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Biomedical subjects

Katsufumi Mizushige

Publications and source records attributed to Katsufumi Mizushige.

At least 19 recordsLinked to original sources
PubMed2006

An antioxidant treatment potentially protects myocardial energy metabolism by regulating uncoupling protein 2 expression in a chronic beta-adrenergic stimulation rat model.

Excessive beta-adrenergic stimulation causes cardiac toxicity, which also contributes to cardiac oxidative stress. Although uncoupling protein 2 (UCP2), a member of the mitochondrial inner membrane carrier family, can regulate energy efficiency and oxidative stress in mitochondria, little data exist regarding interactions between UCP2 expression and beta-adrenergic stimulation induced cardiac oxidative damage. We investigated whether chronic beta-adrenergic stimulation induces myocardial energy metabolism abnormality via oxidative stress, including any role of UCP2. We also examined whether 3-methyl-1-phenyl-2-pyrazolin-5-one (MIC-186; edaravone), a potent free radical scavenger, has cardioprotective effects against beta-adrenergic stimulation. Male Sprague-Dawley rats received isoproterenol (1.2 mg/kg/day) subcutaneously or/and edaravone (30 mg/kg/day) orally. Isoproterenol increased the heart/body weight ratio, accompanied by an increase in the level of myocardial thiobarbituric acid reactive substances (TBARS) and a decreased phosphocreatine (PCr) to adenosine triphosphate (ATP) ratio. Isoproterenol also markedly increased expressions of UCP2 mRNA (1.74 fold vs. non-isoproterenol) and protein (1.93 fold vs. non-isoproterenol). Edaravone had no apparent effect in hypertrophic responses, but significantly prevented both increases in TBARS and decreases in the PCr/ATP ratio. Edaravone also prevented increases in UCP2 mRNA (0.76 fold vs. isoproterenol) and protein (0.62 fold vs. isoproterenol) expressions against isoproterenol administration. Our results suggest that chronic beta-adrenergic stimulation induces myocardial energy inefficiency via excessive oxidative stress. The antioxidant effect of edaravone has potential to improve energy metabolism abnormalities against beta-adrenergic stimulation. Adequate regulation of UCP2 expression through artificial reduction of oxidative stress may play an important role in protection of the myocardial energy metabolism.

Adrenergic beta-Agonists↗
PubMed2006

Contribution of reactive oxygen species to the pathogenesis of left ventricular failure in Dahl salt-sensitive hypertensive rats: effects of angiotensin II blockade.

OBJECTIVE: We investigated the contribution of reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase-dependent reactive oxygen species (ROS) generation to the pathogenesis of diastolic heart failure (DHF) in Dahl salt-sensitive (DS) hypertensive rats, with the aim of testing our hypothesis that the cardioprotective effects of angiotensin II (Ang II) blockade are provided by the suppression of this pathway. METHODS: DS rats were maintained on high (H: 8.0% NaCl) or low (L: 0.3% NaCl) salt diets from age 7 to 17 weeks. DS/H rats were also treated with candesartan cilexetil (10 mg/kg per day, orally) or a superoxide dismutase mimetic, tempol (3 mmol/l in drinking water) from age 7 to 17 weeks. RESULTS: DS/H rats represented hypertension, left ventricular (LV) relaxation abnormality and myocardial stiffening with preserved systolic heart function. As compared with DS/L rats, DS/H rats showed higher levels of transforming growth factor-beta (TGF-beta), connective tissue growth factor (CTGF), p22phox and gp91phox mRNA expression, NADPH oxidase activity and thiobarbituric acid-reactive substance (TBARS) contents in LV tissues. Gene expression of uncoupling protein-2 (UCP-2), an inner mitochondrial membrane proton transporter, was also 2.8 +/- 0.5-fold higher. In DS/H rats, treatment with candesartan did not alter blood pressure, but resulted in a marked improvement of the hemodynamic deterioration; these therapeutic effects were accompanied by decreases in myocardial NADPH oxidase activity, TBARS contents and the expression of TGF-beta, CTGF, p22phox, gp91phox and UCP-2. Similar therapeutic effects were provided by treatment with tempol in DS/H rats. CONCLUSIONS: Our data suggest that NADPH oxidase-mediated ROS production contributes to the pathogenesis of DHF in DS hypertensive rats, and that the cardioprotective effects of AngII blockade are, at least partially, mediated through the suppression of this pathway.

Angiotensin II↗
PubMed2006

The effects of olprinone, a phosphodiesterase 3 inhibitor, on systemic and cerebral circulation.

Olprinone, a phosphodiesterase (PDE) 3 inhibitor, is used to treat heart failure due to its positive inotropic and vasodilative effects. Selective inhibition of the PDE 3 isozyme increases intracellular adenosine 3;5;-cyclic monophosphate and enhances Ca(2+) influx into cardiac muscle cells. The most significant advantage of PDE 3 inhibitors is their ability not only to enhance myocardial contraction, but to reduce, through vasodilatory action, the stress to which the heart is subjected. In peripheral vessels, the decrease of cytosolic free Ca(2+) induces the vasorelaxation of vascular smooth muscle cells. In this way, olprinone reduces mean aortic and pulmonary artery pressures. Additionally, olprinone exerts differential vasodilatory effects on peripheral vessels in each organ, based on the differences in the distribution of PDE 3 among the organs. With respect to the cerebral circulation, olprinone augments blood flow in the cerebral cortex through direct vasodilatory effects on small cerebral arteries or arterioles. Olprinone increases hepatosplanchnic blood flow and improves oxygen supply. While long-term therapy with PDE 3 inhibitors in patients with chronic heart failure may accelerate the progress of the underlying disease and provoke serious ventricular arrhythmia, olprinone shows good potential for short-term treatment in patients who have experienced severe heart failure or patients who have undergone cardiac surgery.

Adult↗
PubMed2005

Association of uncoupling protein-2 expression with increased reactive oxygen species in residual myocardium of the enlarged left ventricle after myocardial infarction.

Left ventricular (LV) dilatation following myocardial infarction (MI) is a major determinant of the patient's prognosis, and myocardial energy metabolism may play a key role in LV remodeling. We aimed to investigate the relative timing of LV dilatation to LV function, myocardial energy regulation by uncoupling protein (UCP)-2, and cellular damage in the noninfarct zone. Myocardial infarction was produced in Sprague-Dawley rats by ligation of the coronary artery. The LV end-diastolic dimension (mm) increased (8.9+/-0.3 vs 6.8+/-0.8 in sham-operated rats, P<0.01) in association with elevation of the LV end-diastolic pressure (mmHg) (18+/-5 vs 6+/-2 in sham-operated rats) at 1 week following the ligation. At 4 weeks, the UCP-2 expression (180% of that in sham-operated rats) and LV end-diastolic dimension increased further (11.1+/-0.5, P<0.01) but there was no change in the LV end-diastolic pressure. The mechanisms for LV dilatation were quite different between the early and late stages after MI. In the late stage, augmentation of UCP-2 expression in the noninfarct zone may be related to the LV dilatation. Further examinations regarding the possibility of the protective role of UCP-2 are needed.

Animals↗
PubMed2005

Spatial distribution of right ventricular perfusion abnormalities following acute right coronary artery occlusion: a study by myocardial contrast echocardiography and blue dye staining.

OBJECTIVE: Although echocardiography is used for diagnosing right ventricular (RV) infarction produced by right coronary artery (RCA) occlusion, there has been no data on the spatial distribution of RV perfusion abnormalities following acute RCA occlusion. We examined this distribution by myocardial contrast echocardiography (MCE) and blue dye staining in canine models. METHODS: The RCA was occluded in 10 open-chest dogs. MCE was performed with 0.27 g/min Levovist infusion by harmonic power Doppler with electrocardiogram gated intermittent triggered imaging at baseline and at 90 min after RCA occlusion. The opacification defects were assessed at the basal, middle, and apical levels of the RV free wall by short-axis view. The extent of the risk area of the occluded RCA, expressed as a percentage of the RV free wall, was measured at each level by injecting blue dye at the end of the experiments. In 10 other dogs, the left anterior descending coronary artery (LAD) was occluded by ligating the proximal portion of the LAD to examine the territory of the LAD on the same levels of the RV free wall by injecting blue dye. RESULTS: Although patchy opacification defects accompanying RV dilation were observed at the basal and middle levels during RCA occlusion, no apical defects were observed in any dogs by MCE. The risk area of the occluded RCA, as delineated by blue dye, was larger in the basal than apical level of the RV free wall in all 10 dogs (basal: 79 +/- 9%; middle: 48 +/- 14%; apical: 3 +/- 6%, p < 0.0001). The risk area of the occluded LAD (basal: 17 +/- 7%; middle: 12 +/- 6%; apical: 6 +/- 6%) was smaller than the risk area of the occluded RCA at the basal and middle levels of the RV free wall (p < 0.0001), and no significant difference was observed at the apical level. CONCLUSIONS: RV perfusion abnormalities produced by RCA occlusion are larger in the basal than apical level of the RV free wall. This finding elucidates the spatial distribution of the territory of the RCA on the RV free wall, and may help in identifying and assessing RV ischemia by echocardiography in humans. Moreover, the data in the current study indicate that RV infarction may be produced by occlusion of the coronary arteries except RCA, because the territory of the LAD on the RV free wall is clearly delineated.

Animals↗
PubMed2004

Effects of pravastatin on progression of glucose intolerance and cardiovascular remodeling in a type II diabetes model.

OBJECTIVES: We examined the effects of early treatment with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor pravastatin on the progression of glucose intolerance and cardiovascular remodeling in a model of spontaneously developing type II diabetes mellitus (DM), the Otsuka Long-Evans Tokushima Fatty (OLETF) rats. BACKGROUND: Clinical trials showed that pravastatin prevented new-onset DM in hypercholesterolemic patients, and that it was effective in prevention of cardiovascular events in diabetics. METHODS: The OLETF rats were treated with pravastatin (100 mg/kg/day) from 5 weeks of age and compared with age-matched untreated OLETF rats and normal Long-Evans Tokushima Otsuka (LETO) rats on serial oral glucose tolerance tests (OGTT) and Doppler echocardiography and on histopathological/biochemical analyses of the heart at 30 weeks. RESULTS: The OGTT revealed that 40% and 89% of untreated OLETF rats were diabetic at 20 and 30 weeks, respectively, but 0% and only 30%, respectively, were diabetic in the treated OLETF. Left ventricular diastolic function was found impaired from 20 weeks in untreated OLETF but remained normal in the treated-OLETF. The wall-to-lumen ratio and perivascular fibrosis of coronary arteries were increased in untreated-OLETF but were limited in the treated-OLETF at 30 weeks. Moreover, cardiac expressions of a fibrogenic growth factor, transforming growth factor-beta1 (TGF-beta1), and a proinflammatory chemokine, monocyte chemoattractant protein-1 (MCP-1), were increased in untreated-OLETF. However, in the treated-OLETF, overexpressions of TGF-beta1 and MCP-1 were attenuated, which was associated with overexpression of endothelial nitric oxide synthase (eNOS) (2.5-fold of control LETO). CONCLUSIONS: Early pravastatin treatment prevented cardiovascular remodeling in the spontaneous DM model by retarding the progression of glucose intolerance, overexpressing cardiac eNOS, and inhibiting overexpressions of fibrogenic/proinflammatory cytokines.

Animals↗
PubMed2004

Latent abnormal fatty acid metabolism in apparently normal perfusion during stress in patients with restenosis after coronary angioplasty: assessment by exercise stress thallium-201 and iodine-123-labeled 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid-dual myocardial single-photon emission computed tomography.

Restenosis is a major problem in patients undergoing coronary angioplasty. Reduced uptake of iodine-123-labeled 15-(p-iodophenyl)-3-R,S-methylpentadecanoic acid (I-BMIPP-123) relatively to thallium-201 (Tl-201) has been attributed to the metabolic damage in the myocardium in patients with coronary artery disease. Therefore, we performed exercise stress Tl-201 and I-BMIPP-123 dual myocardial single-photon emission computed tomography (SPECT) to detect coronary restenosis in 48 patients (35 men and 13 women, mean age 66 +/- 8 years), followed by coronary angiography at follow-up. Patients were divided into 2 groups: those with (n = 24) and without (n = 24) restenosis. Redistribution of Tl-201 was seen more frequently in the restenosis group than in no-restenosis group (58% [14 of 24] vs 8% [2 of 24], p <0.05). Five of 10 patients (50%) with restenosis but without Tl-201 redistribution had Tl-201/I-BMIPP-123 discrepancy during stress. In patients without restenosis, only 1 patient had this discrepancy during stress. Incorporation of Tl-201/I-BMIPP-123 uptake discrepancy during stress significantly improved the sensitivity (58% [14 of 24] to 79% [19 of 24]) with preserved specificity (92% [22 of 24] to 88% [21 of 24]). Exercise stress Tl-201 and I-BMIPP-123 dual myocardial SPECT revealed that latent abnormal fatty acid metabolism may exist in apparently normal perfusion during stress in patients with restenosis after coronary angioplasty. Use of I-BMIPP-123 together with Tl-201 during stress SPECT substantially improved the diagnostic accuracy of restenosis based on Tl-201 redistribution (from 75% to 83%).

Aged↗
PubMed2004

Leukocyte-targeted myocardial contrast echocardiography can assess the degree of acute allograft rejection in a rat cardiac transplantation model.

BACKGROUND: Repetitive endomyocardial biopsies are necessary to monitor the effects of immunosuppressants after cardiac transplantation. Contrast ultrasound with microbubble targeting of leukocytes detects acute leukocyte infiltration. We examined whether leukocyte-targeted myocardial contrast echocardiography (MCE) could provide for the quantitative assessment of acute cardiac rejection. METHODS AND RESULTS: Hearts from Brown Norway rats or Lewis rats were transplanted into other Brown Norway rats. Isografts and groups of allografts either untreated or treated with cyclosporin A (CsA) at a low dose (3 mg x kg(-1) x d(-1)) or high dose (10 mg x kg(-1) x d(-1)) from 3 days before transplantation were compared at posttransplantation day 3. Echocardiography-derived left ventricular wall thickening was comparable among the 4 groups. Myocardial blood flow assessed with MCE, relating pulsing intervals with signal intensity (SI), was slightly decreased only in untreated allografts. However, myocardial SI (in gray levels) obtained after a 10-minute period allowing microbubble-leukocyte interactions after contrast injection exhibited a clear gradient in these groups (12+/-2 in untreated allografts, 9+/-5 in allografts treated with low-dose CsA, 6+/-3 in allografts treated with high-dose CsA, and 2+/-1 in isografts, P<0.001). The pattern of difference in SI among the groups agreed well with that in ED-1-positive cell (macrophage) count (25+/-7, 12+/-4, 5+/-3, and 1+/-0 cells per high-power field, respectively, P<0.001), which correlated with CD3-positive cell (T lymphocyte) count (33+/-5, 22+/-5, 9+/-4, and 1+/-0 cells per high-power field, respectively, P<0.001). CONCLUSIONS: Leukocyte-targeted MCE can noninvasively assess the degree of rejection in transplanted hearts by directly revealing the magnitude of intramyocardial infiltration of macrophages and T lymphocytes.

Acute Disease↗
PubMed2004

Interaction with leukocytes: phospholipid-stabilized versus albumin-shell microbubbles.

PURPOSE: To confirm that BR14 microbubbles (MBs) can be phagocytosed by activated leukocytes, to determine their stability after phagocytosis, and to evaluate how such characteristics influence the fate of neutrophils containing MBs after insonation. MATERIALS AND METHODS: BR14 and human albumin MBs (2 x 10(7)/mL) were incubated with activated human neutrophils (2 x 10(6)/mL) to allow phagocytosis. Deflation rate of the phagocytosed MBs after pulsed insonation (one burst per second for 5 seconds) at 1.8 MHz with peak negative pressure of -540 kPa or -1,340 kPa, lactate dehydrogenase (LDH) leakage, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling stain-positive cell count after insonation were compared between the two agents. RESULTS: At -540 kPa, phagocytosed MBs remained nearly unchanged for both agents after insonation. At -1,340 kPa, although human albumin MBs were disrupted on the first or second burst, BR14 MBs remained undisrupted. After -540-kPa insonation, a similar number of apoptotic cells appeared in neutrophils containing human albumin and BR14 MBs. At -540 kPa, LDH leakage was limited in human albumin MBs and BR14 MBs. At -1,340 kPa, LDH leakage was significantly increased in human albumin MBs and BR14 MBs (P <.01, both vs -540 kPa). Apoptotic cells were significantly decreased in human albumin MBs and BR14 MBs (P <.01, both vs -540 kPa). LDH leakage was lower and apoptotic cell count was greater in BR14 MB-containing neutrophils than in human albumin MB-containing neutrophils (both P <.01). CONCLUSION: Compared with human albumin MBs, BR14 MBs were more stable after phagocytosis with insonation. This stability is associated with less disruption and greater induction of apoptosis in leukocytes after relatively high-pressure insonation in the range for diagnostic use.

Adult↗
PubMed2004

Usefulness of brain natriuretic peptide as a marker for separating cardiac and noncardiac causes of syncope.

We retrospectively evaluated the feasibility of measuring brain natriuretic peptide to identify cardiac syncope in 148 consecutive patients with syncope. Sixty-one patients with cardiac syncope were identified. A cut-off value of 40 pg/ml was used to determine the cardiac causes of syncope; the sensitivity and specificity for identification of cardiac syncope were 82% and 92%, respectively. Thus, measurement of brain natriuretic peptide concentrations may help confirm cardiac causes of syncope, and merits consideration for incorporation into the algorithm used to diagnose syncope.

Aged↗
PubMed2004

The cerebrovascular dilatation effects of olprinone, a phosphodiesterase III inhibitor, in comparison with acetazolamide--a pilot study.

To examine the effects of olprinone, a phosphodiesterase III inhibitor, on cerebral blood flow (CBF), we compared the effects of olprinone on CBF to that of acetazolamide. Using technetium-99m-ethyl cysteinate dimer (99mTc-ECD) brain SPECT, we measured regional CBF (rCBF) at 33 sites, including 16 right and left pairs of non-infarct cerebral cortexes, in seven stroke patients (66.0+/-3.2 years) in a resting state and 15 min after the administration of acetazolamide. Within 1 week, rCBF at each site was measured 15 min after the initiation of olprinone infusion. Resting rCBF showed a significant negative correlation with the change in rCBF (DeltaCBF) during olprinone infusion (r = -0.43, P=0.013), but no significant correlation was seen following acetazolamide administration. The difference in rCBF between the right and left cortex increased more following acetazolamide administration (14.1+/-10.9 ml/(min 100 g)) than during olprinone infusion (5.4+/-4.8 ml/(min 100 g), P=0.013). The rCBF at four regions of interest (ROI) with low-resting CBF (< 49 ml/(min 100 g)) further decreased following the administration of acetazolamide. The vasodilatory effects of olprinone are dependent on resting CBF instead of on the intracerebral steal phenomenon that occurs with acetazolamide.

Acetazolamide↗
PubMed2004

Potential pitfalls of visualization of myocardial perfusion by myocardial contrast echocardiography with harmonic gray scale B-mode and power Doppler imaging.

OBJECTIVE: The present study compared the regional variation of myocardial signal intensity in visualizing myocardial perfusion by myocardial contrast echocardiography (MCE) between harmonic gray scale and power Doppler imaging. METHODS: MCE was performed in 12 patients by electrocardiographic (ECG)-gated intermittent triggered MCE with harmonic gray scale and power Doppler imaging following slow intravenous injection of 0.5 ml contrast agent (Optison). The interval between the ECG triggers (pulsing interval) was increased from every heart beat (1:1) to every 2 (1:2), 4 (1:4), and 8 (1:8) cardiac cycles to allow incremental microbubble (contrast agent) replenishment. The MCE images were recorded when attenuation produced by the left ventricular cavity was minimal. The background-subtracted videointensity was measured in 7 segments in an apical 4-chamber view: 3 (apical, mid, and basal) septal segments, 3 (apical, mid, and basal) lateral segments, and 1 apex segment (apical cap). RESULTS: The background-subtracted videointensity for each segment was greater with the power Doppler than the gray scale imaging (p < 0.01). With the gray scale imaging, the background-subtracted videointensity in the basal septal segment demonstrated a negative value at all pulsing intervals, and the value (-9 +/- 13) was significantly lower than that (22 +/- 20) in the apical lateral segment at a pulsing interval of 1:8 (p < 0.01). With power Doppler imaging, the background-subtracted videointensity was high even in the basal septal segment (112 +/- 33), and no significant difference was observed among each segment. CONCLUSIONS: The findings indicate that quantitative assessment of myocardial perfusion based upon background-subtracted video-intensity may be difficult in the far field with harmonic gray scale imaging although the attenuation is not apparent by visual analysis. Harmonic power Doppler is more sensitive for detecting basilar perfusion in the far field compared with harmonic gray scale imaging.

Aged↗
PubMed2004

A comparison of video and digital data in the assessment of myocardial perfusion abnormalities by myocardial contrast echocardiography.

OBJECTIVE: The objective of the present study was to compare the digital and video data of myocardial contrast echocardiography (MCE) to assess altered myocardial blood flow produced by graded coronary stenoses. METHODS: Three grades of left anterior descending (LAD) coronary artery stenosis and occlusion were created in eight open-chest canine models. MCE was performed with BR1 infusion by harmonic power Doppler with ECG gated intermittent triggered imaging at pulsing intervals ranging from 1:1 to 1:10. For images that were recorded simultaneously on both a videotape (video data) and an optical disk (digital data), myocardial signal intensity in the LAD region was plotted vs. pulsing intervals and was fitted to an exponential function: y = A(1 - e(-bt)), where A is the peak plateau signal intensity, and b is the rate of signal intensity rise for quantification of myocardial blood flow. RESULTS: Both values for A and b progressively decreased with a greater level of stenosis. The correlation of A with myocardial blood flow (determined by use of fluorescent microspheres) was weak with digital data (r = 0.38, p = 0.037), and was insignificant with video data (r = 0.16, p = 0.38). The correlation of b with microsphere-derived myocardial blood flow was better than that of A with both video and digital data, and was similar between the two kinds of data (video: r = 0.69, p < 0.0001; digital: r = 0.68, p < 0.0001). CONCLUSIONS: Video and digital MCE data are equivalent in their ability to quantify altered myocardial blood flow produced by graded coronary stenoses.

Analysis of Variance↗
PubMed2003

Comparison of magnetic resonance imaging and transesophageal echocardiography in detection of thrombus in the left atrial appendage.

BACKGROUND AND PURPOSE: A noninvasive technique of visualizing the left atrial appendage (LAA) and its thrombus in patients with atrial fibrillation would be of great interest. This study examined the utility of MRI for the assessment of thrombus in the LAA. METHODS: We evaluated 50 subjects with nonrheumatic continuous atrial fibrillation and a history of cardioembolic stroke. Each patient received an MRI and a transesophageal echocardiography (TEE) on the same day for thrombus detection in the LAA. Both double- and triple-inversion recovery sequences were used for the MRI evaluations. RESULTS: In all subjects, the LAA was readily visualized with MRI. High-intensity masses in the LAA were clearly distinguishable from the LAA wall in the triple-inversion recovery sequences. Concordance between detection of high-intensity mass with MRI and thrombus with TEE was high: no mass (MRI), no thrombus (TEE), 31 patients; mass (MRI), thrombus (TEE), 16 patients; and mass (MRI), no thrombus (TEE), 3 patients (overall kappa=0.876, SE=0.068). CONCLUSIONS: MRI is a noninvasive and reproducible modality for thrombus detection in the LAA of patients with nonrheumatic continuous atrial fibrillation and previous cardioembolic stroke.

Aged↗
PubMed2003

Quantitative assessment of coronary stenosis by harmonic power Doppler with a simple pulsing sequence and vasodilator stress in patients.

OBJECTIVES: We examined whether myocardial contrast echocardiography (MCE) with harmonic power Doppler (HPD) employing a simple ultrasound pulsing sequence enables estimation of the severity of coronary artery stenosis in patients. BACKGROUND: Contrast intensity (CI) during MCE with intravenous microbubble infusion is dependent on the myocardial blood flow velocity (MBFV) and pulsing interval (PI). METHODS: Based on an in vitro experiment, we devised the MBFV index calculated as the reciprocal of the magnitude of CI decay produced by abrupt PI shortening during intermittent imaging. In 68 coronary artery territories from 49 patients, myocardial HPD images were acquired during intravenous infusion of Levovist, while the long PI with 1:10 electrocardiographic gating was shortened to 1:1, both at baseline and during adenosine triphosphate infusion. The MBFV index in each coronary territory and MBFV reserve as the ratio between hyperemia and baseline were compared with the severity of corresponding coronary artery stenosis assessed by quantitative coronary angiography (QCA) or by pressure guide wire as the fractional flow reserve (FFR). RESULTS: Both the MCE-derived MBFV index during hyperemia and MBFV reserve exhibited significant negative correlations with the QCA-derived stenosis severity (r = -0.56 and r = -0.64, respectively). The MBFV reserve positively correlated with FFR (r = 0.89). By combining the cutoff values of the MBFV index during hyperemia and MBFV reserve, > or =75% of stenoses defined by QCA were determined, with a sensitivity of 77.3%, specificity of 93.4%, and accuracy of 88.3%. CONCLUSIONS: Shortening of PI during intravenous MCE with intermittent HPD imaging under vasodilator stress enables assessment of coronary artery stenoses in patients.

Adult↗
PubMed2003

Assessment of right ventricular perfusion after right coronary artery occlusion by myocardial contrast echocardiography.

OBJECTIVES: The purpose of this study was to examine the ability of myocardial contrast echocardiography (MCE) to assess right ventricular (RV) perfusion. BACKGROUND: Although MCE can readily assess left ventricular perfusion abnormalities, there are no data regarding the ability to assess RV perfusion abnormalities. METHODS: The right coronary artery (RCA) was occluded in 10 open-chest dogs. Myocardial contrast echocardiography was performed with 0.27 g/min Levovist infusion by harmonic power Doppler with electrocardiographically gated intermittent triggered imaging at pulsing intervals ranging from 1:1 to 1:20 at baseline and 90 min after RCA occlusion. Video-intensity of the RV wall was plotted against pulsing intervals and was fitted to an exponential function: y = A(1-exp(-bt)), where A is the plateau video-intensity and b is the rate of video-intensity rise. Myocardial contrast echocardiography and microsphere-derived myocardial blood flow (MBF) measurements were performed at baseline and 90 min after RCA occlusion. RESULTS: Because the severity of RV perfusion abnormalities assessed by MBF varied during RCA occlusion, diverse grades of patchy opacification defects were observed by MCE. The RV wall thickness decreased, and the RV dimension increased, after RCA occlusion in each dog. The correlation of occlusion to baseline MBF ratios in the RV wall was closer to the ratio of b (r = 0.897, p = 0.0004) than A (r = 0.767, p = 0.0097) and was the closest to the ratio of Axb (r = 0.935, p < 0.0001). CONCLUSIONS: The RCA occlusion is manifested by RV wall thinning and dilation as well as by perfusion abnormalities consisting of patchy opacification defects by MCE. Myocardial contrast echocardiography-derived refilling parameters can be applied to assess RV perfusion abnormalities produced by RCA occlusion.

Animals↗
PubMed2003

Potentiation of C-type natriuretic peptide with ultrasound and microbubbles to prevent neointimal formation after vascular injury in rats.

OBJECTIVES: Long-term intravenous infusion of high-dose C-type natriuretic peptide (CNP) is known to prevent neointimal formation after vascular injury. Ultrasound (US) irradiation during microbubbles (MBs) infusion (US/MBs) has been used for local delivery of bioactive agents. We examined whether short-term infusion of CNP could also inhibit neointimal development and whether combined US/MBs treatment at the beginning of the CNP infusion could enhance its effect. METHODS: In the rat carotid artery-balloon injury model, the intima/media area (I/M) ratio 14 days after injury was compared among various short-term post-injury treatments. For combined US/MBs, a commercial echocardiograph (1.8 MHz, mechanical index 1.0) and albumin-coated octafluoropropane gas MBs were used. RESULTS: Infusion of high-dose CNP (1.0 microg/kg/min) immediately after injury for only 24 h successfully reduced the I/M ratio (0.18+/-0.05) to 18% of the ratio in control rats (1.00+/-0.13) that underwent only balloon injury. Although low-dose CNP (0.1 microg/kg/min for 24 h) alone was not effective in reducing the I/M ratio (0.83+/-0.18), combined US/MBs treatment for the first 80 min of the infusion markedly reduced the I/M ratio (0.17+/-0.07), which persisted until 28 days after injury (0.16+/-0.04). CONCLUSIONS: The effects of CNP on the events occurring early after arterial injury may be important in preventing subsequent neointimal development. Thus, intravenous infusion of CNP with US/MBs at its initiation may provide a clinically feasible anti-restenosis therapy applicable immediately after vascular interventions.

Analysis of Variance↗