Transesophageal echocardiographic diagnosis of coronary sinus orifice atresia.
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Abnormalities, Multiple↗
Biomedical subjects
M Inada
Publications and source records attributed to M Inada.
Biplane transesophageal echocardiographic study of left coronary artery to right atrium fistula.
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Adult↗
Human chorionic gonadotropin induces c-myc mRNA expression via TSH receptor in FRTL-5 rat thyroid cells.
To elucidate the gene regulation of the thyroid-cell growth-promoting activity by human chorionic gonadotropin (hCG), we investigated the effect of hCG on c-myc proto-oncogene expression in cultured rat FRTL-5 cells by the Northern blot method. hCG induced c-myc mRNA expression, which peaked at 60-120 min. A dose-dependent increase in c-myc mRNA levels was also ascertained. In the presence of crude immunoglobulin G (IgG) from 2 patients with primary hypothyroidism who had blocking type TSH-receptor antibody, c-myc mRNA expressions induced by hCG were decreased to 82% and 62%, compared with that in the presence of normal IgG. The present results suggest that the expression of c-myc mRNA is a part of the molecular mechanism through which hCG regulates the proliferation of thyroid cells, and that hCG-induced c-myc mRNA expression is presumed to be mediated in part by TSH receptors.
Adenoma↗
Difference in the residual left ventricular pump function between anterior and inferior myocardial infarctions.
To evaluate the left ventricular regional ejection fraction (EF) of noninfarcted area in relation to the left ventricular end-diastolic volume (EDV) in patients with recent myocardial infarction (MI), 75 patients with Q-wave MI (anterior: 51 patients; inferior; 24 patients) were studied. The regional EF of noninfarcted area was obtained by radionuclide angiocardiography 4 weeks after the onset of MI and was used to estimate the left ventricular regional function of the noninfarcted area. Peak creatine kinase and QRS scores were not significantly different between anterior and inferior MI in each left ventricular EDV (EDV < or = 100, 101-139 and > or = 140 ml). Global EF and regional EF of noninfarcted area in anterior MI with left ventricular EDV > or = 140 ml was significantly lower than in those with EDV < or = 139 ml (p < 0.01), whereas there were no significant differences in global EF and regional EF of noninfarcted area in the three groups of left ventricular EDV in inferior MI. Thus, the effect of left ventricular EDV on regional EF of noninfarcted area and on the total cardiac performance was more important in anterior than in inferior MI, because a similar degree of left ventricular dilatation resulted in more severe derangements after anterior MI.
Adult↗
Thyrotropin and triiodothyronine regulate iodothyronine 5'-deiodinase messenger ribonucleic acid levels in FRTL-5 rat thyroid cells.
We investigated the regulation of type I iodothyronine 5'-deiodinase (5'-D) gene expression by TSH and T3 in FRTL-5 rat thyroid cells. Northern blot analysis revealed that these cells express a 5'-D messenger RNA (mRNA) species of 2.1 kilobases. Readdition of TSH to FRTL-5 cells, precultured in both thyroid hormones and TSH-depleted medium for 4 days, increased 5'-D mRNA levels, reaching a maximum (2.8-fold compared to control) after 12 h of TSH (10 microU/ml) stimulation. Dibutyryl cAMP (DBC) and forskolin mimicked this stimulatory effect of TSH on 5'-D mRNA levels. T3 also increased the 5'-D mRNA levels, reaching a maximum (2-fold compared to control) after 8 h of T3 (10(-9) M) stimulation. Addition of TSH (10 microU/ml) or DBC (1 mM) together with T3 (10(-9) M) further increased 5'-D mRNA levels, reaching a maximum (5-fold compared to control) after 12 h of stimulation. Examination of the rate of disappearance of 5'-D mRNA levels after inhibition of mRNA transcription by actinomycin-D revealed that neither TSH nor T3 significantly affected the rate of disappearance. Cycloheximide, a protein synthesis inhibitor, almost completely blocked the induction of 5'-D mRNA by TSH and DBC, but did not block the induction by T3. These results suggest that both TSH and T3 increase 5'-D mRNA levels probably by increasing transcription rate, and that TSH regulates it, in part via the second messenger cAMP, for which cycloheximide-sensitive de novo protein synthesis is required, whereas T3 does without requiring it.
Animals↗
Identification of a 27-kilodalton protein with the properties of type I iodothyronine 5'-deiodinase in human thyroid gland.
N-Bromoacetyl-[125I]T4(BrAc[125I]T4) was used as affinity label to identify type I 5'-deiodinase (5'-D) in human thyroid glands. Affinity labeled proteins were analyzed by autoradiography after sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Human thyroid microsomes labeled with BrAc[125I]T4 showed the most prominent radiolabeled band of protein at a mol wt of approximately 27,000 (p27). BrAc[125I]T4 incorporations into p27 were significantly higher in both Graves' and follicular adenomas than in normal thyroids. On the other hand, four cases out of five carcinomas were lower than the least value of normal thyroids. Furthermore, an excellent correlation was observed between 5'-D activities and quantities of p27 in all cases (r = 0.96; P less than 0.001). Labeling of p27 was strongly inhibited by preferred type I 5'-D substrate rT3, but to a lesser extent by poor substrate T4 or T3, and the type I 5'-D inhibitor, propylthiouracil and iopanoic acid, also inhibited the p27 labeling in normal and various diseases. In addition, the rate of enzyme inactivation by BrAcT4 equaled the rate of p27 labeling. These data suggest that p27 may be a type I 5'-D itself or at These data suggest that p27 may be a type I 5'-D itself or at least the substrate-binding subunit of this enzyme in human thyroid, and that both Graves' and follicular adenoma thyroids contain larger amounts of it, and papillary adenocarcinoma thyroids smaller than normal amounts.
Adenocarcinoma, Papillary↗
Transthyretin (prealbumin) in the pancreas and sera of newly diagnosed type I (insulin-dependent) diabetic patients.
We investigated transthyretin (TTR) in the pancreases and sera of 10 newly diagnosed type I diabetic patients by immunohistochemistry and nephelometry. In the type I diabetic pancreases, glucagon-positive A-cells showed strong immunoreactivity for TTR, the intensity and distribution pattern of which corresponded to those in normal subjects. Morphometric analysis revealed that the amount of strongly TTR-positive A-cells was not significantly different from that in normal subjects. On the contrary, insulin-positive B-cells, which normally show uneven and weak TTR immunoreactivity, decreased in number, and only a few residual B-cells showed faint immunoreactivity. Neither somatostatin cells nor pancreatic polypeptide cells were positive for TTR. The serum TTR concentration showed a significant decrease in type I diabetic patients compared with that in normal subjects (P less than 0.005). These data suggest that the synthesis or storage of TTR in A-cells is not affected, but that in B-cells is impaired in type I diabetes. The decrease in serum TTR might be one of the features of metabolic disorders in type I diabetes.
Adult↗
3,3',5'-Triiodothyronine inhibits collagen-induced human platelet aggregation.
To clarify further the activity of rT3, we examined the effect of rT3 on collagen-induced platelet activation as reflected by aggregation, serotonin release, and protein phosphorylation. rT3, T4, T3, and triiodothyroacetic acid inhibited collagen-induced platelet aggregation and serotonin release from platelets in a dose-dependent manner. However, thyronine did not inhibit collagen-induced platelet aggregation. The concentration at which rT3 inhibited by 50% collagen-induced platelet aggregation was 30 +/- 4 (mean +/- SE) mumol/L. rT3, T4, and T3 did not differ significantly in their abilities to inhibit platelet aggregation. Moreover, rT3 inhibited collagen-induced phosphorylation of the 20-kilodalton protein (myosin light chain) in platelets. In contrast, rT3 did not inhibit 12-O-tetradecanoylphorbol 13-acetate (TPA)- or thrombin-induced platelet aggregation and inhibited only minimally TPA-induced 40-kilodalton protein phosphorylation. These results suggest that rT3 inhibits collagen-induced platelet activation by inhibiting the activity of myosin light chain kinase and that it may be interesting to investigate some kinds of activity of rT3.
Blood Platelets↗
Diastolic time and left ventricular performance during one- and two-handed weight holding.
To evaluate the difference in DT and systolic time intervals during one-handed and two-handed weight holding with the same total load, the DT-heart rate relationship was studied in 12 patients and ten normal volunteers. Heart rate, blood pressure, and pressure-rate product were significantly higher in one-handed compared with two-handed weight-holding exercise in patients with MI. Although there were no significant differences in QS2 and DT between the two types of weight-holding exercise in normal volunteers, QS2 was significantly longer and DT was significantly shorter in one-handed compared with two-handed weight-holding exercise in patients with MI. Disproportionate shortening of DT with higher pressure-rate product during one-handed compared with two-handed weight-holding exercise can initiate an imbalance of myocardial oxygen supply and demand in patients with MI.
Analysis of Variance↗
Disturbance of pulmonary gas exchange in patients with right ventricular infarction.
To evaluate the difference in pulmonary gas exchange in patients with and without right ventricular infarction, 147 consecutive patients with their first inferior wall Q-wave acute myocardial infarction were studied. Thirty-nine patients (group 1) had electrocardiographic evidence of right ventricular infarction and it was absent in 108 patients (group 2). A significantly wider alveolar arterial oxygen difference and higher roentgenographic scores were observed in group 1 compared with group 2. Although there were no significant differences in pulmonary artery wedge pressure and colloid osmotic pressure between groups 1 and 2, mean right atrial pressure was significantly higher, while cardiac output and mixed venous oxygen saturation were lower in group 1 compared with group 2. Patients in group 1 had significantly more left ventricular segments with advanced asynergy and higher incidence of proximal right coronary artery lesions than those in group 2. Thus, our data suggest that disorder of pulmonary gas exchange in patients with right ventricular infarction may be explained by increased permeability of the alveolar capillary membrane secondary to larger extent of ischemic myocardium and by hemodynamic abnormalities associated with right ventricular infarction.
Catheterization, Swan-Ganz↗
Left ventricular function in myocardial infarction. Predictive value during negative low-level exercise three weeks postinfarction.
To evaluate whether the response of left ventricular pump function during low-level exercise in the early postinfarction period can anticipate its change during the first year after acute myocardial infarction (MI), global and regional ejection fractions (EF) were investigated using radionuclide angiography in 52 consecutive patients with negative predischarge exercise test. The changes in left ventricular EF and regional EF of the noninfarcted area during the early exercise test had a good linear relation with the changes during the first year after MI (r = 0.86, p less than 0.001 and r = 0.81, p less than 0.001, respectively). Our results indicate that the mobilization of the Frank-Starling mechanism and myocardial contractility were the important factors related to the change of left ventricular EF, and that the changes of left ventricular EF during exercise in the patient with a negative predischarge exercise test can predict the direction of change (concordant rise or fall) during the first year after MI.
Electrocardiography↗
Role of platelet-activating factor in pulmonary edema after coronary ligation in dogs.
To evaluate whether PAF is related to the precipitation of pulmonary edema after myocardial ischemia, we studied the effect of a specific PAF antagonist, CV-6209, on the extravascular lung water level measured by the thermal-dye double indicator dilution method, ETV, after coronary ligation in dogs. Eight dogs served as sham control animals (group 1). The proximal left anterior descending coronary artery was ligated for 45 min in eight dogs (group 2), and the coronary artery was ligated after pretreatment with CV-6209 (1 mg/kg) in eight dogs (group 3). The ETV increased significantly after coronary ligation in groups 2 and 3. The amount of increase in ETV in group 2 was significantly larger than in group 3. Thus, CV-6209 can prevent the accumulation of extravascular lung water after coronary ligation without producing changes in pulmonary vascular dynamics, indicating that PAF may play an important role in pulmonary edema after myocardial ischemia.
Animals↗
Residual left ventricular pump function after acute myocardial infarction in NIDDM patients.
OBJECTIVE: Left ventricular remodeling occurs immediately after MI, involving structural changes in noninfarcted segment. However, the residual left ventricular pump function in NIDDM patients after acute MI has not been clarified. The purpose of this study was to evaluate the difference in the process of left ventricular remodeling between NIDDM and nondiabetic patients. RESEARCH DESIGN AND METHODS: Left ventricular regional EF images obtained by radionuclide angiography were investigated in 20 NIDDM and 29 nondiabetic patients the 3rd wk after acute MI. RESULTS: Regional EF of the noninfarcted area and P/V had a significant hyperbolic relation with left ventricular EDV in both groups of patients. Despite no difference in the extent of myocardial necrosis and the number of coronary vessels diseased between NIDDM and nondiabetic patients, regional EF of the noninfarcted area and P/V were significantly lower when left ventricular EDV increased in NIDDM patients compared with nondiabetic patients. CONCLUSIONS: Pathogenetic changes of the residual myocardium associated with NIDDM may adversely influence the process of left ventricular remodeling after MI, especially in patients with increased left ventricular EDV.
Adult↗
[Clinical characteristics of pulmonary edema in patients with unstable angina].
To elucidate the clinical characteristics of pulmonary edema in unstable angina, 120 patients with unstable angina who admitted to the hospital within 6 hours after the onset of chest pain were studied. The criteria for the diagnosis of pulmonary edema included interstitial pulmonary edema and diffuse alveolar edema. Pulmonary edema was present in 24 patients. In these patients, the duration of chest pain was relatively longer, and the incidences of diabetes mellitus, emergency coronary revascularization and multiple-vessel coronary artery disease were higher than in those without pulmonary edema. In addition, in-hospital mortality rate in patients with pulmonary edema was higher than in those without it (21 vs 1%, p < 0.001), which is probably due to a large area of myocardial ischemia. For these patients, therefore, early diagnosis and appropriate therapy to save viable segments of the myocardium are mandatory.
Aged↗
[Left ventricular systolic time intervals during paroxysmal supraventricular tachycardia: the difference between A-V nodal re-entry and A-V re-entry].
In this study, the differences in hemodynamic changes during paroxysmal supraventricular tachycardia (PSVT) between A-V nodal re-entry and A-V re-entry were evaluated. In 8 patients with A-V nodal re-entrant tachycardia and 10 with A-V re-entrant tachycardia, electrophysiological studies were performed to measure systolic time intervals (pre-ejection period: PEP, ejection time: ET, PEP/ET ratio: PEP/ET). These measurements were obtained in the control state (atrial pacing at 90/min) and during PSVT with simultaneous recordings of electrocardiogram and femoral arterial pulse tracing. During PSVT, there was no difference in the heart rate between the 2 groups, but ventriculo-atrial conduction time was shorter in A-V nodal re-entry than in A-V re-entry. There was a marked fall in the ET and an increase in PEP/ET in all the patients when PSVT was induced. PEP increased significantly in A-V nodal re-entry, but did not change in A-V re-entry. This resulted in a greater increase in the PEP/ET suggesting a greater deterioration of the hemodynamic consequences in A-V nodal re-entry than in A-V re-ent y. Thus, the hemodynamic changes of PSVT differ between these 2 types of re-entrant circuits, which are mainly influenced by the ventriculo-atrial conduction time.
Adult↗
[The use of a Swan-Ganz catheter with a fast-response thermistor for the measurement of right ventricular performance during anesthetic management of pheochromocytoma].
We used a Swan-Ganz catheter with a fast-response thermistor to measure the right ventricular ejection fraction (RVEF) during the anesthetic management of two patients with epinephrine-dominant pheochromocytomas. Pre-operatively, one patient received alpha adrenergic blocking agents (prazocine, doxazocine) to control the blood pressure but the other patient did not receive any agents. In the latter patient who did not receive alpha adrenergic blocking agents, right ventricular function was depressed post-operatively in the recovery room. The importance of preoperative preparation with alpha adrenergic blocking agents was confirmed by the reductions in RVEF and RVEDVI (right ventricular end-diastolic volume index) after resection of the tumor. Not only left heart monitoring but also right heart monitoring with RVEF and RVEDVI are recommended for the proper management of a patient with pheochromocytoma.
Adrenal Gland Neoplasms↗
[Report of a case with aortic regurgitation in progressive systemic sclerosis].
Aortic valve lesions in progressive systemic sclerosis (PSS) are very uncommon. To our knowledge, aortic regurgitation (AR) associated with PSS has not been reported previously. We would like to report the case of a 58-year-old woman who had PSS with AR due to Raynaud's symptom, fever, positive ANA, accelerated ESR, and diastolic blowing murmur along the left sternal border. After treatment with adreno-cortico steroid and an immunosuppressive agent, the patient improved serologically and symptomatically. However, she was later admitted to our hospital again due to heart failure with progressive AR. She died of refractory heart failure with severe AR and tricuspid regurgitation (TR). The former was caused by aortic cusp lesions and the latter by pulmonary hypertension. An autopsy confirmed the diagnosis of PSS, which was found to have involved the heart, lungs and pancreas. Vasculitis with infiltration and fibrotic changes were noted in these organs. Moreover, there were fibrotic thickenings and shortenings in the aortic cusps with cell infiltration. There were no indications of rheumatic disease. These results suggest that the cause of our patient's aortic valve disease may have been PSS vasculitis.
Aortic Valve Insufficiency↗
Age-related changes in aortic elasticity determined by gated radionuclide angiography in patients with systemic hypertension or healed myocardial infarcts and in normal subjects.
We estimated the aortic volume elasticity (Ve), an index of aortic stiffness, using gated radionuclide angiography, and investigated age-related changes in aortic elasticity in 22 normal control subjects, 30 hypertensive patients and 36 patients with old myocardial infarction. Ve elasticity was calculated noninvasively as a ratio of the pressure change (dP) and the percent volume change (dV/Vo) determined by radionuclide angiography [Ve = dP/(dV/Vo)]. dV/Vo was calculated from the maximal and minimal counts in the aortic arch [dV/Vo = (maximum - minimum)/minimum]. Ve increased significantly with age in normal control subjects (r = 0.62, p less than 0.001), hypertensive patients (r = 0.60, p less than 0.001) and patients with old infarcts (r = 0.59, p less than 0.001). The age-related increase in Ve was significantly greater in hypertensive patients, and that for patients with old myocardial infarcts tended to be greater than in control subjects. Thus, hypertension accelerates the decrease in aortic elasticity with aging. The greater decrease in aortic elasticity resulted in a significant age-related increase in pulse pressure in patients with hypertension and old myocardial infarction.
Adult↗