Development of primary hypothyroidism with the appearance of blocking-type antibody to thyrotropin receptor in Graves' disease in late pregnancy.

Spontaneous remission of Graves' disease with a decrease of thyroid stimulating antibody (TSAb) activity is commonly observed in pregnancy. In this article, however, a Graves' patient who developed primary hypothyroidism with an appearance of thyroid stimulation-blocking antibody (TSBAb) activity in late pregnancy is reported. A 25-year-old woman presented with clinical and biochemical hyperthyroidism with an elevation of 99mTcO4- thyroid uptake (4.7%; normal range, 0.7%-3.0%) and mildly elevated activity of thyrotropin-binding inhibitory immunoglobulin (TBII; 30.4%). She was euthyroid with normal TBII (8.0%) and TSAb (126%) before pregnancy, when the patient was taking a 5-mg daily dose of methimazole (MMI). MMI was stopped by the patient when she became pregnant. Subsequently, the patient progressed into primary hypothyroidism with a marked elevation of TBII activity (78.4%) in the third trimester of the pregnancy (at that time, TSAb activity was not detected). TSBAb measured 2 weeks later was detected at the activity of 85.0%. Replacement therapy was initiated with levothyroxine (LT4) (0.05-0.1 mg/day), which was discontinued on the 55th day postpartum because of the onset of mild thyrotoxicosis followed by short-term euthyroid state despite high TSBAb activity. Subsequently, because the patient developed primary hypothyroidism 5 months after delivery, replacement therapy with LT4 (0.1-0.125 mg/day) was readministered. Thus, it is suggested that the development of hypothyroidism with the appearance of TSBAb in Graves' patients can occur even in late pregnancy.

[Bacteriological evaluation of netilmicin].

The following results were obtained from the bacteriological evaluations of netilmicin (NTL), a newly developed antibiotic agent, with gentamicin (GM), dibekacin (DKB) and amikacin (AMK) as the controls. (1) NTL demonstrated broad antibacterial spectra against both Gram-positive and Gram-negative bacteria, but its antibacterial potency against streptococci was not very strong among other Gram-positive bacteria. (2) In terms of distribution of sensitivity of clinically isolated bacterial strains, NTL proved to have antibacterial potency comparable to that of GM and higher potency than that of DKB of AMK against E. coli K. pneumonia, Enterobacter sp., or H. influenzae. However, its efficacy was inferior to GM against Proteus sp., S. marcescens and P. aeruginosa. (3) In conjunction with the influences of pH of culture media or of addition of horse sera upon the antibacterial efficacy, NTL showed an inclination similar to that of GM, DKB and AKM. Its antibacterial efficacy was fortified on the alkaline side or by addition of sera. In connection with the influences of the amounts of inoculated bacteria upon antibacterial efficacy, there were hardly any appreciable influences on it by any of the tested bacterial strains. (4) The interactions of NTL with carbenicillin were evaluated with the chequerboard titration method to find remarkable cooperative actions in any of E. coli, K. pneumoniae, S. marcescens, A. calcoaceticus and P. aeruginosa. (5) The results of evaluation on the patterns of its antibacterial effects revealed that it acted bactericidal in any tested bacterial strains. (6) As to the therapeutic effects against experimental infections in mice, it was found out that NTL = GM greater than DKB and AMK against E. coli, GM greater than NTL = DKB and AMK against K. pneumoniae and GM and DKB greater than NTL greater than or equal to AMK against A. calcoaceticus and P. aeruginosa in the decreasing order of efficacy.

NONIDEAL BEHAVIOR DURING COMPLETE DISSOLUTION OF ORGANIC IMMISCIBLE LIQUID: 1. IDEAL POROUS MEDIA.

Column experiments were conducted using ideal natural sands and stainless-steel beads to examine the complete dissolution behavior of an organic immiscible liquid. Trichloroethene (TCE) was used as the representative organic liquid. The elution curves exhibited multi-step behavior, with multiple extended periods of relatively constant contaminant flux. These secondary steady-state stages occurred at concentrations several orders-of-magnitude below aqueous solubility for the well-sorted sands. In contrast, the secondary steady-state stages occurred within one log of aqueous solubility for the poorly-sorted sand. The nonideal behavior is hypothesized to result from constraints to hydraulic accessibility of the organic liquid to flowing water, which may be expected to be mediated by the pore-scale configuration of the flow field and the fluid phases.

[Studies on the genesis of the aortic thudding sound in patients with aortic insufficiency, with special reference to the aortic flow pattern (author's transl)].

To clarify the genesis of the aortic thudding sound (AK), phono-, mechano- and pulsed Doppler echocardiography were performed in 16 patients with pure aortic insufficiency (AI), 3 with AI associated with mild aortic stenosis (AIs) and 5 with AI associated with mitral insufficiency (AI + MI). The results obtained were as follows: 1) AK was composed of two components, that is, one (AK1) occurred in early systole and the other (AK2) near the end point of an ejection systolic murmur. Patients studied were divided into 4 groups following the appearance of AK1 and/or AK2: group with only AK1 (4 cases), group with only AK2 (7 cases), group with both AK1 and AK2 (5 cases) and group without AK (8 cases). 2) AK1 was a low frequency sound and was well recorded from the cardiac base to the right supraclavicular region. AK1 was not observed in cases with mild to moderate AI and with AI associated with mild AS. In atrial fibrillation, when the preceding R-R intervals were long, AK1 was loud and appeared in early systole, and when short, small and in mid-systole. Marked augmentation of AK1 was observed in the first beat after premature ventricular contraction with a compensatory pause. 3) AK2 was also low in frequency and was most intensively recorded near the apex. Although the intensity of AK2 tended to increase in the severe cases of AI, AK2 could be observed in mild to moderate cases. Intensity of AK2 also showed the post-extrasystolic potentiation similar to that of AK1. 4) The carotid pulse showed pulsus bisferiens in all cases with AK2 (group with only AK2 and group with both AK1 and AK2). On the other hand, in cases without AK2 (group without AK and group with only AK1), carotid pulse showed a monophasic systolic wave except 3 cases. These results suggested that there was a close relationship between AK2 and pulsus bisferiens in the carotid pulse. (5) In the apex cardiogram (ACG), systolic notches coincident with AK1 and/or AK2 were observed in 10 of 12 cases with AK2 and in 4 of 9 cases with AK1. In cases without AK, however, no notch was seen in ACG. Therefore, these notches might be resulted from the shock of the anterior chest wall produced simultaneously with the occurrence of AK. 6) Flow patterns at the left ventricular outflow tract (aortic flow patterns) were recorded in 13 cases, including 3 with only AK1, 2 with only AK2, 3 with both AK1 and AK2 and 5 without AK. In 5 of 13 cases the flow patterns were recorded simultaneously with phonocardiograms. Systolic aortic flow showed biphasic patterns in all cases with AK2, and monophasic patterns in cases without AK2. AK1 occurred coincidentally with the first peak of the biphasic flow patterns, and AK2 with the second peak. These results suggested that AK1 might be produced by rapid ejection of massive amount of blood containing a regurgitant flow into the aorta with the ordinarily distensiblwe aortic wall, and AK2 by the clash between the second ejected flow and the reflected flow returning from the peripheral artery against the first ejected flow.

[Echocardiographic study on systolic left ventricular posterior wall motion in patient with atrial septal defect].

Systolic motion of the left ventricular posterior wall (LVPW) was studied by M-mode and long-axis two-dimensional echocardiography in 35 patients (pts) with secundum type of atrial septal defect (ASD), comparing with that of 19 surgically closed ASD (post ASD), 27 with hypertrophic cardiomyopathy (HCM), 15 with old anteroseptal myocardial infarction (a-s MI) and 28 normal subjects. The results obtained were as follows: 1) Excursion of LVPW (PWE) was significantly increased in the pts with ASD compared with normal subjects (P less than 0.001), but there was no significant difference in PWE between the pts with ASD and the pts with HCM or a-s MI. 2) Mean systolic posterior wall velocity (MPWVs) was significantly decreased in the pts with ASD compared with the pts with HCM (p less than 0.05). However, no significant difference could be found in MPWVs between the pts with ASD and a-s MI or normal subjects. 3) End-systolic thickening of LVPW was significantly increased in the pts with ASD compared with normal subjects (p less than 0.05), the pts with a-s MI (p less than 0.05) and the pts with post ASD (p less than 0.01), except for the pts with HCM. There was a significant difference in % end-systolic thickness of lVPW between the pts with ASD and the pts with a-s MI or post ASD (p less than 0:05). 4) Mid-systolic thickening and % mid-systolic thickening of LVPW were significantly increased in the pts with ASD compared with normal subjects, the pts with a-s MI, the pts with post ASD and the pts with HCM (p less than 0.01). This characteristic mid-systolic bulging of LVPW in the pts with ASD was coincident with early-systolic anterior motion of IVS. 5) Basal portion of LVPW indicated the marked inward contraction during end-systole in 30 of 35 pts (86%) with ASD. In these 30 pts, association of mitral valve (MV) prolapse was observed. 6) Following surgical closure of ASD in 19 pts, MV prolapse disappeared following normalization of excessive endsystolic contraction of the LVPW in 16 pts (functional MV prolapse). In 3 pts, however, posterior MV showed multiple abnormal echoes, indicating MV prolapse or mitral regurgitation (organic MV prolapse). In conclusion, these results suggested that mid-systolic bulging of LVPW in ASD is compensatory reaction for systolic anterior IVS motion, and that mechanism of MV prolapse in ASD is related to abnormal left ventricular geometry due to excessive inward contraction of basal portion of LVPW during end-systole.

[Mode of splitting of the second heart sound in patients with hypertrophic cardiomyopathy].

Mode of the splitting of the second heart sound ( IIs ) and left ventricular systolic time intervals (STIs) in patients (pts) with hypertrophic cardiomyopathy were compared with those in hypertension (HT) with the global hypertrophy of the left ventricular wall. Forty-seven pts with hypertrophic cardiomyopathy [non-obstructive type (HCM, 30 pts), obstructive type (HOCM, 17 pts)] and 21 pts with HT were studied. The pts with HCM were classified as septal hypertrophic type (19 pts) and apical hypertrophic type (11 pts) on the basis of the echocardiographic findings. The pts with HOCM were classified as resting type (13 pts) and latent type (provoked by amyl nitrite: 4 pts) on the basis of the obstructive sign at rest. Mode of the splitting of the IIs : a) The pts with HCM showed a wide splitting of the IIs . The mean split interval during held expiration (IIA-IIP) was 41.0 +/- 9.9 msec. Twenty pts (67%) showed abnormal respiratory splitting. The mean IIA-IIP interval in septal hypertrophic type (45.3 +/- 9.0 msec) was significantly wider than that in apical hypertrophic type (33.6 +/- 6.7 msec) (p less than 0.05). There was a positive correlation between IIA-IIP interval and the thickness of the upper portion of the interventricular septum (r = 0.63). b) Nine out of 13 pts with resting type of HOCM showed a paradoxical (reversed) splitting with a mean IIA-IIP interval of -23.8 +/- 24.4 msec. On the other hand, pts with latent type showed a wide splitting similar to HCM with a mean IIA-IIP interval of 35.0 +/- 7.1 msec. c) The pts with HT showed a single IIs or physiological splitting. The mean IIA-IIP interval was 14.5 +/- 9.3 msec, which was significantly decreased than that of normals or the pts with HCM (p less than 0.01). Left ventricular systolic time intervals: a) The pts with an either type of HCM showed a short corrected left ventricular electromechanical systole [(Q-IIA)c] due to the shortening of the corrected left ventricular ejection time (LVETc). b) The pts with resting type of HOCM showed a long (Q-IIA)c due to the prolongation of LVETc, but latent type showed the same change as in HCM. c) The pts with HT showed a tendency of prolongation of (Q-IIA)c due to slightly short LVETc and long corrected pre-ejection period (PEPc). Fractional shortening of the left ventricle (%FS) and mean velocity of circumferential fiber shortening (mean VCF) calculated from echocardiograms were significantly greater in both types of HCM than those in normals and HT (p less than 0.05). Left ventricular end-diastolic dimension was significantly decreased in the pts with septal hypertrophic type of HCM than in others.(ABSTRACT TRUNCATED AT 400 WORDS)

[Exercise echocardiography in different types of hypertension classified by left ventricular geometry; comparison with hypertrophic cardiomyopathy].

We investigated left ventricular (LV) function in 40 patients (pts) with hypertension (HT), 16 pts with hypertrophic cardiomyopathy (HCM), 3 pts with ASH and HT and in 27 control subjects by M-mode echocardiography using supine exercise (50 watts, 3 minutes). The hypertensive subjects were echocardiographically divided into three subsets; the normal LV (17 cases), the hypertrophied LV (17 cases) and the dilated LV (6 cases). Similarly, pts with HCM were echocardiographically and cineangiographically divided into three subsets; ASH (asymmetric septal hypertrophy, 6 cases), APH (predominant apical hypertrophy, 6 cases) and DFH (diffuse left ventricular hypertrophy, 4 cases). Changes of left ventricular dimension Controls and HT: Stroke volume was increased during exercise in the controls, normal LV and hypertrophied LV groups by decreasing LV end-systolic dimension ( LVDs ), but it was increased in dilated LV group by increasing LV end-diastolic dimension ( LVDd ) (Frank-Starling mechanism). LVDd was increased transiently in the controls and normal LV group during recovery, but its grade and duration were more pronounced in the latter. LVDd did not change significantly in hypertrophied and the dilated LV groups. HCM: LVDd and LVDs did not change significantly during exercise in all 3 groups. LVDd was increased transiently during recovery in ASH group, but not in the other groups. Changes of peak velocity of circumferential fiber shortening (VCF) and the ratio of peak systolic blood pressure to LV end-systolic volume (PSP/ LVVs ). Controls and HT: Peak VCF was increased during exercise most markedly in the normal LV group, but it was not increased in the dilated LV group. PSP/ LVVs was increased significantly during exercise in the controls, the normal and hypertrophied LV groups, but not in the dilated LV group. HCM: Peak VCF showed a significant increase during exercise in ASH group, but not in the other two groups. Changes of the D/S ratio. The ratio of systolic to diastolic velocity of the LV posterior wall was expressed as a D/S. This ratio did not change significantly in the controls, HT and APH groups, but it was decreased significantly in ASH and DFH groups. LV end-systolic wall stress and LVDs relationship ( ESWst - LVDs ).(ABSTRACT TRUNCATED AT 400 WORDS)

[Pulsed Doppler echocardiographic assessment of diastolic left ventricular hemodynamics in hypertrophic cardiomyopathy: relationship between the mode of left ventricular filling and the distribution of left ventricular hypertrophy].

In order to clarify left ventricular relaxation and filling in different types of hypertrophic cardiomyopathy (HCM), velocity patterns of blood flow at the inflow tract of the left ventricle (LV) were recorded by pulsed Doppler echocardiography and compared with those of normal subjects (26 cases). Forty-one patients with HCM were classified into the following 4 groups according to the distribution of LV hypertrophy and the evidence of cavity obstruction of the LV; with asymmetric septal hypertrophy (ASH: 15 patients), apical hypertrophy (APH: 10), diffuse hypertrophy ( DIH : five) and obstruction of the LV cavity (HOCM: 11). The HOCM group consisted of five cases of ASH type and six of APH or DIH type. Acceleration time (AT), deceleration time (DT) and the A/D ratio were measured on the pulsed Doppler echocardiogram. The M-mode echogram of the LV was recorded and subsequently digitized to obtain peak LV filling rate. The results were as follows: AT was significantly prolonged in 4 groups of HCM compared with that of the normal subjects. But there was no significant difference in AT among various HCM groups. DT was markedly prolonged in 4 groups of HCM compared with that of the normal subjects, but DT was significantly shortened in the ASH group compared with that of the APH or HOCM group. DT of the HOCM group was divided into the following 2 types according to the duration; normal or slightly prolonged DT (three cases) and markedly prolonged DT (eight). The former group belonged to the ASH type of LV hypertrophy in all cases, and two of them showed a third heart sound. An apical diastolic murmur was recorded in four patients of the ASH group, and six of the HOCM (five cases with ASH type and one with APH type). The A/D ratio was significantly increased in 4 groups of HCM compared with that of the normal subjects. But there was no significant difference among HCM groups. Diastolic descent rate (DDR) of the mitral valve echogram was significantly reduced in 4 groups of HCM compared with that of the normal subjects, particularly in the ASH and HOCM groups. DDR was roughly correlated with DT in the HCM group (r = -0.40, p less than 0.02). Peak LV filling rate was markedly decreased in the ASH, APH and HOCM groups compared with that of the normal subjects. There was a significant negative correlation between peak LV filling rate and DT (r = -0.49, p less than 0.01). In conclusion, the mode of LV filling in HCM showed various patterns according to the location of ventricular hypertrophy and the presence of cavity obstruction of the LV.(ABSTRACT TRUNCATED AT 400 WORDS)

[Studies on the mechanisms of the third and fourth heart sounds: with special reference to the phase analysis of mitral flow velocity pattern].

To investigate the genesis of the third ( IIIs ) and fourth heart sounds (IVs), apical phonocardiograms were recorded simultaneously with pulsed Doppler signals of the mitral flow and interventricular septal (IVS) and left ventricular posterior wall (PW) echoes by M-mode echocardiography in 26 cases with the IIIs and 11 cases with the IVs. The following results were obtained: Cases with the IIIs were classified into the following three groups according to the time relationship between the IIIs and a rapid filling wave (D wave) of the mitral flow velocity pattern. IIIs -peak group: The IIIs occurred coincidently with the peak of the D wave in five healthy adolescents and in 12 cases with absolute left ventricular volume overload including mitral regurgitation (MR: eight cases), postoperative atrial septal defect (ASD: three cases) and ventricular septal defect (one case). IIIs -delay group: The IIIs occurred about 38 msec after the peak of the D wave in eight cases with relative left ventricular volume overload including congestive cardiomyopathy (CCM: three cases) and ischemic heart disease (IHD: five cases). IIIs -early phase group: The IIIs occurred about 35 msec before the peak of the D wave in a case with acute MR due to chordal rupture. In the IIIs -peak group, the IIIs coincided in time with the points of inflection (check points) of both the IVS and PW during rapid filling phase in three cases with MR of mild to moderate degree and one case of postoperative ASD. In the IIIs -delay group, the IIIs occurred simultaneously with either the check point of the IVS or PW in two cases with CCM and one case with IHD, and it occurred before the check points of both the IVS and PW in two cases with severe MR of IIIs -peak group and in a case with acute MR due to chordal rupture of IIIs -early phase group. Cases with the IVs were classified into following 2 groups according to the time relationship between the IVs and the atrial contraction wave (A wave) of the mitral flow velocity pattern. IVs-peak group: The IVs occurred coincidentally with the peak of the A wave in six cases with left ventricular hypertrophy including hypertrophic cardiomyopathy (five cases) and hypertension (one case). IVs-delay group: The IVs occurred about 33 msec after the peak of the A wave in five cases with left ventricular dilatation or dysfunction including old myocardial infarction (two cases), CCM (one case), postoperative ASD (one case) and aortic regurgitation (one case). There were two types of IVs in time relationship between the IVs and the check points of the left ventricular wall during atrial contraction phase.(ABSTRACT TRUNCATED AT 400 WORDS)