Possible role for atrial natriuretic peptide in polyuria associated with paroxysmal atrial arrhythmias.
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Biomedical subjects
Publications and source records attributed to J Fujii.
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Segmental wall motion abnormalities are common in patients with myocarditis. Left ventricular (LV) regional wall motion was assessed in six patients with myocarditis by two-dimensional echocardiography. Some of our patients demonstrated regional thinning of the wall, similar to myocardial infarction. Therefore, segmental wall motion abnormalities with or without regional wall thinning detected by two-dimensional echocardiography cannot be used to differentiate myocarditis from coronary artery disease. Nevertheless, echocardiography can be performed repeatedly and is useful for evaluating the severity of myocarditis by assessing LV regional wall motion abnormalities, changes in LV wall thickness and cardiac pump function during the course of the disease.
Inflow characteristics of left and right ventricular filling were assessed in 40 patients with myocardial infarction and in 10 normal subjects by pulsed Doppler echocardiography. Patients with myocardial infarction were subdivided into four groups, focusing on the involvement of right ventricular and septal branches of the coronary arteries. Group I consisted of 11 patients with anterior infarction who showed an obstructive lesion of the proximal left anterior descending branch involving the first septal perforator with a patent right coronary artery. Group II consisted of 10 patients with inferior infarction who showed an obstructive lesion of the proximal right coronary artery involving the right ventricular branch. Group III consisted of 12 patients with both anterior and inferior infarction who showed obstructive lesions of both the proximal left anterior descending branch and the right coronary artery involving the right ventricular branch. Group IV consisted of seven patients with lateral infarction who showed an obstructive lesion of the diagonal branch or branches of the circumflex coronary artery with a patent left anterior descending branch and right coronary artery. Three measurements were performed from the transmitral and transtricuspidal inflow velocity patterns to assess the left and right ventricular diastolic behaviors. These measurements were: acceleration half-time, deceleration half-time of early diastolic rapid inflow, and the ratio of the peak velocity of early diastolic rapid inflow to that of the late diastolic inflow due to the atrial contraction. Impaired diastolic filling of the left ventricle compensated by enhanced left atrial contraction was observed in patients with myocardial infarction from groups I, II, III and IV.(ABSTRACT TRUNCATED AT 250 WORDS)
Plasma levels of thromboxane B2 (TXB2) and 6-keto PGF1 alpha in the blood samples taken at the coronary sinus and ascending aorta from twenty-one Japanese patients with variant angina and twenty with effort angina were measured by radioimmunoassay, the objective being to search for the contribution of prostanoids in coronary spasm. The data were compared with data on thirteen subjects free from coronary artery diseases. In coronary sinus blood, plasma TXB2 in patients with effort angina exhibited statistically significant high levels, as compared with data in the controls. These with variant angina also had high levels, albeit without a statistically significant difference. Eight patients with variant angina and for whom the coronary angiogram showed more than 50% of narrowing had statistically significant high levels of TXB2, and the other thirteen with variant angina and normal coronaries or less than 50% of narrowing had the same plasma levels of TXB2 as the controls. In contrast to TXB2, the plasma levels of 6-keto PGF1 alpha in both coronary sinus and aortic blood of patients with variant angina were very low, as compared with normal controls. Statistically significant low levels of 6-keto PGF1 alpha were noted in the coronary sinus blood of patients with variant angina with normal coronaries and in the aortic blood of those with variant angina, as compared with data on the normal controls. Neither ergonovine test nor spontaneous attacks in patients with variant angina revealed characteristic changes in levels of TXB2 and 6-keto PGF1 alpha in the coronary sinus. These data suggest that high levels of TXB2 in patients with atherosclerotic coronaries may be one factor leading to spasm, while low levels of PGI2 may be a contributing factor.
To elucidate the contribution of prostanoids in coronary spasm, plasma levels of thromboxane B2 (TXB2) and 6-keto PGF1 alpha at the coronary sinus and ascending aorta in 21 patients with variant angina were measured, as compared with findings in 20 with effort angina and 13 subjects with normal coronaries. In the coronary sinus blood, plasma TXB2 in patients with effort angina exhibited statistically significant high levels, as compared with data in the controls. On the contrary, the data obtained from patients with variant angina were not statistically significant. However, eight patients whose coronary angiogram revealed more than 50% of coronary stenoses had statistically significant high levels of TXB2 and other patients with normal coronaries or less than 50% of narrowing showed almost the same levels of TXB2 as the controls. In contrast to TXB2, the plasma levels of 6-keto PGF1 alpha in patients with variant angina were very low in both groups with variant angina. These data suggest that high levels of TXB2 observed in patients with atherosclerotic coronaries may be an accelerating factor while low levels of prostacyclin may be an essential factor leading to spasm. HLA analysis of 23 patients with variant angina was performed to search for genetic factors, under the hypothesis that such may contribute to the low levels in prostacyclin. This preliminary study revealed statistically significant high frequencies of Bw52 and B-40 in the patients, as compared with frequencies among 152 normal Japanese. Genetic studies are ongoing in our clinic.
A case with fistulas from both coronary arteries and the bronchial artery to the pulmonary artery is reported. We believe this is the first case report of an uncommon form of complex arteriovenous fistula diagnosed by selective angiography.
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Seven patients with advanced inoperable carcinoma of the lung were treated with combination chemotherapy consisting of adriamycin, mitomycin-C, and tegafur (AMF therapy). There was, at least, no progress of the carcinoma during treatment and objective response was obtained in 28.6% of patients. With regard to side effects, leukopenia and gastrointestinal symptoms were found in each of 3 patients.
To investigate whether lithium carbonate ameliorates the leukopenia and infectious complication that accompany systemic chemotherapy, we studied 19 patients with small cell carcinoma of the lung receiving combination chemotherapy. Eight patients received systemic chemotherapy and lithium carbonate and 11 patients received systemic chemotherapy alone. The mean leukocyte count nadir during chemotherapy was significantly higher in the patients of the lithium group than in the patients of the control group (p less than 0.05). Percentage of infectious complication related to leukopenia was lower in the lithium group than in the control group, although there was no significant difference between these two groups. There was almost no significant side effect except for liver dysfunction in one patient. We therefore believe that lithium carbonate is an effective and safe drug against leukopenia during cytotoxic chemotherapy.
Echocardiographic findings of 11 patients with dilated cardiomyopathy (DCM) were compared with those of 11 patient with coronary triple vessel disease, who showed extensive left ventricular (LV) wall motion abnormalities (abnormal LV regional wall motion observed in more than six of seven segments as classified by AHA) and a dilated LV cavity (LVEDVI: 120 ml/m2 or greater), consistent with so-called ischemic cardiomyopathy (ICM). Short-axis two-dimensional echocardiograms of the left ventricle at the mitral valve, papillary muscle, and apical levels were divided equally into eight segments starting from the posterior aspect of the right side of the interventricular septum. Non-uniformity of LV regional wall motion abnormalities was demonstrated in seven patients (64%) with DCM and 11 patients (100%) with ICM, and that of LV regional wall motion abnormalities of more than two degrees was observed in one patient (9%) with DCM and nine patients (82%) with ICM. LV regional wall thinning was observed in two patients (18%) with DCM and 11 patients (100%) with ICM. Increased echo intensity of the LV regional wall was observed in only four patients with ICM. Two patients (18%) with DCM and 11 patients (100%) with ICM had episodes of chest pain and the former two had LV regional wall thinning, suggesting the possibility of post-myocarditis cardiomegaly. Abnormal Q waves in the electrocardiograms were observed in 10 patients (91%) with ICM and in two (18%) with DCM. Exercise ECG tests were positive in nine of 11 patients with ICM, but in none of the five DCM examined.(ABSTRACT TRUNCATED AT 250 WORDS)
The clinical records of 1187 patients starting antihypertensive treatment during the period 1969-1979 were reviewed at the end of 1983. The annual drop-out rate was 21.0% in the first year, decreased in subsequent years and was about 1% after five years. The medication compliance of 381 patients was estimated by interview in 1980. Of all 381 patients, 243 (63.8%) reported taking 95-100% of prescribed drugs. Medication compliance was related to the frequency and timing of dosing rather than to the number of drugs. Once daily regimens had better compliance than three times daily ones, and medication compliance was greatest for morning dosing, second greatest for evening dosing, and least for dosing at noon. Repeated assessment of medication compliance on three successive years was followed by gradual improvement of compliance without any other intervention.
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The distribution of left ventricular hypertrophy determined by two-dimensional echocardiography was compared with the ECG findings of 15 patients with so-called apical hypertrophic cardiomyopathy. In most patients, hypertrophy was localized from the anterior septum at the mid-level of the left ventricle to the apex. Giant negative T waves and ST depressions were observed in II, III, aVF and V4-6 in all cases. Negative U waves in the same leads and prolongation of the QTc were also observed in most cases. The cause of these ECG abnormalities was unknown, but ST-T changes and negative U waves may be related to marked, localized hypertrophy of the apex. The depth of the negative T waves and the ST segments changed significantly by hour, from day to day, or from year to year. However, these changes were not associated with significant changes in blood pressure, cardiothoracic ratio, physical condition or therapy. The cause of these changes was unknown, but alterations in activity of the sympathetic nervous system may be one possible cause. In patients with monthly or yearly changes in ST-T, the progression of hypertrophy may also be the cause. ST-T variations revealed in this study might be one of the causes for the different incidences of giant negative T waves in the reports with apical hypertrophic cardiomyopathy. In some patients, an exercise test was positive, but, the coronary angiogram and left ventriculogram were normal for all patients.
A system for reconstructing three-dimensional images of the left ventricle from randomly-recorded multiple short-axis two-dimensional images was developed. This system consisted of a real-time phased array sector scanner, a transducer-locating arm system for registering the spatial coordinates of the images, and a digitizer-computer system for digitizing the endocardial edge to display the reconstruction image and to calculate the left ventricular volume. The clinical applicability of this system was assessed by comparing the calculated left ventricular volumes by this system (3DE) with those measured by cineventriculography (LVG) for 10 patients. For end-diastolic volumes (EDV) determined by 3DE and LVG, the linear regression equation was EDV (LVG) = 1.07 EDV (3 DE)-3.4, SEE = 19.0 ml, r = 0.959. For end-systolic volumes (ESV), it was ESV (LVG) = 1.16 ESV (3 DE)-6.0, SEE = 13.1 ml, r = 0.970, and for stroke volumes (SV), it was SV (LVG) = 0.70 SV (3 DE) + 32.3, SEE = 24.5 ml, r = 0.606. This method was considered applicable to clinical non-invasive measurements of left ventricular volumes. Digitized images were easily processed by a computer, and much informations, such as volumes, shapes and wall motion, were assessable.