the presence of mRNAs of Kir6.2 and Kir6.1 but not mRNAs of sulfonylurea receptor 1 or 2. Isosorbide dinitrate, diazoxide, and nicorandil reduced leukocyte migration and microvascular obstruction in reperfused ischemic tissue of rat mesenteric microcirculation. In conclusion, nicorandil attenuates ischemia/reperfusion-induced PMNL activation via donation of nitric oxide and K channel-related cascade.

Animals↗

PubMedDate not supplied

Noninvasive tissue characterization of coronary arterial plaque by 16-slice computed tomography in acute coronary syndrome.

Noninvasive characterization of coronary plaques is challenging for cardiologists. The authors' goal was to explore the clinical feasibility of newly developed 16-slice computed tomography (CT) in tissue characterization of coronary arterial plaques in patients with acute coronary syndrome. Sixteen patients with acute coronary syndrome underwent 16-slice CT (Aquillion, Toshiba) and coronary arteriography with intravascular ultrasound (IVUS) within 7 days. Twenty-three plaques were classified by IVUS according to plaque echogenicity: 6 soft plaques, 11 intermediate plaques, and 6 calcified plaques. Mean (+/- SD) CT numbers (Hounsfield units [HU]) of these 3 types of plaques were 50.6 +/-14.8 HU, 131 +/-21.0 HU, and 721 +/-231 HU, respectively. Sixteen-slice CT facilitates noninvasive tissue characterization of coronary arterial plaques.

Adult↗