Biomedical subjects

Masakazu Kohno

Publications and source records attributed to Masakazu Kohno.

71 records · Page 4Linked to original sources

PubMed2003

Improvement of cerebral blood flow by olprinone, a phosphodiesterase-3 inhibitor, in mild heart failure.

Cerebral blood flow (CBF) is reduced in heart failure (HF). For the treatment of acute HF, a phosphodiesterase-3 inhibitor, olprinone (OL), yields an increase in myocardial contractility and a decrease in arterial afterload. During a 15-min intravenous infusion of OL (0.2 microg/kg/min), regional CBF at 6 sites of each cerebral cortex was examined using technetium-99m-ethylcysteinate dimer brain SPECT in 18 HF patients and 7 age-matched normal subjects. The baseline CBF was significantly reduced in HF (43.0 +/- 3.9 ml/min/100 g) compared to that in normal subjects (48.0 +/- 4.6 ml/min/100 g, p < 0.01). The baseline CBF showed a significant negative correlation with the increase in CBF during the OL infusion in HF (r = -0.38, p < 0.01) and normal subjects (r = -0.65, p < 0.01). The percent increase in CBF was significantly greater in HF (13.7%) than in normal subjects (9.8%, p < 0.046). In patients with HF, the CBF of the cerebral cortex was decreased, but was increased by OL infusion.

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PubMed2003

Renal sympathetic nerve responses to tempol in spontaneously hypertensive rats.

Recent studies have implicated a contribution of oxidative stress to the development of hypertension. Studies were performed to determine the effects of the superoxide dismutase (SOD) mimetic 4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl (Tempol) on vascular superoxide production and renal sympathetic nerve activity (RSNA) in anesthetized Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Compared with WKY rats (n=6), SHR showed a doubled vascular superoxide production, which was normalized by treatment with Tempol (3 mmol/L, n=7). In WKY rats (n=6), Tempol (30 mg/kg IV) significantly decreased mean arterial pressure (MAP) from 108+/-5 to 88+/-6 mm Hg and HR from 304+/-9 to 282+/-6 beats/min. In SHR (n=6), Tempol significantly decreased MAP from 166+/-4 to 123+/-9 mm Hg and HR from 380+/-7 to 329+/-12 beats/min. Furthermore, Tempol significantly decreased RSNA in both WKY rats and SHR. On the basis of group comparisons, the percentage decreases in MAP (-28+/-4%), HR (-16+/-3%) and integrated RSNA (-63+/-6%) in SHR were significantly greater than in WKY rats (-17+/-3%, -9+/-2%, and -30+/-4%, respectively). In SHR, changes in integrated RSNA were highly correlated with changes in MAP (r=0.85, P<0.0001) during administration of Tempol (3, 10, and 30 mg/kg IV). In both WKY rats and SHR (n=4, respectively), intracerebroventricular injection of Tempol (300 micro g/1 micro L) did not alter MAP, HR, or RSNA. Intravenous administration of a SOD inhibitor, diethyldithio-carbamic acid (30 mg/kg), significantly increased MAP, HR, and integrated RSNA in both WKY rats and SHR (n=6, respectively). These results suggest that augmented superoxide production contributes to the development of hypertension through activation of the sympathetic nervous system.

Animals↗

PubMed2002

Correlation of functional and structural alterations of the coronary arterioles during development of type II diabetes mellitus in rats.

OBJECTIVE: Cardiac complications in diabetes mellitus (DM) are frequently ascribed to microangiopathy. Therefore, we sought to directly correlate the serial changes in coronary arterial function with the extent of coronary arteriolar remodeling in a model spontaneously developing type II DM. METHODS: Otsuka Long-Evans Tokushima Fatty (OLETF) rats and control Long-Evans Tokushima Otsuka (LETO) rats were used. At 5, 15 and 30 weeks of age, ten rats in each group were subjected to systemic and coronary hemodynamic measurements using the colored microsphere technique before and during maximal coronary hyperemia and histological assessment with Azan-Mallory stain of the coronary arterioles. RESULTS: As early as 15 weeks of age, at which time fasting plasma glucose concentration remained normal, OLETF rats exhibited a lower coronary flow reserve and a greater coronary vascular resistance during hyperemia than did LETO rats. On histomorphometry, OLETF rats exhibited a greater wall-to-lumen ratio and a greater degree of perivascular fibrosis of arterioles at 15 weeks of age and thereafter, both of which exhibited a significant correlation with the minimal coronary vascular resistance. CONCLUSIONS: The degree of functional deterioration in coronary circulation was directly correlated with the severity of coronary arteriolar structural remodeling during the development of microangiopathy in early stage of DM.

Animals↗

PubMed2002

Vascular proliferation and transforming growth factor-beta expression in pre- and early stage of diabetes mellitus in Otsuka Long-Evans Tokushima fatty rats.

The roles of transforming growth factor (TGF)-beta 1 in vascular proliferation, atherosclerosis, and plaque still remain controversial. TGF-beta 1 has been previously reported to inhibit the proliferation and migration of vascular smooth muscle cells and endothelial cells, in vitro. On the other hand, administration or transgenic overexpression of TGF-beta 1 enhances extracellular matrix synthesis and cellular hyperplasia of the intima and media in the normal artery and injured artery in vivo. We evaluated the correlation of arterial proliferation with plasma levels of TGF-beta 1 and TGF-beta receptor type II, respectively, in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a new strain of spontaneous non-insulin-dependent diabetes mellitus (NIDDM) models. OLETF rats (n=30) were divided into three groups aged 5,15, and 30 weeks. Long-Evans Tokushima Otsuka (LETO) rats (n=30) were used as age-matched non-diabetic controls. Plasma TGF-beta1 and insulin were determined by enzyme-linked immunosorbent assay. Immunoreactive TGF-beta receptor type II antigen was detected by immunohistochemistry on the thoracic artery. Arterial media area was measured microscopically. Oral glucose tolerance test was performed to examine the stage of diabetes mellitus. The thoracic aorta wall section area increased significantly from the age of 15 weeks in OLETF rats, versus LETO rats. In both OLETF and LETO rats, plasma TGF-beta 1 increased significantly from the age of 15 weeks. In OLETF rats, plasma TGF-beta 1 increased significantly over that in LETO rats (P<0.001). Furthermore, TGF-beta receptor type II was detected on aortic wall as strong signals in OLETF rats, but only weakly in LETO rats. OLETF rats showed hyperinsulinemia and insulin resistance from the age of 15 weeks. With oral glucose tolerance test, from the age of 15 weeks, the high glucose level in OLETF rats was prolonged to 2 h after loading, and the insulin levels at both fasting and after loading were significantly higher than those of LETO rats (P<0.001). There are significant linear relations between plasma TGF-beta 1 antigen and aorta wall section area, and plasma TGF-beta 1 antigen and fasting insulin level (P<0.001, respectively). We found that plasma TGF-beta 1 and vascular TGF-beta type II receptors existed to a greater extent in pre- and early stages of diabetes mellitus (DM) in OLETF rats compared with LETO rats. The greater extent of each in OLETF rats was associated with hyperinsulinemia and/or vascular thickening.

Aging↗

PubMed2002

Myocardial blood flow measurements in rats with simple pulsing contrast echocardiography.

Relationship between contrast intensity and ultrasound (US) pulsing interval has been utilized to quantify myocardial blood flow (MBF) during myocardial contrast echocardiography (MCE). We tested if an MCE method employing a simple pulsing sequence during intravenous contrast infusion has the ability to quantify MBF in rats. We performed MCE in 17 rats using a 5- to 12-MHz broadband transducer during microbubble infusion via the femoral vein. Acoustic density (AD) from the anterior wall of the left ventricle imaged in the short axis plane was plotted against the frame number after shortening the pulsing interval (PI) from 1:20 to 1:1 end-systolic ECG gating. The relation between AD and frame number was fitted to a decay function. The rate of the AD decay was decreased during dipyridamole infusion, but was increased by causing coronary stenosis. The AD during long PI imaging remained unchanged during the interventions. Estimated MBF by MCE after correction by heart rate exhibited a close correlation (r = 0.83) with the present "gold standard" of colored microsphere-derived MBF. Thus, the decay rate of the contrast intensity obtained with the high-frequency transducer after abrupt shortening of PI during intravenous microbubble infusion may provide for noninvasive measurement of MBF in rats.

Animals↗

PubMed2002

Carotid turbulent flow observed by convergent color Doppler flowmetry in silent cerebral infarction.

AIM: A newly developed convergent color Doppler (CCD) was used for evaluating the possible relationship of the flow dynamics of the internal carotid artery to silent cerebral infarction (SCI). METHODS: In 108 patients (65+/-8 years) with stroke risk factors, the CCD simultaneously images information, on both flow direction and Doppler signal energy. The relation between turbulent flow and the incidence of brain lesions of SCI as identified by magnetic resonance imaging was investigated in 212 vessels, excluding four occluded vessels. Percent area stenosis was measured as (vessel area - lumen area)/(vessel area) on cross-sectional echo image of stenotic site. RESULTS: Incidence of turbulent flow in SCI patients with 50-70% or 70-90% stenosis was higher (76.5 or 59.1%) than that in non-SCI patients (17.4 or 33.3%, both p < 0.0001). CONCLUSION: Non-invasive assessment of flow dynamics by CCD imaging can be useful for proposing the early stages of brain damage even in patients free from neurological deficits.

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PubMed2002

Improvement of aortic wall distensibility and reduction of oxidative stress by pioglitazone in pre-diabetic stage of Otsuka Long-Evans Tokushima fatty rats.

We tested the hypothesis that pioglitazone (insulin sensitizer) reduces oxidative stress and improves aortic wall distensibility in the pre-diabetic stage of Otsuka Long-Evans Tokushima Fatty rats, type 2 diabetes mellitus (DM) model. 20 DM and 9 nonDM male rats were divided into 3 groups: treated-DM, untreated-DM, and untreated-nonDM. Pioglitazone (0.01%) was mixed in chow in the treated group from 15 to 20 weeks of age. At baseline and 20 weeks, plasma malondialdehyde (MDA) was measured. At 20 weeks, intravascular ultrasound images and aortic pressure were simultaneously recorded. Stiffness parameter beta was calculated from the cyclic variations of aortic diameter and pressure. From an excised thoracic aorta, aortic wall collagen was measured, and the morphology was histopathologically evaluated by hematoxylin-eosin staining. At 20 weeks, MDA (nmol/ml) in treated-DM (2.3 +/- 0.3) was lower than in untreated-DM (3.2 +/- 0.6, p < 0.0001). beta in treated-DM (0.53 +/- 0.21) was smaller than that in untreated-DM (0.88 +/- 0.26, p = 0.0067). Aortic wall collagen (mg/100 mg dry weight) did not decrease in treated-DM (22.3 +/- 3.2 vs untreated-DM : 19.6 +/- 4.7). Lumen/medial area ratio (L/M) increased in treated-DM (2.79 +/- 0.40 vs untreated-DM : 2.22 +/- 0.20, p = 0.0041, untreated-nonDM : 2.25 +/- 0.55, p = 0.0075). MDA was significantly correlated with beta (r = 0.65, p = 0.0005) or L/M (r = -0.60, p = 0.0008). Pioglitazone may reduce oxidative stress and contribute to improvement of aortic wall stiffness without decrease in collagen content at an early prediabetic stage of type 2 DM.

Age Factors↗

PubMed2002

Assessment of myocardial viability in prior myocardial infarction by intravenous bolus microbubble injection: a new time domain index to estimate regional relative myocardial blood volume.

We tested whether the duration of myocardial opacification by harmonic power Doppler imaging after intravenous bolus microbubble injection (with a definition of "the end of opacification") would reflect the remaining vascular bed in infarcted segments. In 28 patients with previous myocardial infarction and 20 control patients, we performed harmonic power Doppler imaging after intravenous bolus injection of 1.5 g of Levovist. Using multiframe trigger mode in which 4 consecutive frames were imaged at every sixth end systole, which formed 1 "burst," we recorded anterior/septal and inferior/posterior walls separately on the center of each apical view with individual boluses. The duration of segmental opacification was measured as the number of "bursts" in which color signals persisted until the fourth frame. The duration was similar between the anterior/septal and inferior/posterior walls (13 +/- 3 vs 13 +/- 3 bursts, not significant) in the control group. In myocardial infarction patients, the duration was significantly shorter in the infarcted than in the control segments (6 +/- 6 vs 14 +/- 3 bursts, P < .001) and their ratio and difference exhibited significant correlations (r = 0.82, P < .001 and r = 0.91, P < .001, respectively) with the activity ratio on thallium Tl 201 single-photon emission computed tomography at rest. Thus, the duration of opacification by harmonic power Doppler imaging after intravenous bolus microbubble injection, the measurement of which was standardized by using multiframe trigger mode, may be useful in assessing regional myocardial viability in patients with previous myocardial infarction.

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PubMed2002

Role of adenosine A(1) receptor in angiotensin II- and norepinephrine-induced renal vasoconstriction.

We investigated the contributions of adenosine A(1) receptors to angiotensin II- and norepinephrine-induced renal vasoconstriction. Intrarenal administrations of angiotensin II (3, 10, and 30 ng) or norepinephrine (100 and 500 ng) produced dose-dependent renal vasoconstriction in anesthetized dogs. Under resting conditions, angiotensin II (30 ng) and norepinephrine (500 ng) significantly decreased renal blood flow by -43 +/- 3 and -19 +/- 2%, respectively (n = 21). Intra-arterial infusion of adenosine (5 microg/kg/min) significantly augmented renal blood flow responses to both angiotensin II and norepinephrine (-64 +/- 4 and -45 +/- 14%, n = 7). Renal blood flow responses to angiotensin II and norepinephrine were also augmented by inhibition of cellular uptake of adenosine with dipyridamole (10 microg/kg/min, n = 6). Blockade of adenosine A(1) receptors with 8-(noradamantan-3-yl)-1,3-dipropylxanthine (KW-3902; 10 microg/kg/min) did not alter basal renal blood flow but significantly attenuated angiotensin II- and norepinephrine-induced renal vasoconstriction (-34 +/- 6 and -9 +/- 3%, n = 7). Furthermore, KW-3902 completely prevented augmentation of renal blood flow responses to angiotensin II and norepinephrine produced by adenosine or dipyridamole (n = 7 and 6, respectively). Administrations of angiotensin II (30 ng) or norepinephrine (500 ng) into the common carotid artery significantly decreased carotid blood flow by -20 +/- 5 and -41 +/- 10%, respectively; however, neither adenosine (5 microg/kg/min) nor KW-3902 (10 microg/kg/min) affected the carotid blood flow responses to angiotensin II and norepinephrine (n = 5, respectively). Adenosine concentrations in dialysates were not significantly changed by administrations of angiotensin II (from 19 +/- 3 to 24 +/- 4 nM, n = 6) or norepinephrine (from 16 +/- 3 to 19 +/- 3 nM, n = 6). These results suggest that basal interstitial adenosine levels influence both angiotensin II and norepinephrine-induced vasoconstriction via A(1) receptors in the kidney but not in the area drained by the common carotid artery. The responses of adenosine to angiotensin II- and norepinephrine-induced renal vasoconstriction may not be mediated through de novo intrarenal adenosine accumulation due to angiotensin II- and norepinephrine-induced renal vasoconstriction.

Adenosine↗

PubMed2002

Perindopril effect on uncoupling protein and energy metabolism in failing rat hearts.

Uncoupling proteins, inner mitochondrial membrane proton transporters, are important for regulating myocardial energy efficiency. We investigated the effects of the ACE inhibitor perindopril on cardiac performance, myocardial energy efficiency, and uncoupling protein expression in an aortic regurgitation rat model. Twenty male Sprague-Dawley rats, in which aortic regurgitation was produced, were divided into untreated and perindopril-treated (5 mg x kg(-1) x d(-1)) rats. The treatments were initiated 3 days after operation. Ten control rats were sham-operated. Measurements of blood pressure and echocardiography were repeated before and 100 days after operation (endpoint). Left ventricular uncoupling protein-2 expression, creatine phosphate, and adenosine triphosphate were measured at endpoint. In perindopril-treated rats, systolic and diastolic blood pressure decreased after treatment (92+/-4/65+/-2 mm Hg). At endpoint, left ventricular end-diastolic dimension in untreated (10.7+/-0.2 mm) and treated rats (9.2+/-0.2 mm) was increased, and fractional shortening was reduced in untreated rats (28+/-1%) but did not change in treated rats (36+/-2%). Uncoupling protein-2 mRNA expression increased in untreated rats (3.7-fold) and was suppressed by perindopril (1.5-fold). The creatine phosphate was reduced in untreated rats (10.6+/-0.7 micro mol/g) but not in treated rats (15.9+/-2.0 micro mol/g). In the chronic stage of aortic regurgitation, perindopril improved cardiac performance and myocardial energy efficiency, in which the suppression of uncoupling protein-2 may play an important role.

Adenosine Triphosphate↗

PubMed2002

Adrenomedullin inhibits doxorubicin-induced cultured rat cardiac myocyte apoptosis via a cAMP-dependent mechanism.

We previously reported that adrenomedullin produced by cardiac myocytes acts as a local modulator in some cardiac disorders. However, the role of adrenomedullin (AM) in cardiomyocyte apoptosis remains to be clarified. The present study investigated the effect of AM on doxorubicin-induced cardiac myocyte apoptosis. Doxorubicin increased the number of cells with pyknotic nuclei and lactate dehydrogenase release, and AM dose-dependently (10(-10)-10(-8)6 M) inhibited these increases produced by doxorubicin. Treatment with AM also suppressed doxorubicin-induced DNA fragmentation and caspase-3 activation. 8-Bromo-cAMP, a cAMP analog, mimicked these antiapoptotic effects of AM. An AM/calcitonin gene-related peptide (CGRP) receptor antagonist CGRP-(8-37) and a protein kinase A inhibitor H89 attenuated the antiapoptotic effect of AM. CGRP-(8-37) and H89 had no apoptotic effect alone, but accelerated doxorubicin-induced apoptosis. Under serum-free conditions, AM secretion into the culture medium and expression of AM mRNA were significantly increased after treatment with doxorubicin. Hydrogen peroxide scavenger catalase and antioxidant N-acetyl-L-cysteine inhibited the doxorubicin-mediated increase in AM secretion and its gene expression. These results indicate that AM inhibits doxorubicin-induced cardiac myocyte apoptosis through a cAMP-dependent mechanism and suggest that augmented production of AM by doxorubicin has an endogenous antiapoptotic effect. AM, as an autocrine factor, may play a protective role against cardiomyocyte injury by doxorubicin.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2002

Inhibition of migration and proliferation of rat vascular smooth muscle cells by a new HMG-CoA reductase inhibitor, pitavastatin.

The migration and proliferation of vascular smooth muscle cells (SMCs) are known to play roles in the pathogenesis of atherosclerosis. Therapy with a reductase inhibitor of 3-hydroxy-3 methylglutaryl coenzyme A (HMG-CoA) ("statin") produces significant alterations in various SMC functions. The objectives of the present study were to determine whether pitavastatin, a new chemically synthesized and powerful statin, can affect angiotensin II (Ang II)- and platelet-derived growth factor (PDGF)-induced migration and proliferation of cultured rat vascular SMCs. The effect of pitavastatin on cell viability was also examined in these cells. Migration was evaluated by the Boyden's chamber method using microchemotaxis chambers. As expected, Ang II and PDGF BB potently stimulated cell migration in a concentration-dependent manner. Pitavastatin significantly inhibited Ang II (10(-6) mol/l)-induced migration at the concentrations of 10(-8) and 10(-7) mol/l. Pitavastatin also inhibited PDGF BB (1 ng/ml)-induced migration at concentrations between 10(-9) and 10(-8) mol/l in a relatively concentration-dependent manner. This statin modestly but significantly inhibited Ang II (10(-6) mol/l)- and PDGF BB (1 ng/ml)-induced DNA synthesis at concentrations between 10(-9) and 10(-7) mol/l. In addition, pitavastatin clearly inhibited Ang II (10(-6) mol/l)- and PDGF BB (1 ng/ml)-induced increases of cell number at concentrations between 10(-9) and 10(-7) mol/l. Pitavastatin did not affect lactate dehydrogenase release from these cells at the concentrations used in this experiment. In a trypan blue exclusion test, dead cells stained with trypan blue were not found 24 h after treatment with 10(-9), 10(-8) or 10(-7) mol/l of pitavastatin. These findings suggest that pitavastatin suppresses the migration and proliferation stimulated by Ang II and PDGF BB without affecting cell viability. Pitavastatin may exert an anti-atherogenic effect, in part, through these mechanisms.

Animals↗

PubMed2002

A new method for evaluation of split renal cortical blood flow with contrast echography.

The recent development of contrast echography has made renal enhancement possible through an intravenous injection of microbubble-based contrast. In animal models, tissue perfusion can be quantified using contrast echography by measurement of the rate at which microbubbles replenish tissue after their ultrasound-induced destruction. Our purpose in this study was to evaluate renal blood flow with contrast echography in humans. To increase the sensitivity for microbubbles, we used a combination of power Doppler harmonic and intermittent imaging. The pulsing interval (PI) was changed from 10 cardiac cycles to 1 cardiac cycle during an intravenous infusion of the contrast agent, and alterations in the intensity of the renal cortex were represented as a decline ratio (DR). In 24 patients with various renal diseases, we were able to observe all 48 kidneys with adequate enhancement of the renal cortex. At PI of 10 cardiac cycles, the enhancement was homogeneous and strong, while, obviously, changing PI from 10 to 1 cardiac cycles caused a decline of enhancement. An excellent correlation was found between DR using contrast echography and renal plasma flow determined by clearance and radionuclide measurements. An excellent correlation was found between the DR values determined by contrast echography and the renal plasma flow values determined using clearance and radionuclide measurements. These results suggest that DR may be useful for evaluation of both total and split renal blood flow. Thus the contrast echographic method presented here could succeed in assessing renal cortical blood flow less invasively than conventional methods in humans.

Adolescent↗

PubMed2002

A role of oxidative stress-generated eicosanoid in the progression of arteriosclerosis in type 2 diabetes mellitus model rats.

Diabetes mellitus (DM) is a well-established risk factor of cardiovascular diseases. We investigated the mechanism of the progression of arteriosclerosis in DM, focusing on the role of oxidative stress and insulin resistance in vivo. Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, an experimental model of type 2 DM, were assigned to 3 groups, based on supplementation with vitamin E (VE) or troglitazone (TR), a VE-derived agent which improves insulin-resistance. At 36 weeks, plasma and aortic tissue 8-iso-PGF2alpha contents, a vascular proliferating eicosanoid produced in vivo by oxidative stress, were measured by EIA. TGF-beta1 and TGF-beta1 receptor II were immunohistochemically analyzed. Histopathologically, medial area and the nuclear number of smooth muscle cells of the aorta were measured. The tissue 8-iso-PGF2alpha content (pg/g tissue) was significantly decreased by either VE or TR in the aorta (untreated-OLETF, 15,332+/-3,254 vs. TR-treated-OLETF, 7,092+/-1,992 or VE-treated-OLETF, 5,394+/-836, both p<0.01), but that in plasma decreased by only VE. VE and TR improved the increased the level of the actual medial area and the number of smooth muscle cells. The expression of TGF-beta1 was reduced, but TGF-beta1 receptor II was not. 8-iso-PGF2alpha may play an important role in the progression of arteriosclerosis. Antioxidant treatment may promise significant clinical benefits in the early diabetic stage.

Animals↗

PubMedDate not supplied

Assessment of adenosine-induced coronary steal in the setting of coronary occlusion based on the extent of opacification defects by myocardial contrast echocardiography.

The authors examined the ability of real-time myocardial contrast echocardiography (MCE) to assess adenosine-induced coronary steal in the setting of coronary artery occlusion. The left anterior descending (LAD) coronary artery was occluded in 8 open-chest dogs. Real-time MCE was performed during LAD occlusion, and the extent of opacification defects from MCE was measured without and with adenosine infusion. Microsphere-derived myocardial blood flow (MBF) was measured in the LAD and left circumflex (LCx) coronary artery beds, and the LAD/LCx ratio of MBF was calculated. The LAD/LCx ratio of MBF decreased in response to adenosine administration (without adenosine: 0.66, with adenosine: 0.43, p < 0.01). The extent of opacification defects from MCE increased in response to adenosine administration (without adenosine: 18%, with adenosine: 22%, p < 0.01). Thus, real-time MCE allows for the detection of adenosine-induced coronary steal as changes in the extent of opacification defects in the setting of occlusion of 1 coronary artery accompanying another normally patent coronary artery.

Adenosine↗

PubMedDate not supplied

Contrast transesophageal echocardiography in diagnosing congenital enlargement of the right atrium--a case report.

Congenital malformation of the right atrium or the coronary sinus is rare, and cases are classified into 1 of the following 4 categories: (1) congenital enlargement of right atrium, (2) single diverticulum, (3) multiple diverticula of the right atrium, and (4) diverticulum of the coronary sinus. This report presents a 63-year-old man with cardiomegaly and no chest symptoms. A chest radiograph revealed an enlarged cardiac silhouette with a prominent right heart border. Although a transesophageal echocardiography revealed marked enlargement of the right atrium, neither further anomaly nor massive regurgitation was observed. The systolic pulmonary artery pressure derived from the peak velocity of mild tricuspid regurgitation was 38 mm Hg. Secondary enlargement of the right atrium due to atrial septal defect or pulmonary venous connection anomaly was deemed negligible by use of transesophageal contrast echocardiography, and primary enlargement of the right atrium was confirmed. Transesophageal echocardiography using ultrasound contrast was determined to be feasible for diagnosing congenital malformation of the right atrium.

Cardiomegaly↗

PubMedDate not supplied

Left atrial thrombosis in achalasia--a case report.

An 81-year-old woman came to the clinic with aphasia and gait disturbance. A transthoracic echocardiogram showed left atrial (LA) thrombus at the posterobasal site, which was compressed by a large mass with high echo intensity. A chest computed tomography scan revealed dilatation of the esophagus, compressing the LA from the posterior side. An endoscopy showed a bolus and much foulness in the distended esophagus, which were immediately eliminated by an endoscopic procedure. The LA thrombus, as shown by transesophageal echocardiography, spontaneously resolved without any neurologic signs. The authors assumed that the dilatated esophagus compressed the LA, and this may have produced the abnormal flow dynamics in the LA. The injury of endocardial surface produced by the distension or turbulent flow, in addition to dehydration, may have augmented a coagulability in the LA.

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