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Biomedical subjects

J Yoshikawa

Publications and source records attributed to J Yoshikawa.

At least 127 records · Page 7Linked to original sources
PubMed1999

Combination effects of TAS-103, a novel dual topoisomerase I and II inhibitor, with other anticancer agents on human small cell lung cancer cells.

PURPOSE: TAS-103 [6-((2-(dimethylamino) ethyl)amino)-3-hydroxy-7H-iindeno(2,1-c)quinolin-7-one dihydrochloride] is a newly synthesized dual inhibitor of topoisomerase I and II. Since anticancer drugs are used in combination with other drugs for effective chemotherapy, we investigated the cytotoxic effect of TAS-103 in combination with other conventional anticancer agents, such as cisplatin, vindesine, doxorubicin, 5-fluorouracil, and the antitopoisomerase inhibitors SN-38 and etoposide in vitro. METHODS: Inhibition of the growth of the human small-cell lung cancer cell line SBC-3 was evaluated using the tetrazolium dye (MTT) assay. Drug interactions were evaluated by isobologram analysis and the determination of combination indices supplemented by a three-dimensional model. RESULTS: Simultaneous use of TAS-103 and cisplatin had a supraadditive effect, but combinations of TAS-103 with other drugs had an additive or marginally subadditive effect. Three-dimensional model analysis added more information about the synergistic concentration ranges of two drugs (cisplatin 200-400 nM and TAS-103 7 10 nM). Sequential use of TAS-103 and cisplatin had only an additive effect. CONCLUSION: These results suggest that the concomitant use of TAS-103 and cisplatin has a greater cytotoxic effect on cancer cells than single drug use, and may provide a beneficial effect in the treatment of small-cell lung cancer.

Aminoquinolines↗
PubMed1999

Mucin-producing biliary papillomatosis associated with gastrobiliary fistula.

We report a case of mucin-producing biliary papillomatosis in a 78-year-old woman. Abdominal ultrasound (US) and computed tomography (CT) showed wall thickening and dilatation of the intrahepatic bile duct (IHBD), as well as a nodular lesion, 1.2 cm in diameter, in the left branch of the IHBD. Gastric endoscopy revealed excretion of bile-containing mucin on the anterior wall of the body of the stomach. Endoscopic ultrasonography (EUS) showed gastrobiliary fistula and discharge of mucin into the stomach. Needle biopsy of the biliary tumor revealed papillary proliferation, but no malignant cells were recognized histologically. Therefore this patient was diagnosed as having mucin-producing biliary papillomatosis forming gastrobiliary fistula. She did not present with obstructive jaundice, probably because of the fistula. She is alive, without obstructive jaundice, 16 months after the diagnosis without having had surgery. This is, to our knowledge, the first reported case of biliary papillomatosis forming gastrobiliary fistula and with the patient free of obstructive jaundice.

Aged↗
PubMed1999

Association between angiotensin-converting enzyme gene polymorphisms and regression of left ventricular hypertrophy in patients treated with angiotensin-converting enzyme inhibitors.

PURPOSE: An insertion/deletion (ID) polymorphism of the angiotensin-converting enzyme (ACE) gene is associated with left ventricular hypertrophy. The present study examined polymorphisms of the ACE gene in patients with essential hypertension and left ventricular hypertrophy who were participants in a long-term trial of therapy with an ACE inhibitor. PATIENTS AND METHODS: ACE inhibitor therapy was administered for >2 years to 54 patients with hypertension who had moderate or severe left ventricular hypertrophy. Cardiac dimensions were monitored by echocardiography before the initiation of therapy and after 1 and 2 years of treatment. Serum ACE activity and plasma concentrations of brain natriuretic peptide, a marker for left ventricular hypertrophy, were also monitored. RESULTS: Eighteen patients had the II genotype for the angiotensin-converting enzyme gene, 19 had the ID genotype, and 17 had the DD genotype. Baseline (mean +/- SD) serum ACE activity was significantly greater (P <0.05) in the DD (18 +/- 7 IU/L) group than in the II (7 +/- 4 IU/L) or ID (12 +/- 6 IU/L) groups. ACE inhibitor therapy was effective in controlling blood pressure, and it reduced posterior and septal wall thickness, left ventricular mass index, and plasma brain natriuretic peptide concentration in all three groups. Despite similar blood pressure reductions, after 2 years, mean (+/- SD) regression in posterior wall thickness was significantly less (P <0.05) in the DD group (-9% +/- 5%) than in the ID (-21% +/- 7%) and II (-21% +/- 9%) groups. Similar results were seen for the reductions in brain natriuretic peptide levels. The magnitudes of regression of septal wall thickness and left ventricular mass index during therapy were less in the DD group than the II group (P <0.05). CONCLUSION: Hypertensive patients with the DD genotype are less likely to have regression of left ventricular hypertrophy when treated with ACE inhibitors than are patients with other ACE genotypes.

Aged↗
PubMed1999

Plasma levels of nitric oxide and related vasoactive factors following long-term treatment with angiotensin-converting enzyme inhibitor in patients with essential hypertension.

Several mechanisms other than the inhibition of systemic and local formation of angiotensin II (Ang II) have been proposed to play a role in mediating the hypotensive effects of angiotensin-converting enzyme (ACE) inhibitors. In the present study, we measured plasma levels of nitric oxide (NO) and the related vasoactive factors bradykinin, 6-keto prostaglandin F1alpha (6-keto PGF1alpha) a stable metabolite of prostacyclin, and cyclic guanosine-3',5'-monophosphate (cGMP) before and after a 4-week treatment with the ACE inhibitor lisinopril in 17 patients with essential hypertension. Plasma NO levels were measured by the Griess method after conversion of nitrate to nitrite. Long-term lisinopril treatment significantly reduced blood pressure and increased plasma NO and 6-keto PGF1alpha. The treatment also tended to increase plasma levels of bradykinin and cGMP, but not to a significant extent. The posttreatment NO level was inversely correlated with posttreatment systolic, diastolic, and mean blood pressure (n = 17, r= -.68, P< .01, n = 17, r= -.54, P < .05, and n = 17, r= -.66, P< .01, respectively). The posttreatment bradykinin level was also modestly correlated with posttreatment systolic and mean blood pressure (n = 17, r = -.51, P < .05 and n = 17, r = -.55, P < .05, respectively). In contrast, posttreatment 6-keto PGF1alpha and cGMP levels were not correlated with posttreatment systolic, diastolic, or mean blood pressure. These findings raise the possibility that increased formation of NO and bradykinin, as well as inhibition of the renin-angiotensin system, contribute to the hypotensive effect of the ACE inhibitor observed in our hypertensive patients.

6-Ketoprostaglandin F1 alpha↗
PubMed1999

Noninvasive evaluation of pulmonary capillary wedge pressure in patients with acute myocardial infarction by deceleration time of pulmonary venous flow velocity in diastole.

OBJECTIVES: This study investigates the correlation between deceleration time of diastolic pulmonary venous flow (PV-DT) and of early filling mitral flow (LV-DT), and pulmonary capillary wedge pressure (PCWP) in patients with acute myocardial infarction (AMI). BACKGROUND: An earlier study suggests that Doppler-derived LV-DT provides an accurate means of estimating PCWP in postinfarction patients with left ventricular systolic dysfunction. Furthermore, recent studies have suggested that PCWP correlates better with PV-DT than with LV-DT. However, the value of PV-DT and LV-DT for assessment of PCWP in patients with AMI has not been evaluated. METHODS: In 141 consecutive patients with AMI, we measured PV-DT and LV-DT by Doppler echocardiography, and compared these variables with PCWP measured using a Swan-Ganz catheter. RESULTS: There was a weak negative correlation between the LV-DT and PCWP (r = -0.54). Although the sensitivity of < or =130 ms in LV-DT in predicting > or =18 mm Hg in PCWP was high (86%), its specificity was low (59%). On the other hand, a very close negative correlation was found between PV-DT and PCWP (r = -0.89). The sensitivity and specificity of < or =160 ms in PV-DT in predicting > or =18 mm Hg in PCWP were 97% and 96%, respectively. CONCLUSIONS: In patients with AMI, Doppler-derived PV-DT showed a stronger correlation with PCWP than LV-DT.

Adult↗
PubMed1999

Potential applications of intracardiac echocardiography in the assessment of the aortic valve from the right ventricular outflow tract.

Intracardiac echocardiography (ICE) is a developing technology and a promising method for visualizing intracardiac structures. However, its applications are currently limited to guidance during mitral valvuloplasty, catheter ablation, or electrophysiologic examination. The goal of this study was to observe the aortic valve, measure the annular diameter of the valve by ICE through a right-sided approach, and compare the results by ICE with those by transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE). We studied 18 patients (9 men, 9 women, aged 19 to 72 years) with various heart diseases, including 15 patients with mitral or aortic valvular disease. An imaging catheter was advanced through a long sheath into the outflow tract of the right ventricle. We obtained good longitudinal views of the aortic valve in all patients. Two of the 18 patients had poor image quality by TTE. The annular diameter by ICE correlated more closely with TEE than with TTE. In conclusion, right-sided ICE is a safe, simple, and useful procedure for observing the aortic valve during cardiac catheterization without additional discomfort in the patients. Right-sided ICE is superior to TTE in observing the aortic valve and measuring the annular diameter of the valve. The annular diameter can be measured by ICE as precisely as by TEE.

Adult↗
PubMed1999

Assessment of transmural coronary blood flow with intraoperative transesophageal color Doppler echocardiography during coronary revascularization.

Intraoperative color Doppler transesophageal echocardiography with a 4- to 7-MHz transducer was performed on 28 consecutive patients who underwent coronary artery bypass grafting to image and evaluate the transmural coronary blood flow before and after cardiopulmonary bypass. The transmural coronary flow was visualized in 26 (92.8%) of 28 patients in the inferior wall and in 13 (46.4%) of 28 patients in the lateral wall. The peak diastolic flow velocity of the transmural coronary artery in the inferior and lateral wall was significantly increased after coronary revascularization in patients with a successful bypass graft to the right coronary artery (from 34.0 +/- 19.7 to 64.9 +/- 30.9 cm/s, P <.001, n = 10) and to the left circumflex coronary artery (from 35.1 +/- 18.6 to 62.1 +/- 21.1 cm/s, P <.001, n = 10). No significant changes were observed in patients with no bypass graft to the right or left circumflex coronary artery. Coronary blood flow can be mapped and the velocity measured with Doppler transesophageal echocardiography with a high-frequency (4- to 7-MHz) transducer. Assessment of the transmural coronary flow may provide valuable information and aid in decision making during surgical revascularization.

Adult↗
PubMed1999

Effect of diltiazem on cardiac remodeling in rats assessed by Doppler echocardiography and mRNA expression.

The purpose of this study was to examine the effect of diltiazem on cardiac dysfunction and the change in cardiac gene expression after myocardial infarction in rats. On the first day after myocardial infarction, rats were randomly assigned to a diltiazem treatment (Dil, n = 7) or an untreated group (MI, n = 8). We then performed Doppler echocardiographic examinations on the rats and measured their hemodynamics at 4 weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. Diltiazem decreased the mean aortic pressure and heart rate. Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 18 +/- 2 mmHg and 5 +/- 1 mmHg (P < 0.01). Diltiazem reduced LVEDP to 14 +/- 1 mmHg (P < 0.05), but it did not change CVP. The weight of the right ventricle in MI was significantly larger than in the control rats (control, n = 7, 0.46 +/- 0.02 g/kg vs. MI, 0.81 +/- 0.06 g/kg; P < 0.01). The left ventricular end-diastolic dimension (LVDd) in MI increased to 8.8 +/- 0.3 mm (P < 0.01, control, 6.1 +/- 0.3 mm). Diltiazem prevented an increase in the weight of the right ventricle (0.69 +/- 0.03 g/kg, P < 0.05) and LVDd (7.7 +/- 0.2 mm, P < 0.05 to MI). The rats within MI showed systolic dysfunction, defined by a decreased ejection fraction (control, 67 +/- 2% vs. MI, 36 +/- 3%, P < 0.01), and diastolic dysfunction, defined by the E-wave deceleration rate (control, 13.4 +/- 1.6 m/s2 vs. MI, 30.4 +/- 3.4 m/s2; P < 0.01). Diltiazem significantly prevented systolic and diastolic dysfunction. The increases in beta-MHC, ANP, and collagen type I and III mRNAs in the noninfarcted left ventricle and right ventricle were significantly suppressed by treatment with diltiazem. alpha-Skeletal actin increased in MI, and alpha-skeletal actin was more increased with Dil. In conclusion, diltiazem prevents cardiac dysfunction and morphological change due to left ventricular remodeling after experimental myocardial infarction.

Actins↗
PubMed1999

Exercise four hour redistribution thallium-201 single photon emission computed tomography and exercise induced ST segment elevation in detecting the viable myocardium in patients with acute myocardial infarction.

OBJECTIVE: To investigate the specificity and sensitivity of the combination of redistribution in exercise thallium-201 single photon emission computed tomography (SPECT) and exercise induced ST elevation for detecting the viable myocardium in patients with acute myocardial infarction. DESIGN: 37 patients were studied within seven weeks of onset of Q wave myocardial infarction (anterior in 22, inferior in 15). All patients underwent exercise four hour redistribution thallium-201 SPECT and positron emission tomography using fluorine-18-fluorodeoxyglucose (FDG) and nitrogen-13 ammonia under fasting conditions. RESULTS: Sixteen patients showed exercise induced ST elevation >/= 1.5 mm, and 15 of these had increased FDG uptake in the infarct region. Eleven of 16 patients (10 of 11 patients with anterior infarctions) with irreversible thallium-201 defects and increased FDG uptake showed exercise induced ST elevation. The sensitivity, specificity, and predictive accuracy of redistribution, exercise induced ST segment elevation, or both for detecting increased FDG uptake were 82%, 75%, and 67% (94%, 75%, and 91% for anterior infarctions), respectively. CONCLUSIONS: In patients with acute Q wave myocardial infarction, the combination of redistribution in exercise thallium-201 SPECT and exercise induced ST elevation can detect the viable myocardium in the infarct region with high sensitivity and specificity, especially in patients with anterior infarctions.

Adult↗
PubMed1999

Administration of SIN-1 induces guinea pig airway hyperresponsiveness through inactivation of airway neutral endopeptidase.

BACKGROUND: Peroxynitrite plays an important role in the pathogenesis of airway inflammation. We have already found that peroxynitrite may contribute to decreased beta(2)-adrenoceptor responses in airway smooth muscle. However, it is not known whether peroxynitrite can alter neutral endopeptidase (EC 3.4.24.11; NEP) activity in the airways. This study was designed to determine whether peroxynitrite induces airway hyperresponsiveness to substance P (SP) and endothelin-1 (ET-1) through the inactivation of airway NEP. METHODS: We examined whether the administration of S-morpholinosydnonimine (SIN-1), a compound that releases peroxynitrite, increased bronchoconstrictor responses to SP and ET-1 in anesthetized guinea pigs. In addition, we assayed NEP activity in the airways of SIN-1-exposed guinea pigs. RESULTS: Though SIN-1 (10(-7) M) alone had no effect on pulmonary resistance, pretreatment with SIN-1 significantly enhanced SP- and ET-1-induced bronchoconstriction. Pretreatment with phosphoramidon, an NEP inhibitor, also enhanced SP- and ET-1-induced bronchoconstriction. However, simultaneous administration of phosphoramidon and SIN-1 had no additive effect on SP- and ET-1-induced bronchoconstriction. Peroxynitrite formation by SIN-1 was completely inhibited by N-acetylcysteine (NAC) and glutathione (GSH) in vitro, and pretreatment with NAC and GSH significantly reversed the potentiation by SIN-1 of SP-induced bronchoconstriction. In addition, the NEP activity of the trachea after SIN-1 exposure was significantly reduced compared to the level in control guinea pigs (solvent for SIN-1: 30.0+/-4.2 fmol.min(-1).mg tissue(-1); 10(-7) M SIN-1; 15.5+/-4.5 fmol.min(-1).mg tissue(-1), p<0.05). CONCLUSIONS: These findings suggest that peroxynitrite induces airway hyperresponsiveness to SP and ET-1 through the inactivation of airway NEP, and that peroxynitrite is an important mediator of the alterations in airway functions.

Animals↗
PubMed1999

Plasma endothelin-1 level in chronic obstructive pulmonary disease: relationship with natriuretic peptide.

BACKGROUND AND OBJECTIVE: Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by the vascular endothelium. The purpose of this study was to elucidate the pathophysiological role of ET-1 in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD). METHOD: We measured plasma ET-1 levels during right heart catheterization both at rest and during exercise on room air and while breathing oxygen in patients with COPD. In addition, we simultaneously measured plasma levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). RESULTS: Plasma ET-1 levels at rest were significantly higher in 21 patients with COPD than in 16 control subjects (p < 0.001). For COPD patients, there was no correlation between the plasma ET-1 level and pulmonary arterial pressure or pulmonary vascular resistance at rest. On the other hand, there was a significant negative correlation between plasma ET-1 level and mixed venous oxygen tension (r = -0. 503, p < 0.05). Also, the plasma ET-1 level was positively correlated with those of ANP (r = 0.540, p < 0.05) and BNP (r = 0. 533, p < 0.05) at baseline. Oxygen administration significantly decreased plasma ET-1 levels at rest (p < 0.05). Plasma ET-1 levels did not change significantly with exercise despite the progression of pulmonary hypertension and hypoxemia. In contrast, plasma ANP and BNP levels both increased markedly with exercise (p < 0.01). CONCLUSION: We conclude that in patients with COPD, the plasma ET-1 level is not affected by acute progression of pulmonary hypertension and hypoxemia during exercise, and persistent hypoxemia may be associated with an increase in the plasma ET-1 level. In addition, our findings suggest that ANP and BNP may modulate the pulmonary vascular tone by interacting with ET-1 in these patients.

Aged↗
PubMed1999

Effects of candesartan and cilazapril on rats with myocardial infarction assessed by echocardiography.

The purpose of this study was to compare the angiotensin II type 1 receptor antagonist candesartan cilexitil (candesartan) and the angiotensin-converting enzyme inhibitor cilazapril on cardiac function, assessed by Doppler echocardiography and cardiac gene expression associated with cardiac remodeling, in rats with myocardial infarction. Candesartan or cilazapril was administered after myocardial infarction. At 1 and 4 weeks after myocardial infarction, cardiac function and mRNA expression in noninfarcted myocardium were analyzed. Candesartan and cilazapril equally prevented increases in hypertrophy in noninfarcted myocardium, left ventricular dilatation, and ejection fraction at 4 weeks. The E-wave/A-wave velocity ratio and the rate of E-wave deceleration, measures of diastolic function, increased to 9.2+/-0.6 and 26.3+/-2. 6 m/s2 at 1 week after myocardial infarction. Candesartan and cilazapril, administered at a dose of 1 mg/kg per day, prevented increases in E-wave/A-wave velocity ratio and E-wave deceleration at 1 and 4 weeks. Candesartan and cilazapril significantly suppressed increased mRNA expression of beta-myosin heavy chain, alpha-skeletal actin, and atrial natriuretic peptide in noninfarcted ventricle at 1 and 4 weeks and expression of collagen I and III at 4 weeks to a similar extent. When given at a dose of 10 mg/kg per day, both candesartan and cilazapril prevented cardiac dysfunction and gene expression to the same extent as when given at 1 mg/kg per day. In conclusion, Doppler echocardiography showed that candesartan and cilazapril equally improved systolic and diastolic function and that ventricular remodeling accompanied modulation of cardiac gene expression.

Angiotensin Receptor Antagonists↗
PubMed1999

Guinea pig airway hyperresponsiveness induced by blockade of the angiotensin II type 1 receptor. Role for endogenous nitric oxide.

Losartan is the first angiotensin II type 1 (AT1) receptor antagonist to become available for the treatment of hypertension. However, recent reports have revealed several cases of losartan-induced bronchoconstriction. We investigated to determine the mechanism of losartan-induced bronchoconstriction, considering in particular the involvement of endogenous nitric oxide (NO). In this study, we examined the effects of losartan on airway obstruction and endogenous NO production using anesthetized guinea pigs and cultured airway epithelial cells. Five minutes after administration of angiotensin II (Ang II), the bronchoconstriction induced by acetylcholine was not changed. In contrast, Ang II in the presence of losartan caused a significant increase in the acetylcholine responsiveness. Pretreatment with L-N omega-nitroarginine-methylester (L-NAME) potentiated acetylcholine-induced bronchoconstriction 5 min after administration of Ang II, and L-arginine reversed this action of L-NAME on the acetylcholine responsiveness. Moreover, Ang II administration increased NO concentration in expired air (12.5 +/- 1.5 ppb for saline, 40 +/- 5 ppb for Ang II, p < 0.01), and losartan significantly inhibited Ang II-stimulated NO release (20 +/- 3.5 ppb) from guinea pig airway. In cultured airway epithelial cells, Ang II also increased NO release (160 +/- 25 nM), and the effect of this Ang II-induced NO release was significantly inhibited by pretreatment with losartan (25 +/- 8 nM, p < 0.01). These findings suggest that losartan-induced bronchoconstriction may result from inhibition of endogenous NO release in the airway.

Acetylcholine↗
PubMed1999

Inhibition of bronchoprotective effects of beta2-adrenoceptor agonists by peroxynitrite in guinea pig airways.

Peroxynitrite plays an important role in the pathogenesis of inflammatory diseases, including those affecting the lung. In inflamed airways, simultaneous cellular production of superoxide anion (.O2-) and nitric oxide (NO) may occur, potentially resulting in continuous formation of peroxynitrite. However, because peroxynitrite has a short half-life, its in vivo physiologic effects in the airways may not be sufficiently evaluated with a single administration. Accordingly, this study was designed to use 3-morpholinosydnonimine (SIN-1), a compound that releases peroxynitrite, to determine whether peroxynitrite could alter airway beta2-adrenoceptor (beta2-AR) function in anesthetized guinea pigs. Though SIN-1(10(-)7 M) alone had no effect on pulmonary resistance, pretreatment with SIN-1 significantly attenuated isoprenaline- and salbutamol-induced bronchoprotection against acetylcholine. Pretreatment with SIN-1 also attenuated forskolin-induced bronchoprotection. S-Nitroso-N-acetylpenicillamine (SNAP), a potent NO donor, did not have the same effect as SIN-1. N-Acetylcysteine and glutathione each significantly reversed the inhibitory effect of SIN-1 on isoprenaline-induced bronchoprotection in a dose-dependent manner. These striking findings suggested that peroxynitrite, but not NO, is an important mediator of alteration of beta2-AR function in airway smooth muscle. Additionally, the action of peroxynitrite seems to be directed either at adenylate cyclase activity or at effects downstream of such activity.

Acetylcholine↗
PubMed1999

A case of diffuse pulmonary arteriovenous fistula.

A 30-year-old Japanese woman was admitted to hospital for dyspnea. She had a history of corrective surgery for a large atrial septal defect and partial anomalous pulmonary venous drainage, which had produced cyanosis in her infancy. However, her cyanosis continued postoperatively. Angiography revealed a double inferior vena cava (IVC), with the left IVC connected with the hemiazygos vein and the right IVC with the left atrium through a very small orifice. Most of the blood from the 2 IVCs flowed into the superior vena cava via the distended azygos and hemiazygos veins. Pulmonary arteriography revealed no abnormal structures. Pulmonary arterial pressure was normal. There was marked pulmonary venous oxygen desaturation. Perfusion lung scintigraphy revealed multiple segmental perfusion defects. These findings suggested the presence of diffuse microscopic pulmonary arteriovenous fistulas bilaterally in the lungs. The patient appears to be the first reported adult case of microscopic and diffuse arteriovenous fistulas. Neither resection of the arteriovenous fistulas nor corrective surgery for the diversion was indicated, and heart-lung transplantation might be the only treatment able to relieve her dyspnea.

Adult↗
PubMed1999

Detection of a biphasic response of hibernating myocardium by dobutamine-stress electrocardiography-gated technetium-99m-tetrofosmin single photon emission computed tomography--a case report.

A woman with coronary artery disease underwent a new imaging technique: dobutamine-stress electrocardiography (ECG)-gated tetrofosmin-single photon emission computed tomography (SPECT). Dobutamine-stress ECG-gated tetrofosmin-SPECT with automatic left ventricular function analysis software programs detected improvement and a biphasic response of dysfunctional myocardium during dobutamine infusion, which suggested viable but hibernating myocardium. Dobutamine-stress ECG-gated tetrofosmin-SPECT with automatic left ventricular function analysis software programs has the potential to detect viable but dysfunctional myocardium with contractile reserve.

Aged↗