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Biomedical subjects

J Yoshikawa

Publications and source records attributed to J Yoshikawa.

At least 91 records · Page 5Linked to original sources
PubMed2000

Angiotensin blockade inhibits SIF DNA binding activities via STAT3 after myocardial infarction.

The in vivo activation of transcription factors, which is important for cell regulation by gene expression, has not been well examined in myocardial infarcted heart. The purpose of this study was to determine whether myocardial signal transducer and activator of transcription (STAT) pathway is activated as sis-inducing factor (SIF) in infarcted heart, and to assess the angiotensin blockade on SIF activity in ischemic and non-ischemic myocardium of rat. Myocardial infarction was made by ligation of the coronary artery in Wistar rats. In electrophoretic mobility shift assay, myocardial SIF DNA binding activities gradually increased and reached to peak at 1 week in infarcted and non-infarcted regions after myocardial infarction. Imidapril and candesartan cilexitil significantly prevented the increase in SIF DNA binding activity in infarcted and non-infarcted regions. This increased SIF DNA complex was supershifted by specific anti-STAT3 antibody, indicating that increased SIF complex at least contained activated STAT3 proteins in myocardial infarcted heart. Furthermore, immunoprecipitation-Western blot analysis revealed that STAT3 of infarcted and non-infarcted regions were tyrosine-phosphorylated at 1 week after myocardial infarction. Imidapril and candesartan cilexitil prevented the increase in phosphorylated STAT3. Thus, the transcriptional activation of STAT3 through AT1 receptor may be partially involved in cardiac remodeling after myocardial infarction.

Angiotensin Receptor Antagonists↗
PubMed2000

Point mutations in mitochondrial DNA of patients with alcoholic cardiomyopathy.

The pathogenesis of alcoholic cardiomyopathy (ACM) is not well understood. However, recent reports have shown that mutations in mitochondrial DNA (mtDNA) were associated with mitochondrial encephalomyopathy and cardiomyopathy. Our objective was to explore point mutations in mtDNA and the pathogenesis of ACM. We obtained heart biopsy specimens from ten male habitual drinkers with congestive heart failure. We amplified the total mtDNA obtained from these specimens using a two-step polymerase chain reaction method and analyzed the products using automated fluorescence-based direct sequencing. The sequences were compared with those of controls. MtDNA from the ACM patients contained multiple point mutations. Specifically, four of the ten patients carried five point mutations that had been detected previously in several other mitochondrial diseases. These point mutations were not observed in controls. These results suggest that mtDNA abnormalities are involved in the pathogenesis of ACM.

Adult↗
PubMed2000

Prognostic value of Doppler transmittal flow patterns and cardiac natriuretic peptides in patients with chronic congestive heart failure admitted for episodes of acute decompensation.

This study was designed to determine whether the restrictive filling transmitral flow velocity pattern is associated with increased plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). It was also designed to evaluate the prognostic value of these parameters from patients with chronic congestive heart failure (CHF) admitted for episodes of acute decompensation. We performed Doppler echocardiography, measured plasma levels of ANP and BNP in 33 patients at the time of admission, and assessed the subsequent cardiac mortality for 3 months. Eleven patients (33%) had a restrictive filling pattern of deceleration time (DcT) < 120ms. Plasma ANP and BNP levels were markedly increased in all patients to 189 +/- 145 pg/ml and 865 +/- 559 pg/ml, respectively. Seventeen patients (52%) showed more than 700 pg/ml of plasma levels of BNP. There was a significant correlation of DcT with the plasma ANP level (r = -0.41, P = 0.017), and a better correlation of DcT with the plasma BNP level (r =-0.50, P = 0.003). The combined index of both shorter DcT (< 120 ms) and higher plasma BNP levels (>700 pg/ml) was the best predictor of cardiac mortality by Cox univariate analysis (chi2 = 5.87, P = 0.015). Furthermore, the sensitivity and specificity of this index for the detection of cardiac mortality were 80% and 86%, respectively. In conclusion, the combined analysis of the Doppler transmitral flow velocity pattern and measurement of the plasma BNP level is noteworthy since it is noninvasive and convenient. Moreover, it is extremely useful in predicting the prognosis for patients with chronic CHF admitted for episodes of acute decompensation.

Acute Disease↗
PubMed2000

Differences in time course of myocardial mRNA expression in non-infarcted myocardium after myocardial infarction.

In non-infarcted myocardium after myocardial infarction, the change of cardiac phenotypic modulation of contractile protein, extracellular matrix and intracellular Ca2+ transport protein, such as sarcoplasmic reticulum Ca2+(SR-Ca2+)-ATPase, Na+-Ca2+ exchanger, have a important role during cardiac remodeling. However, the time course in this gene expression in the adjacent and remote left ventricular, or right ventricular myocardium after myocardial infarction has not been well examined. The purpose of this study was to examine the left ventricular function and regional cardiac gene expression after myocardial infarction. Myocardial infarction was produced in Wistar rats by the ligation of the left anterior descending coronary artery. After 3 weeks, 2 months and 4 months from myocardial infarction, we performed Doppler echocardiography and measured the systolic and diastolic function. Then, we analyzed the contractile protein, extracellular matrix and intracellular Ca2+ transport protein mRNAs of cardiac tissues in the adjacent and the remote noninfarcted myocardium, and right ventricular myocardium by Northern blot hybridization. Fractional shortening of infarcted heart progressively decreased. Peak early diastolic filling wave (E wave) velocity increased, and the deceleration rate of the E wave velocity was more rapid in myocardial infarction areas. Atrial filling wave (A wave) velocity decreased, resulting in a marked increase in the ratio of E wave to A wave velocity. Expression of myocardial alpha-skeletal actin, beta-MHC and ANP mRNA, or collagen I and III mRNA were higher at 3 weeks after myocardial infarction. SR Ca2+-ATPase mRNA in the adjacent non-infarcted myocardium was decreased at 2 months, and that in remote myocardium was decreased at 4 months after infarction. Na+-Ca2+ exchanger mRNA levels were increased at 3 weeks, but was decreased at 2 months in the adjacent non-infarcted myocardium and at 4 months in the remote myocardium. These findings suggest that the compensation for myocardial infarction by myocardial gene expression in non-infarcted myocardium may occur at an early phase after myocardial infarction, and myocardial dysfunction may begin from adjacent to remote non-infarcted myocardium during progressive cardiac remodeling.

Animals↗
PubMed2000

Impact of Doppler-derived left ventricular diastolic performance on exercise capacity in normal individuals.

BACKGROUND: Doppler-derived left ventricular (LV) diastolic indexes have been shown to correlate with exercise capacity in patients with heart diseases as well as healthy individuals. However, it is uncertain whether they predict exercise capacity independent of noncardiac factors. METHODS: To clarify the impact of the LV diastolic index on exercise capacity, 160 healthy individuals were investigated. All underwent Bruce protocol treadmill stress testing and 2-dimensional and Doppler echocardiography. Estimated metabolic equivalent was calculated from exercise time (metabolic equivalent = 1.11 + 0.016 x exercise time). Diastolic performance was assessed by Doppler transmitral flow velocity pattern. Pulmonary function tests and complete blood cell count were also performed. RESULTS: LV diastolic indexes correlated well with metabolic equivalent (peak transmitral filling velocity (A): r = -0.51, P <.0001; ratio of early and late transmitral filling velocities (E/A): r = 0.58, P <. 0001). However, there was no significant correlation between LV systolic indexes and metabolic equivalent. Independent predictors for a higher metabolic equivalent by multivariate analysis were higher E/A (P <.0001), higher vital capacity (P =.001), smaller body mass index (P =.0003), younger age (P =.0050), and higher hemoglobin concentration (P =.0026). CONCLUSION: Doppler-derived LV diastolic index may help in predicting exercise capacity in normal individuals independent of other cardiac and extracardiac factors.

Adult↗
PubMed2000

Suppression by eicosapentaenoic acid of oxidized low-density lipoprotein and lysophosphatidylcholine-induced migration in cultured rat vascular smooth muscle cells.

The migration of medial smooth muscle cells into the intima is proposed to be an initial process of intimal thickening in atherosclerotic lesions. The present study was designed to determine whether pretreatment with the antiatherogenic agent eicosapentaenoic acid (EPA) inhibits the migration induced by oxidized low-density lipoprotein (LDL) and its major phospholipid component, lysophosphatidylcholine (lyso-PC), in cultured rat vascular smooth muscle cells (VSMCs) using Boyden's chamber method. The effects of EPA pretreatment on angiotensin II (Ang II)- and platelet-derived growth factor BB (PDGF BB)-induced migration were also examined in these cells. Oxidized LDL and lyso-PC induced migration in a concentration-dependent manner. EPA pretreatment clearly suppressed oxidized LDL (200 microg/mL)- and lyso-PC (10(-5) mol/L)-induced migration between 40 and 160 micromol/L. EPA pretreatment also suppressed Ang 11 (10(-7) mol/L)- and PDGF BB (5 ng/mL)-induced migration at a concentration of 80 and 160 micromol/L. However, in a trypan blue exclusion test, dead cells stained with trypan blue were not found 24 hours after treatment with EPA. These results suggest that EPA suppresses VSMC migration induced by oxidized LDL and lyso-PC, as well as Ang II and PDGF BB. These preliminary data concerning the effects of EPA may partly explain the antiatherosclerotic effects of this agent.

Animals↗
PubMed2000

Cerebellar hemorrhage after coil embolization for a ruptured vertebral dissecting aneurysm.

BACKGROUND: We present a case of ruptured vertebral dissecting aneurysm that exhibited cerebellar hemorrhage after successful embolization of the vertebral artery including the dissected site. CASE PRESENTATION: A 59-year-old man suffered a sudden onset of severe occipital headache when he looked up. Computed tomography demonstrated subarachnoid hemorrhage. Angiography revealed a right vertebral dissecting aneurysm distal to the posterior inferior cerebellar artery. Endovascular embolization of the aneurysm was performed with preservation of the posterior inferior cerebellar artery. The next day, the patient suffered a cerebellar hemorrhage in the vermis. The intracranial pressure was controlled by external ventricular drainage. The patient was discharged with mild cerebellar ataxia and bilateral abducens nerve palsy. CONCLUSION: In a case of vertebral dissecting aneurysm distal to the posterior inferior cerebellar artery, blood circulation in the vertebral arterial system may change after embolization of the aneurysm. In our case, the preserved posterior inferior cerebellar artery might have been hemodynamically stressed postoperatively, resulting in cerebellar hemorrhage. Therefore, strict control of blood pressure is essential in the acute stage after occlusion of the aneurysm.

Aneurysm, Ruptured↗
PubMed2000

Value of acceleration flow and the prestenotic to stenotic coronary flow velocity ratio by transthoracic color Doppler echocardiography in noninvasive diagnosis of restenosis after percutaneous transluminal coronary angioplasty.

OBJECTIVES: The study evaluated the value of coronary flow velocity measurement by transthoracic color Doppler echocardiography (TTCDE) for the noninvasive diagnosis of restenosis after percutaneous transluminal coronary angioplasty (PTCA) for left anterior descending coronary artery (LAD) lesions. BACKGROUND: Recent advances in TTCDE provide coronary flow velocity measurements in the LAD under the guidance of color flow mapping. METHODS: We studied 53 patients who underwent successful PTCA for LAD lesions and follow-up coronary angiography (18 patients with restenosis [Group-R], 35 patients without restenosis [Group-N]). We searched localized color aliasing corresponding to local flow acceleration to obtain coronary flow velocity at PTCA sites in the LAD. When localized aliasing was detected, we measured coronary flow velocity at the aliasing (stenotic site) and the prestenotic site. RESULTS: Using TTCDE, it was possible to measure mean diastolic velocity (MDV) in the LAD in 41 (77%) of 53 patients (14 of 18 patients in Group-R; 27 of 35 patients in Group-N). Localized aliasing was displayed by color flow mapping in 14 (100%) of 14 patients in Group-R, and 15 (56%) of 27 patients in Group-N. Stenotic MDV in Group-R was significantly higher than that in Group-N (60.3 +/- 21.1 vs. 35.1 +/- 7.6 cm/s, p < 0.01), although prestenotic MDV did not differ between Group-R and Group-N (20.2 +/- 3.0 vs. 19.6 +/- 2.3 cm/s). There were significant differences in the prestenotic to stenotic MDV ratio between Group-R and Group-N (0.36 +/- 0.10 vs. 0.57 +/- 0.09, p < 0.001). Localized aliasing with the prestenotic to stenotic MDV ratio <0.45 as the optimal cutoff value had a sensitivity of 86% and a specificity of 93% for the presence of restenosis in LAD lesions. CONCLUSIONS: Detection of localized color aliasing and measurement of the prestenotic to stenotic MDV ratio in the LAD by TTCDE are useful in the noninvasive diagnosis of restenosis after PTCA for LAD lesions.

Aged↗
PubMed2000

Possible mechanism of bronchoprotection by SIN-1 in anaesthetized guinea pigs: roles of nitric oxide and peroxynitrite.

BACKGROUND: S-morpholinosydnonimine (SIN-1) is thought to generate peroxynitrite. Recent reports suggested that peroxynitrite possessed a potent vascular relaxant activity via guanylate cyclase activation. However, no previous studies have examined the relaxant effect of peroxynitrite on airway smooth muscle. OBJECTIVE: To determine the mechanism of bronchoprotection by SIN-1, considering in particular the involvement of nitric oxide (NO) and peroxynitrite. METHODS: Peroxynitrite formation was assayed by monitoring the oxidizing activity of dihydrorhodamine 123, and NO was measured polarographically as a redox current in vitro. We examined the effect of SIN-1 delivered to the airway by ultrasonic nebulization against bronchoconstriction induced by acetylcholine in anaesthetized guinea pigs. RESULTS: SIN-1 produced peroxynitrite in a time- and concentration-dependent manner, but did not produce NO in vitro. However, when mixed with glutathione (GSH) and bronchoalveolar lavage fluid (BALF), peroxynitrite formation by SIN-1 was inhibited and SIN-1 induced the release of NO. SNAP (S-nitroso-N-acetyl-penicillamine) and SIN-1 each inhibited acetylcholine-induced bronchoconstriction in a dose-dependent manner in vivo. Though GSH alone did not have any effect on baseline airway resistance and acetylcholine-induced bronchoconstriction, pretreatment with GSH significantly enhanced SNAP- and SIN-1-induced bronchoprotection. In addition, pretreatment with carboxy-PTIO, a NO scavenger, completely inhibited bronchoprotective effect of SNAP on acetylcholine-induced bronchoconstriction, but partially inhibited SIN-1-induced bronchoprotection. CONCLUSION: These findings demonstrated that SIN-1 is a potent peroxynitrite-releasing compound and caused significant bronchoprotection against acetylcholine. The mechanism of bronchoprotection by SIN-1 appears to be mediated by peroxynitrite but also at least in part through NO regeneration, which may involve GSH and airway thiols as a consequence of exposure to peroxynitrite.

Acetylcholine↗
PubMed2000

Effect of angiotensin-converting enzyme inhibitor on left ventricular parameters and circulating brain natriuretic peptide in elderly hypertensives with left venticular hypertrophy.

In the elderly, left ventricular hypertrophy (LVH) is a powerful risk factor for cardiovascular events and cardiovascular death. The purpose of the present study is to investigate the effect of long-term effective blood pressure control with the angiotensin-converting enzyme (ACE) inhibitor temocapril on left ventricular (LV) mass and function indices and the circulating concentration of the cardiac hormone brain natriuretic peptide (BNP) in elderly hypertensives with LVH. Temocapril treatment was administered for 1 year to 11 elderly hypertensives (mean age, 72 years) with LVH. Cardiac dimensions and circulating concentrations of BNP were monitored before initiation of treatment and after 1 year of treatment. At entry, BNP levels were positively correlated with the LV mass index, but were not correlated with the mean blood pressure, LV ejection fraction, or E/A ratio (the ratio of peak transmitral flow velocity in early diastole, peak E, to that in late diastole, peak A). After 1 year, temocapril treatment resulted in effective control of blood pressure. The treatment did not affect the LV ejection fraction, but modestly increased the E/A ratio. Temocapril significantly reduced septal and posterior wall thickness and the LV mass index. BNP significantly declined after 1 year. Changes in BNP were significantly related to changes in the LV mass index, but were not related to changes in the mean blood pressure, LV ejection fraction, or E/A ratio. The results suggest that long-term ACE inhibitor treatment with temocapril can induce the regression of LV mass and reduce elevated plasma BNP in elderly hypertensive patients with LVH. In this study, changes in BNP reflected the magnitude of regression of LVH.

Aged↗
PubMed2000

Role of endogenous nitric oxide in exercise-induced airway narrowing in patients with bronchial asthma.

BACKGROUND: Increased amounts of nitric oxide (NO) in expired air and induced sputum have been found in asthmatic patients, and the role of excessively produced NO in the pathogenesis of bronchial asthma is under active investigation. OBJECTIVE: This study was designed to investigate the involvement of endogenous NO in exercise-induced bronchoconstriction (EIB) in asthmatic patients by using the sputum induction method. METHODS: The concentration of NO derivatives and inflammatory indices in induced sputum were examined in 18 asthmatic subjects and 10 normal control subjects. All asthmatic subjects performed an exercise test for 6 minutes. For 8 weeks after the first exercise testing, 400 microg of beclomethasone dipropionate twice daily was administered for asthmatic subjects with EIB, and the exercise testing and sputum induction were repeated in these patients. RESULTS: The concentration of NO derivatives in induced sputum was significantly higher in 9 asthmatic subjects with EIB (1580 +/- 280 micromol/L) than in 9 asthmatic subjects without EIB (1130 +/- 210 micromol/L) and normal control subjects (510 +/- 150 micromol/L). Moreover, there was a significant correlation between the concentration of NO derivatives and the percentage of maximal fall in FEV(1) (r = 0.569, P =.019). The concentration of NO derivatives was also more closely correlated with the area under the curve of the percentage fall in FEV(1) plotted against time for 30 minutes (AUC(0-30); r = 0.812, P <.001). After treatment with inhaled beclomethasone dipropionate in asthmatic subjects with EIB, there was a significant decrease in the concentration of NO derivatives in induced sputum. The change in the concentration of NO derivatives was significantly correlated with the change in the AUC(0-30) (r = 0.896, P =.0114) but not with the change in the percentage of maximal fall in FEV(1). CONCLUSION: These findings suggest that excessive production of NO is associated with EIB in patients with asthma and contributes to the prolonged airway narrowing phase rather than to the maximal airway narrowing evoked by exercise.

Adult↗
PubMed2000

A dopamine-secreting pheochromocytoma.

We describe a patient with pheochromocytoma, which secretes dopamine. He was admitted to hospital because of chronic diarrhea. After surgical resection of the tumor, dramatic cessation of the diarrhea and blood pressure elevation were observed. Decreased expression of dopamine beta-hydroxylase in the tumor was considered a possible mechanism of producing a pathophysiological concentration of dopamine. This case shows that excessive excretion of dopamine, a vasodilative hormone, may affect blood pressure.

Adrenal Gland Neoplasms↗
PubMed2000

Three-dimensional echocardiography using a muliplane transesophageal probe: the clinical applications.

The use of multiplane transesophageal echocardiography has provided three-dimensional image sets of the heart from multiple two-dimensional images with high-image quality through rotation of the transducer without changing its position (rotational scanning). We discuss the methods, clinical applications, and current limitations of this three-dimensional technique.

Echocardiography, Three-Dimensional↗
PubMed2000

Effects of cardiac natriuretic peptides on oxidized low-density lipoprotein- and lysophosphatidylcholine-induced human mesangial cell migration.

The objectives of the present study were (1) to determine whether oxidized LDL and lysophosphatidylcholine (lyso-PtdCho), a major phospholipid component of oxidized LDL, stimulate the migration of cultured human mesangial cells and (2) to investigate the possible effects on mesangial cell migration of the cardiac natriuretic peptides atrial and brain natriuretic peptide (ANP and BNP). Oxidized LDL (10 and 100 microg/mL) and lyso-PtdCho (10(-7) to 10(-5) mol/L) stimulated migration in a concentration-dependent manner. In contrast, the effects of native LDL and phosphatidylcholine were modest or nonexistent. Protein kinase C (PKC) inhibitor and downregulation of PKC activity by phorbol ester inhibited oxidized LDL- and lyso-PtdCho-induced migration. Human ANP(1-28) and human BNP-32 significantly inhibited oxidized LDL- and lyso-PtdCho-induced migration in a concentration-dependent manner. C-ANF (des-[Glu(18),Ser(19),Gly(20),Leu(21),Gly(22)]ANP(4-23)), a specific ligand for ANP clearance receptors, could not inhibit oxidized LDL- and lyso-PtdCho-induced migration. Inhibition by ANP and BNP of lyso-PtdCho-induced migration was paralleled by an increase in the cellular level of GMP. Oxidized LDL- and lyso-PtdCho-induced migrations were inhibited by 8-bromo-cGMP. The results suggest that oxidized LDL and lyso-PtdCho stimulate the migration of human mesangial cells, at least in part, through a PKC-dependent process and that ANP and BNP inhibit this stimulated migration, probably through a cGMP-dependent process.

Atrial Natriuretic Factor↗
PubMed2000

Aldose reductase inhibitor improves insulin-mediated glucose uptake and prevents migration of human coronary artery smooth muscle cells induced by high glucose.

We examined involvement of the polyol pathway in high glucose-induced human coronary artery smooth muscle cell (SMC) migration using Boyden's chamber method. Chronic glucose treatment for 72 hours potentiated, in a concentration-dependent manner (5.6 to 22.2 mol/L), platelet-derived growth factor (PDGF) BB-mediated SMC migration. This potentiation was accompanied by an increase in PDGF BB binding, because of an increased number of PDGF-beta receptors, and this potentiation was blocked by the aldose reductase inhibitor epalrestat. Epalrestat at concentrations of 10 and 100 nmol/L inhibited high glucose-potentiated (22.2 mmol/L), PDGF BB-mediated migration. Epalrestat at 100 nmol/L inhibited a high glucose-induced increase in the reduced/oxidized nicotinamide adenine dinucleotide ratio and membrane-bound protein kinase C (PKC) activity in SMCs. PKC inhibitors calphostin C (100 nmol/L) and chelerythrine (1 micromol/L) each inhibited high glucose-induced, PDGF BB-mediated SMC migration. High glucose-induced suppression of insulin-mediated [(3)H]-deoxyglucose uptake, which was blocked by both calphostin C (100 nmol/L) and chelerythrine (1 micromol/L), was decreased by epalrestat (100 nmol/L). Chronic high glucose treatment for 72 hours increased intracellular oxidative stress, which was directly measured by flow cytometry using carboxydichlorofluorescein diacetate bis-acetoxymethyl ester, and this increase was significantly suppressed by epalrestat (100 nmol/L). Antisense oligonucleotide to PKC-beta isoform inhibited high glucose-mediated changes in SMC migration, insulin-mediated [(3)H]-deoxyglucose uptake, and oxidative stress. These findings suggest that high glucose concentrations potentiate SMC migration in coronary artery and that the aldose reductase inhibitor epalrestat inhibits high glucose-potentiated, PDGF BB-induced SMC migration, possibly through suppression of PKC (PKC-beta), impaired insulin-mediated glucose uptake, and oxidative stress.

Aldehyde Reductase↗
PubMed2000

Deletion polymorphisms in the angiotensin converting enzyme gene are associated with pulmonary hypertension evoked by exercise challenge in patients with chronic obstructive pulmonary disease.

Angiotensin converting enzyme (ACE) plays an important role in the pathogenesis of pulmonary hypertension. In this study we determined whether the deletion (D)/insertion (I) polymorphism in the ACE gene may be associated with pulmonary hypertension evoked by exercise challenge in patients with chronic obstructive pulmonary disease (COPD). ACE genotypes were determined in 19 patients with COPD. All patients underwent right heart catheterization followed by a constant-load exercise test while breathing room air or oxygen. Subgroups were created of seven patients with the II genotype, six with the ID genotype, and six with the DD genotype who were well-matched with respect to age, blood gas data at rest or after exercise, baseline lung function, results of incremental exercise testing, and hemodynamic data at rest. The mean pulmonary arterial pressure (Ppa) and pulmonary vascular resistance (Rpv) at rest in the three subgrpoups did not differ significantly during breathing of either room air or oxygen. However, the Ppa after exercise challenge in patients with the DD genotype (55.7 +/- 4.9 mm Hg [mean +/- SD]) was significantly higher than in patients with the II genotype (42.6 +/- 7.1 mm Hg, p = 0.008). The Rpv after exercise in patients with the DD genotype was also significantly higher than in patients with the ID and II genotypes. During breathing of oxygen to diminish acute hypoxic pulmonary vasoconstriction, the Ppa in patients with the DD genotype (52.3 +/- 3.1 mm Hg) was higher than in patients with the ID genotype (40.5 +/- 5.9 mm Hg, p = 0.0049) or the II genotype (37.7 +/- 5.9 mm Hg, p = 0.0027). In addition, the Rpv in patients with the DD genotype was higher than in patients with the ID and II genotypes. These results suggest that D-I polymorphism in the ACE gene may be associated with pulmonary hypertension evoked by exercise challenge in patients with COPD. However, the number of patients in this study was very small for a genetic association study, and our results should be examined in larger studies.

Aged↗
PubMed2000

Reverse redistribution of thallium-201 myocardial single photon emission tomography and contractile reserve.

The present study investigated the contractile reserve of myocardium exhibiting reverse redistribution (RRD) of thallium-201 (201Tl) after acute myocardial infarction. Forty patients experiencing their first acute myocardial infarction underwent resting 201Tl single-photon emission computed tomography (SPECT) and low-dose (5-10 microgxkg(-1)xmin(-1)) dobutamine stress echocardiography (DSE) within 4 weeks after the onset of infarction. The left ventricle was divided into 13 segments for analysis. The severity of defects in 201Tl SPECT and the extent of wall motion abnormality in DSE were visually assessed and scored. The sum of each defect score and wall motion score of infarct-related segments were defined as total defect score (TDS) and total wall motion score (TWM), respectively. Quantitative analysis of 201Tl uptake was also performed. Resting 201Tl SPECT revealed RRD in 16 patients (group RRD), fixed defect (FIX) in 23 patients (group FIX), and redistribution in one. There was a significant difference in improvement of TWM between rest and stress in TWM in both the RRD and FIX groups (p<0.0001, each case). The improvement of TWM with dobutamine was significantly greater in RRD than in FIX (1.6+/-1.0 vs 0.6+/-0.7, p=0.001). There was a positive correlation between the magnitude of RRD and improvement of TWM with dobutamine (r=0.48, p=0.002). Myocardium exhibiting RRD on 201Tl SPECT in patients with acute myocardial infarction has greater contractile reserve than that exhibiting a fixed defect.

Adult↗