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Biomedical subjects

J Yoshikawa

Publications and source records attributed to J Yoshikawa.

At least 109 records · Page 6Linked to original sources
PubMed2000

Effects of metabolically ischemic, but viable, myocardium on QT dispersion in patients with acute myocardial infarction: a study with resting I-123-BMIPP/thallium-201 myocardial single-photon emission computed tomography.

In chronic Q-wave myocardial infarction, QT dispersion is closely correlated with infarct size, but this correlation has not been evaluated for acute myocardial infarction (AMI). The effects of abnormal fatty acid metabolism on QT dispersion were examined in 123 patients with AMI who underwent resting iodine-123-15-iodophenyl 3-methyl pentadecanoic acid (BMIPP)/thallium-201(201Tl) myocardial single photon emission computed tomography (SPECT) and electrocardiographic analysis in the subacute phase. The relationship between BMIPP and 201Tl was defined as match when the total defect score for BMIPP was equal to or smaller than that for 201Tl, and as mismatch when the total defect score for BMIPP was larger than that for 201Tl. Twenty-six patients (21%) demonstrated BMIPP-201Tl match and 97 (79%) demonstrated mismatch. Infarct size was closely correlated with QT dispersion (r=0.67, p<0.001) in patients with BMIPP-201Tl match, but weakly correlated (r=0.30, p<0.005) in patients with BMIPP-201Tl mismatch. For small infarctions, QT dispersion was significantly larger in patients with BMIPP-201Tl mismatch than in those with BMIPP-201Tl match (62+/-24 ms vs 41+/-18 ms, p=0.03), but did not differ between the 2 groups for large infarctions. This study shows that QT dispersion is influenced by infarct size and by the presence of metabolically ischemic but viable myocardium in patients with AMI.

Adult↗
PubMed2000

A reverse flow-metabolism mismatch pattern: a new marker of viable myocardium with greater contractility during dobutamine stress than myocardium with a flow-metabolism mismatch pattern.

Few studies have investigated the contractility of myocardium with a reverse flow-metabolism pattern; that is, greater uptake of nitrogen- 13-ammonia (NH3) than fluorine- 18-fluorodeoxyglucose (FDG) on positron emission tomography (PET). This study examined the contraction thickening represented by count increase in ECG-gated FDG-PET of myocardium with a reverse flow-metabolism pattern during low-dose dobutamine stress. Fifty-four patients with myocardial infarction were studied. Relative NH3 and FDG uptake (%NH3, %FDG) and %count increase were measured in 216 apical and 216 lateral segments on ECG-gated FDG-PET. The %count increase during low-dose dobutamine stress was greater in myocardium with a reverse flow-metabolism mismatch pattern than in myocardium with a flow-metabolism mismatch pattern (35.9+/-25.7% vs 24.6+/-15.9%, p=0.0221 in apical segments, and 38.4+/-22.6% vs 27.6+/-18.4%, p=0.0040 in lateral segments) despite smaller %FDG. A reverse flow-metabolism mismatch pattern should be noted as a new marker of viable myocardium with greater contractility during dobutamine stress than myocardium with a flow-metabolism mismatch pattern.

Aged↗
PubMed2000

Effects of valsartan on angiotensin II-induced migration of human coronary artery smooth muscle cells.

The migration as well as proliferation of coronary artery medial smooth muscle cells (SMC) into the intima is proposed to be an important process of intimal thickening in coronary atherosclerosis. In the current study, we examined the effects of the angiotensin type 1 receptor antagonist valsartan on angiotensin II (Ang II)-induced migration of cultured human coronary artery SMC using Boyden's chamber methods. Ang II significantly stimulated human coronary artery SMC migration in a concentration-dependent manner between 10(-6) and 10(-8) mol/l when cells of passage 4 to 6 were used. However, the migration response to Ang II was moderately decreased in cells of passage 10 to 12, and was markedly decreased in cells of passage 15 to 17, compared to that of passage 4 to 6. Ang II-induced migration was blocked by the Ang II type 1 (AT1) receptor antagonist valsartan in a concentration-dependent manner. By contrast, the Ang II type 2 (AT2) receptor antagonist PD 123319 did not affect Ang II-induced migration. Ang II modestly increased the cell number of human coronary artery SMC after a 24-h incubation. This increase in cell numbers was also clearly blocked by valsartan, but not by PD 123319. These results indicate that Ang II stimulates migration as well as proliferation via AT1 receptors in human coronary artery SMC when cells of passage 4 to 6 are used. Valsartan may prevent the progression of coronary atherosclerosis through an inhibition of Ang II-induced migration and proliferation in these cells, although in vivo evidence is lacking.

Angiotensin II↗
PubMed2000

Ruptured irregularly shaped aneurysms: pseudoaneurysm formation in a thrombus located at the rupture site.

OBJECT: The authors describe the clinical, radiological, and pathological findings of ruptured cerebral aneurysms with irregular configurations. METHODS: Eight patients with subarachnoid hemorrhage due to ruptured irregularly shaped aneurysms were examined. The preoperative radiological findings in these cases were compared with the pathological and operative findings of endovascular or open surgery. All of the aneurysms exhibited delayed opacification and delayed washout of contrast medium from the irregularly shaped portion of the aneurysm on digital subtraction angiography and/or helical computerized tomography scanning. Endovascular embolization with platinum coils was attempted in the first four patients who underwent treatment. In three of these patients the aneurysm ruptured again during the endovascular procedure. In the fourth patient an intraaneurysm thrombus was observed during the procedure and clipping was performed. In the subsequent four patients, three underwent clipping without complication and one underwent partial aneurysm embolization because of poor general status. A thrombus adjacent to the aneurysm dome was observed in the patients who underwent open surgery. Pathological examination of the operative specimens revealed a pseudoaneurysm-like cavity in the thrombus that was adherent to the aneurysm. CONCLUSIONS: Ruptured irregularly shaped aneurysms may be accompanied by fragile pseudoaneurysm-like cavities located at the rupture point. Because these aneurysms have a high risk of repeated rupture during an endovascular procedure, advancing microinstruments to the weaker portion of the aneurysm should be avoided.

Adult↗
PubMed2000

[Prediction of restenosis after percutaneous transluminal coronary angioplasty using coronary flow reserve. Kansai Doppler Guide Wire Study Group].

This multi-center prospective study attempted to predict restenosis after percutaneous transluminal coronary angioplasty(PTCA) using coronary flow reserve. Intracoronary blood flow velocity was measured in 47 patients(37 males, 10 females, mean age 66 +/- 9 years) with a Doppler guide wire, following successful PTCA. Twenty-four patients had prior myocardial infarction. After successful PTCA, a Doppler guide wire was placed at the distal portion of the target lesion, and coronary blood flow velocity was measured before and during intravenous administration of adenosine triphosphate. Follow-up coronary angiography was performed 154 +/- 69 days after PTCA, and the diameter stenosis of the target lesion was measured using quantitative coronary angiography. Follow-up angiography showed restenosis in 13 patients(28%). Sensitivity and specificity for predicting restenosis were low(50%, 45%, respectively) with a post-PTCA% diameter stenosis cut-off point of 27%. Sensitivity and specificity were 67% and 61% with a minimal lumen diameter cut-off of 1.8 mm. The reference coronary artery diameter(cut-off point 2.5 mm) was better for predicting restenosis(sensitivity 78% and specificity 76%). Sensitivity and specificity were 62% and 67%, respectively, using coronary flow reserve(cut-off point 2.0). The restenosis rate of patients with a reference diameter of more than 2.5 mm was 10%, but 54% for those with less than 2.5 mm(p < 0.05). In patients with a reference diameter of less than 2.5 mm, coronary flow reserve was useful for predicting restenosis(cut-off point 1.9, sensitivity 71% and specificity 83%). Coronary flow reserve is useful for predicting restenosis after PTCA, when combined with reference coronary artery diameter.

Aged↗
PubMed2000

Effects of preinfarction angina on myocardial injury in patients with acute myocardial infarction: a study with resting 123I-BMIPP and 201T1 myocardial SPECT.

METHODS: Recent studies have suggested that patients with preinfarction angina have smaller infarcts and a better in-hospital outcome than those without angina. The mechanisms responsible for limitation of infarct size in the presence of preinfarction angina are unclear. We examined the effects of preinfarction angina on myocardial injury in patients with the first acute myocardial infarction with resting 123I-15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) 201TI myocardial scanning performed within 1 mo of infarction. RESULTS: Of 136 patients tested, 48 (35%) had preinfarction angina within 72 h before infarction, whereas 88 (65%) did not. BMIPP and 201TI defects were scored in 9 segments of the left ventricle (0 = normal, 1 = mild defect, 2 = moderate defect, 3 = severe defect, and 4 = no uptake). The total defect score was defined as the sum of the defect scores. There was no significant difference in percentage diameters of stenoses of infarct-related arteries, collateral circulation, total defect scores for BMIPP, or 201TI between the groups with and without preinfarction angina. However, the ratio of total defect score for 201TI to that for BMIPP was significantly smaller for patients with than for those without preinfarction angina (0.64 +/- 0.21 versus 0.74 +/- 0.25, respectively; P = 0.007). CONCLUSION: Preinfarction angina did not affect the areas at risk in acute myocardial infarction, as shown by BMIPP defect, but decreased necrotic myocardium in the areas at risk, as shown by 201TI defect, and increased metabolically damaged but viable myocardium, as shown by BMIPP and 201TI mismatch through unidentified mechanisms other than collateral circulation (e.g., ischemic preconditioning).

Angina, Unstable↗
PubMed2000

[Clinical usefulness of intracoronary Doppler for prediction of coronary restenosis].

The Doppler guide wire is widely used in the diagnosis of heart diseases, and in particular including ischemic heart disease. It offers various advantages for application in tortuous and peripheral arteries, and in the detection of functional coronary stenosis that coronary angiography cannot detect. A number of multicenter trials have also shown that the Doppler guide wire is of value in predicting coronary restenosis after coronary intervention. On the other hand, the Doppler guide wire is influenced not only by the stenosis in the epicardial coronary artery, but also by stenosis in the vascular beds of coronary microcirculation. An appreciation of both the advantages and disadvantages of the Doppler guide wire and its usefulness is of considerable importance.

Clinical Trials as Topic↗
PubMed2000

Cytomegalovirus associated pancreatitis in a patient with systemic lupus erythematosus.

Pancreatitis can develop as a complication of systemic lupus erythematosus (SLE). Steroids are considered one of the possible causes of this complication, but the pathological mechanism is unclear. We describe an autopsy case of a 29-year-old woman with cytomegalovirus (CMV) associated pancreatitis that developed during steroid therapy for her SLE. Many parenchymal cells with cytomegalic inclusions were seen in the patient's pancreas, especially in lesions showing active inflammation, and transcripts of CMV major immediate-early and late genes, markers of active viral replication, were detected. These findings suggest that CMV played an etiological role in the pancreatic disorder.

Adult↗
PubMed1999

Effect of red wine on coronary flow-velocity reserve.

An increase in coronary flow-velocity reserve may be one of the important cardioprotective effects of red wine. Some polyphenols may have potent vasorelaxing effects on coronary microvessels during hyperaemia.

Adult↗
PubMed1999

Antioxidants improve impaired insulin-mediated glucose uptake and prevent migration and proliferation of cultured rabbit coronary smooth muscle cells induced by high glucose.

BACKGROUND: To explore the role of intracellular oxidative stress in high glucose-induced atherogenesis, we examined the effect of probucol and/or alpha-tocopherol on the migration and growth characteristics of cultured rabbit coronary vascular smooth muscle cells (VSMCs). METHODS AND RESULTS: Chronic high-glucose-medium (22. 2 mmol/L) treatment increased platelet-derived growth factor (PDGF)-BB-mediated VSMC migration, [3H]thymidine incorporation, and cell number compared with VSMCs treated with normal-glucose medium (5.6 mmol/L+16.6 mmol/L mannose). Probucol and alpha-tocopherol significantly suppressed high glucose-induced increase in VSMC migration, cell number, and [3H]thymidine incorporation. Probucol and alpha-tocopherol suppressed high glucose-induced elevation of the cytosolic ratio of NADH/NAD+, phospholipase D, and membrane-bound protein kinase C activation. Probucol, alpha-tocopherol, and calphostin C improved the high glucose-induced suppression of insulin-mediated [3H]deoxyglucose uptake. Chronic high-glucose treatment increased the oxidative stress, which was significantly suppressed by probucol, alpha-tocopherol, suramin, and calphostin C. CONCLUSIONS: These findings suggest that probucol and alpha-tocopherol may suppress high glucose-induced VSMC migration and proliferation via suppression of increases in the cytosolic ratio of free NADH/NAD+, phospholipase D, and protein kinase C activation induced by high glucose, which result in reduction in intracellular oxidative stress.

Animals↗
PubMed1999

Intravascular ultrasound-guided balloon angioplasty for treatment of in-stent restenosis.

We investigated the usefulness of intravascular ultrasound (IVUS)-guided balloon angioplasty for in-stent restenosis in 37 lesions of 34 consecutive patients. We divided these patients into two groups: a group in which the balloon size was determined by quantitative coronary angiography (QCA group; 17 patients, 19 lesions) and a group in which the balloon size was determined by IVUS (IVUS group; 17 patients, 18 lesions). We compared short-term and 6-month outcomes for these groups. In the IVUS group, we used a balloon of a size equal to 95% of the media-to-media diameter at the distal to the stent, as determined by IVUS. No significant differences were observed in patient or lesion characteristics between the two groups. The clinical success rate was 100% in both groups, and no clinical events were observed in either of the groups. The balloon/artery ratio was larger in the IVUS group than in the QCA group (1.33 +/- 0.35 vs. 1.16 +/- 0.13, P < 0.05), and the recurrent restenosis rate was lower (17% vs. 53%, P < 0.05). These results suggest that repeat balloon angioplasty using a balloon size determined by IVUS is useful for in-stent restenosis. Cathet. Cardiovasc. Intervent. 47:298-303, 1999.

Angioplasty, Balloon, Coronary↗
PubMed1999

Usefulness of newly designed pigtail catheter with multiple side holes by reducing incidence of ventricular ectopy.

This study was designed to determine whether a newly designed 5 Fr pigtail catheter of Jet Balance with multiple side holes reduces the incidence of ventricular ectopy during left ventriculography. To examine the catheter movement in vitro, we injected a colored glycerin solution by an injector through 5 Fr Jet Balance catheter and 6 Fr conventional pigtail catheter suspended in a water filled, glass container. A recoil of the catheter caused by injection was observed for a 6 Fr conventional catheter; however, no catheter movement was observed when a 5 Fr Jet Balance was used. To evaluate clinical usefulness of the 5 Fr Jet Balance, we compared the number of incidence of ventricular ectopy during left ventriculography between 5 Fr Jet Balance and 6 Fr conventional pigtail catheters. In 104 consecutive patients who underwent left ventriculography, a 5 Fr Jet Balance was used in 55 patients (5 Fr Jet Balance group), and a 6 Fr conventional pigtail in 49 patients (6 Fr conventional pigtail group). The 5 Fr Jet Balance group had a significantly lower incidence of VPB (21.8% vs. 42.9%, P = 0.02), ventricular tachycardia (1.9% vs. 14.3%, P = 0.02), and multiple VPB (9.0% vs. 34.7%, P = 0.001), respectively, than the 6 Fr conventional pigtail group. In conclusion, a 5 Fr Jet Balance pigtail catheter is useful and safe as regard to the incidence of ventricular ectopy during left ventriculography. Cathet. Cardiovasc. Intervent. 48:220-225, 1999.

Aged↗
PubMed1999

Activation of mitogen-activated protein kinases in in vivo ischemia/reperfused myocardium in rats.

In this study, we investigate the in vivo activation of mitogen-activated protein kinases (MAPK) as important signal transduction cascades observed after myocardial ischemia/reperfusion. Myocardial continuous ischemia and ischemia/reperfusion was produced in Wistar rats. The activities of MAPKs in the ischemic and ischemia/reperfused regions were measured using an in-gel kinase assay, an in vitro kinase assay and Western blot analysis. Activator protein-1 (AP-1) DNA binding activity was determined using an electrophoretic mobility shift assay. DNA fragmentation was detected as DNA ladders by agarose gel electrophoresis. The p46JNK and p55JNK activities of continuous ischemia were significantly increased at 30 min (5.9 and 4.2 fold, respectively P<0.05). Coronary reperfusion increased both p42ERK and p44ERK activities at 30 min (3.0 and 2.3 fold P<0.01), and both p46JNK and p55JNK activities at 30 min (1.4 and 1.7 fold P<0.05). The AP-1 DNA binding activities of continuous ischemia were significantly increased at 1, 3 and 7 days (28, 21 and 17 fold, respectively P<0.01). Coronary reperfusion markedly decreased AP-1 DNA binding activities at 1 (41%P<0.01) and 3 days (48%P<0.05). Myocardial DNA fragmentation was considerably more enhanced by reperfusion than continuous ischemia. In conclusion, our present work provides the first in vivo evidence that ERK and JNK are activated by reperfusion from the activities of continuous ischemia. These signal transduction mechanisms may be partially responsible for the myocardial injury.

Animals↗
PubMed1999

Increased JNK, AP-1 and NF-kappa B DNA binding activities in isoproterenol-induced cardiac remodeling.

The in vivo signal transduction pathway, responsible for isoproterenol-induced cardiac hypertrophy or remodeling, remains to be clarified. The purpose of this study was to examine c-Jun NH2-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK), activator protein-1 (AP-1) and nuclear factor-kappa B (NK-kappa B) DNA binding activity, which seem to be important in a signal transduction cascade upstream of the increased level of mRNA expression observed in isoproterenol-induced cardiac remodeling. Rats were continuously infused with saline and isoproterenol by intravenous injection (a short period; 0.5 microgram/kg/min) and an osmotic minipump (a long period; 0.5 or 3 mg/kg/day). Cardiac morphology was measured by echocardiography. JNK and ERK were measured by in gel kinase assay. AP-1 and NF-kappa B DNA binding activity was determined using an electrophoretic mobility shift assay. Echocardiogram showed that the thickness of the left ventricular anterior wall (AW) and left ventricular posterior wall (PW) increased at day 1 in low doses, and at day 1 in high doses. Isoproterenol significantly increased ERK and JNK activity at 15 min after intravenous infusion of 0.5 microgram/kg/min isoproterenol. At late phase about JNK and ERK activity, only a high dose of isoproterenol increased JNK. AP-1 DNA binding activities spurred by low or high doses of isoproterenol administration increased at 12 h, reached their peak of 24.1- and 37.1-fold (P < 0.01), respectively, at 24 h, and thereafter decreased. Although low doses of isoproterenol did not change the level of NF-kappa B DNA binding activities, high doses increased it to 10.9-fold (P < 0.01) at day 2. This study showed increased JNK, ERK, AP-1 and NF-kappa B DNA binding activities in isoproterenol-induced cardiac remodeling. AP-1 may contribute to the isoproterenol-induced cardiac remodeling, and JNK or NF-kappa B may also play some roles in it.

Animals↗
PubMed1999

Long-acting calcium channel antagonist pranidipine prevents ventricular remodeling after myocardial infarction in rats.

The purpose of this study was to examine the effects of the long-acting calcium channel antagonist pranidipine on ventricular remodeling, systolic and diastolic cardiac function, circulating humoral factors, and cardiac mRNA expression in myocardial infarcted rats. Myocardial infarction (MI) was produced by ligation of the coronary artery in Wistar rats. Three mg/kg per day of pranidipine was randomly administered to the infarcted rats. Hemodynamic measurements, Doppler echocardiographic examinations, analyses of the plasma levels of humoral factors, and myocardial mRNA expression were performed at 4 weeks after myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 24.2 +/- 1.2mmHg and 5.4 +/- 0.6 mmHg. Pranidipine reduced LVEDP and CVP to 13.6 +/- 1.4mmHg (P < 0.01) and 2.5 +/- 0.4mmHg (P < 0.01). The weight of the left and right ventricles in MI was significantly higher than in the sham-operated rats (sham, 2.02 +/- 0.04 and 0.47 +/- 0.02g/kg; MI, 2.18 +/- 0.05 and 0.79 +/- 0.04g/ kg; P < 0.01). Left ventricular end-diastolic dimension (LVDd) in MI increased to 10.3 +/- 0.3mm (P < 0.01) (sham, 6.4 +/- 0.3mm). Pranidipine prevented an increase in the weight of the left and right ventricles (2.02 +/- 0.04 and 0.6 +/- 0.03g/kg, P < 0.01) and LVDd (7.9 +/-0.2mm, P < 0.01 to MI). Plasma renin activity (PRA), and plasma epinephrine, norepinephrine, and dopamine concentrations in MI were higher than those of the sham-operated rats. Pranidipine decreased the PRA and plasma cathecolamine levels of the myocardial infarcted rats to the level of the sham-operated rats. Moreover, the rats in MI showed systolic dysfunction, shown by decreased fractional shortening (sham, 31 +/- 2% vs MI, 15 +/- 1%; P < 0.01) and diastolic dysfunction shown by the E-wave deceleration rate (sham, 12.8 +/- 1.1 m/s2; MI, 32.6 +/- 2.1 m/s2; P < 0.01). Pranidipine significantly prevented systolic and diastolic dysfunction. The increases in beta-myosin heavy chain (MHC), alpha-skeletal actin, and atrial natriuretic polypeptide mRNAs in the noninfarcted left ventricle and right ventricle at 4 weeks after the myocardial infarction were significantly suppressed by the treatment with pranidipine. On the other hand, depressed alpha-MHC was restored to normal levels by pranidipine in both regions. In conclusion, pranidipine prevents the left ventricular remodeling process accompanied by systolic and diastolic dysfunction, and inhibits abnormal cardiac gene expression after myocardial infarction.

Analysis of Variance↗
PubMed1999

Endomyocardial biopsy findings in patients with atrioventricular block in the absence of apparent heart disease.

The purpose of this study was to examine the histopathological findings of right ventricular endomyocardial biopsies from ten patients less than 60 years of age (47 +/- 9.8 (mean +/- SD) years) with documented atrioventricular block but without apparent heart disease. They underwent electrophysiological testing, echocardiography, coronary angiography, and right ventricular endomyocardial biopsy. Biopsy specimens were assessed for morphologic changes in myocyte diameter, fibrosis, disarray, and degeneration. Electrophysiological testing demonstrated atrioventricular nodal block in 2, intra-His bundle block in 2, and infra-His bundle block in 6 patients. Histology revealed evidence of myocardial fibrosis with either myocyte hypertrophy or disarray in 7 of the 10 patients. The results of electrophysiological testing did not correlate with the histopathological findings or severity. In one patient, heart failure appeared during the follow-up period. We conclude that patients with atrioventricular block of unknown etiology have histological abnormalities of the ventricular endomyocardium in addition to the conduction system disturbances. We consider such cases as constituting one of the disease groups of cardiomyopathy, and suggest that it is necessary to follow up the clinical course in these patients.

Adult↗