Diagnosis of quinolone-induced arthropathy in juvenile dogs by use of magnetic resonance (MR) imaging.

The present study was carried out to confirm whether arthropathy in juvenile dogs induced by ofloxacin, a new quinolone antibacterial agent, may be diagnosed by magnetic resonance (MR) imaging. Three-month-old male beagle dogs were orally administered ofloxacin at 20 mg/kg once daily for 7 consecutive days. On day 8, MR images were obtained with a 4.7-tesla (T) super-conductive high magnetic field strength unit. An irregular cartilage surface and dissecans changes in the distal femoral condyle were observed. These MR findings were essentially consistent with pathologic observation showing multifocal blisters on the articular cartilage with an increased amount of turbid synovial fluid in the joint. The results demonstrate that occurrence of ofloxacin arthropathy in juvenile dogs can be clearly diagnosed by use of MR imaging.

Tc-99m(V) DMSA uptake in cardiac amyloidosis.

Tc-99m(V) DMSA scintigraphy was performed on two patients with primary cardiac amyloidosis. Scintigraphy performed (after radionuclide administration) showed accumulation in the myocardium.

Cellulose in the house of the appendicularian Oikopleura rufescens.

By electron diffraction analysis, highly crystalline cellulose I beta was found in the house (a special structure in which the tunicate lives) of the appendicularian Oikopleura rufescens. Cellulose microfibrils 20 nm in width were observed in a random array or highly organized with rectangular spacing of 2 to 10 microns in the house. The bundled cellulose microfibrils formed in the inlet filters, which are highly ordered meshwork structures. This paper provides the first account of the existence of cellulose in the house of an appendicularian. Our findings showed that the house and tunic are homologous tissues among the tunicates, and that the common ancestor of the tunicates (ascidians, thaliaceans, and appendicularians) already possessed cellulose-biosynthetic ability.

[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.

Pharmacokinetic disposition and arthropathic potential of oral ofloxacin in dogs.

We examined the relation between the pharmacokinetic disposition and arthropathic potential of ofloxacin, a new quinolone antibacterial agent, using both male immature (3-month-old) and mature (18-month-old) beagles. Ofloxacin was orally administered to these dogs at 20 mg/kg once daily for 8 consecutive days, and the animals were killed 2 h after the last treatment. Serum ofloxacin concentrations were repeatedly measured on days 1 and 7 by use of high-performance liquid chromatography (HPLC), and pharmacokinetic parameters were calculated. In addition, on day 8, the drug concentrations in the joint synovial fluid and humeral and femoral condyles were measured. Clinico-pathological tests of blood and serum or histopathological examination of bone specimens were also performed. Arthropathy was macroscopically observed in the cartilage surface of all immature dogs, but not in mature dogs. There were, however, no noticeable differences in pharmacokinetic parameters between the two age groups of dogs or between single and 7-day treatments. In contrast to the occurrence of arthropathic lesions, the synovial fluid and condylar drug concentrations in immature dogs was equal to or lower than those in mature dogs, suggesting that the pharmacokinetic disposition of ofloxacin may not be essential for cartilage lesions.

Effect of the novel high affinity choline uptake enhancer 2-(2-oxopyrrolidin-1-yl)-N-(2,3-dimethyl-5,6,7,8-tetrahydrofuro[2,3-b] quinolin-4-yl)acetoamide on deficits of water maze learning in rats.

The pharmacological properties of MKC-231 (2-(2-oxopyrrolidin-1-yl)-N- (2,3-dimethyl-5,6,7,8-tetrahydrofuro[2,3-b]quinolin-4-yl) acetoamide, CAS 135463-81-9) in comparison with an acetylcholinesterase (AChE) inhibitor, tacrine (CAS 1684-40-8) were studied. MKC-231(10(-10)-10(-6) moll) significantly increased high affinity choline uptake (HACU) when it was incubated with the hippocampal synaptosomes of ethylcholine mustard aziridinium ion (AF64A) treated rats, but not of normal rats. MKC-231 did not affect the AChE activity, [3H]- quinuclidinyl benzilate binding, and [3H]-pirenzepine binding. Oral administration of MKC-231 (1-10 mg/kg) significantly improved the learning deficits in the Morris' water maze of AF64A-treated rats, but it did not produce any significant side effects, like tremor, salivation or hypothermia, which were observed in rats treated with high doses of tacrine. Tacrine (0.1-3 mg/kg p.o.) failed to ameliorate the learning deficits in AF64A-treated rats. These results suggest that MKC-231 is a novel and quite unique compound, which improves the memory impairment induced by AF64A through the enhancement of HACU without any side effects at the effective doses.

[Phono- and echocardiographic studies of the genesis of mitral valve prolapse in patients with funnel chest].

Two-dimensional echocardiograms (2-DE) and phonocardiograms (PCG) were used to clarify the genesis of mitral valve prolapse (MVP) and mitral regurgitation (MR) in 44 patients with funnel chest. These patients were categorized in three groups on the basis of the fronto-sagittal index (FSI) as determined from chest radiographs; 17 as mild, 15 as moderate and 12 as severe funnel chest. Their ages ranged from 5 to 65 years and averaged 24 years. MVP was diagnosed using the long-axis view of the 2-DE, and MR was diagnosed phonocardiographically including provocative test using angiotensin II. The results were as follows: In 44 patients with funnel chest, 20 (45%) had MVP and 15 (34%) had MR, respectively. The incidence of MVP increased directly in proportion to the severity of index, but the incidence of MR did not. In the short-axis view of the left ventricle at the level of the papillary muscles, there was more marked flattening of the interventricular septum than of the left ventricular posterior wall, resulting in deformity of the left ventricular geometry. A distortion index (DI) was used to quantify the degree of distortion of left ventricular shape, calculated as follows: DI = (R-r)/r, where R and r were radii of the curvatures of the interventricular septum and the left ventricular posterior wall, respectively. The DI in end-diastole (DId) and end-systole (DIs) increased in proportion to the severity of funnel chest. Patients were subdivided into four groups on the basis of DId. Incidence of MVP increased in proportion to the degree of distortion of the left ventricular shape. There was, however, no significant difference in the incidence of MR among the four groups. Patients were subdivided; one group of 13 under 14 years of age; another, 31 over 15 years old. The incidence was much higher in the latter than the former, but the incidence of MVP increased in proportion to the severity of funnel chest in both groups. MR was complicated by MR in nearly all cases in the latter group, but none had MR in the former. The DI of patients, whose FSI improved with surgery, apparently improved in addition to the disappearance and/or improvement of their MVP and MR. However, patients whose FSI did not improve with surgery showed little change in DI and persistence of MVP and/or MR.(ABSTRACT TRUNCATED AT 400 WORDS)

[Left ventricular function in patients with right ventricular overload evaluated by exercise echocardiography: comparison of pulmonary hypertension and atrial septal defects].

To evaluate left ventricular function in patients (pts) with right ventricular overload, exercise echocardiographic studies using a bicycle ergometer were performed for seven pts with pulmonary hypertension (PH), two with cor pulmonale (CP) and 16 with atrial septal defects (ASD), and the results were compared with those of 10 (control I) and 27 (control II) normal persons. These subjects were categorized in two study groups; study I consisting of PH, CP and control group I with an exercise workload of 25 watts for 3 min; and study II consisting of ASD and control group II with an exercise workload of 50 watts for 3 min. The results were as follows: M-mode echocardiography revealed that: During exercise, the stroke volume (SV) was increased with a significant decrease of left ventricular end-systolic dimension (LVDs), but without a change in left ventricular end-diastolic dimension (LVDd) in control groups I and II, with a marked increase of LVDd and a slight decrease of LVDs in the ASD group. By contrast, the SV in the PH group tended to decrease during exercise with a slight decrease of LVDd, but without a significant change in LVDs. Right ventricular dimension (RVD) was significantly increased during exercise in the PH group, but was decreased in the ASD group. In control groups I and II, RVD did not change during exercise. In ASD, and control groups I and II, the peak velocity of circumferential fiber shortening (Vcf) was increased during exercise, and the peak negative Vcf was significantly decreased. However, these parameters exhibited impaired responses during exercise in the PH group. Abnormal interventricular septal (IVS) motion at rest tended to become normal during exercise in 12 of 16 pts with ASD. In all pts with PH, however, IVS motion did not change substantially during exercise. There were similar parameter responses between the PH and CP groups. Two-dimensional echocardiography showed that: The left ventricular short-axis view demonstrated a diastolic left ventricular configuration which changed from oblique to relatively circular orientation during exercise in the ASD group. In four of five pts with PH, the diastolic configuration of the left ventricle was oblique because of a loss of the normal curvature of the IVS at rest and during exercise. The diastolic left ventricular configuration improved during exercise in only one pt with PH, with slightly elevated pulmonary arterial systolic pressure as in the ASD group.(ABSTRACT TRUNCATED AT 400 WORDS)

[Genesis of protodiastolic extra heart sound in mitral stenosis: a phono-, apex-, echo- and cineangiographic study].

To clarify the genesis of a protodiastolic extra heart sound (S3') which was occasionally recorded at about the beginning of a diastolic rumble in mitral stenosis (MS), phono-, apex- and echocardiography were performed for 33 patients with MS, and left ventricular (LV) cineangiography was performed for eight of them. The patients were classified as S3'(+) and S3'(-) groups, according to whether they had S3'. Results were as follows: The S3' was synchronous with the rapid filling (RF) wave of the apexcardiogram (ACG). Its amplitude was proportional to the size of the RF wave. The RF wave was significantly sharper in the S3'(+) group as compared with that of the S3'(-) group. The S3' always appeared after onset of dispersion of dots in the velocity pattern of blood flow at the mitral valve orifice according to pulsed Doppler echocardiography. There was no significant difference between the S3'(+) and S3'(-) groups in the region of the mitral valve orifice according to two-dimensional echocardiography, and at the peak rate of change of the LV dimension during diastole as determined by M-mode echocardiography. The peak rate of change of the long-axis dimension of the LV during diastole as determined by cineangiography was significantly greater in the S3'(+) group than in the S3'(-) group. However, there was no significant difference between the two groups regarding the peak rate of change in the short-axis dimension of the LV during diastole as determined by cineangiography. The amplitude of the early diastolic dip of the interventricular septum (IVS) was significantly greater in the S3'(+) group as compared with that of the S3'(-) group. The amplitude of the S3' and the size of the RF wave correlated positively with the amplitude of the early diastolic dip of the IVS in pts with atrial fibrillation. Fractional shortening of the LV ascertained by M-mode echocardiography was significantly greater in the S3'(+) group than in the S3'(-) group. The end-systolic dimension of the LV tended to be less in the former than in the latter group. In conclusion, the S3' in MS was considered to be a third heart sound. Expansion along the long-axis of the LV and its sudden change in early diastole may account for the genesis of the S3', and this expansion may be accentuated by restoring force and active diastolic suction of the LV, and by velocity, direction and spread toward the cardiac apex of the stenotic mitral jet flow.

[Noninvasive studies of dynamic left ventricular outflow obstruction in patients with sigmoid septum].

In order to evaluate the clinical significance of the markedly protruding interventricular septum into the left ventricular (LV) cavity (sigmoid septum), we performed non-invasive studies including amyl nitrite (AN) inhalation in 21 patients (pts) with two-dimensional echocardiographic (2DE) documentations. LV outflow tract (LVOT) obstruction was determined by the presence at least three of the following findings at rest or during AN inhalation: 1) a loud apical ejection systolic murmur (ESM), 2) a midsystolic dip in the carotid pulse, 3) systolic anterior motion (SAM) of the mitral valve (MV) or chordae tendineae, and 4) systolic semiclosure of the aortic valve (AV). The 21 pts were subdivided into six pts (group I) with resting (two pts) or provocative (four) obstruction, and 15 pts (group II) without obstruction. Their ages ranged from 40 to 85 years with an average of 65. No pt had evidence of hypertrophic cardiomyopathy. Results were as follows: In five pts of group I a long ESM with a mid-systolic peak was recorded near the apex. After AN inhalation, this murmur was markedly intensified. On the contrary, all pts of group II had a short and early systolic murmur, which was not markedly intensified by AN. In contrast to group II, group I pts had a significantly smaller LV end-diastolic dimension, a smaller LVOT dimension, higher percent thickening of the LV posterior wall, higher fractional shortening and decreased aorto septal angle (the angle between the anterior aortic wall and the interventricular septum by 2DE). On 2DE, each pt of group I showed significant narrowing between the protruded septum and the hypercontractile LV posterior wall with the papillary muscle. Anteriorly shifted chordae tendineae noted as the SAM on the M-mode echocardiogram might also play an important role on the genesis of obstruction. The signs of LVOT obstruction at rest disappeared following oral administration of propranolol in two pts of group I. These observations suggested that LVOT obstruction might occur in some pts with sigmoid septum and the hypercontractile state, and that a systolic murmur observed in this condition should be differentiated from a functional murmur in the aged or a systolic murmur in hypertrophic obstructive cardiomyopathy.

[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)

[Phase analysis of mitral regurgitation in mitral valve prolapse: comparison of pulsed Doppler echocardiography with phonocardiography].

The clinical implication of the timing of mitral regurgitation (MR) in mitral valve prolapse (MVP) was investigated by comparison of the phonocardiographic patterns of the regurgitant murmur with either prolapsing phase of the mitral valve determined by two-dimensional echocardiography (TDE) or regurgitant flow patterns by pulsed Doppler echocardiography (PDE). A total of 23 patients (pts) with MVP was classified into five subsets on the basis of the phonocardiographic findings: six pts with a pansystolic murmur, seven with a late systolic murmur, two with an early systolic murmur, three with only a click(s) and five with a angiotensin II-induced regurgitant murmur (provocative MR). A comparative study between the regurgitant murmur and regurgitant flow patterns was also made in 10 pts with MR due to other etiology (four pts of rheumatic MR, three of ruptured chordae tendineae and three of papillary muscle dysfunction). MR was detected at or just above the mitral orifice using a combined system of the PDE and TDE from a transcutaneous approach. The results obtained were as follows: Phase of MR detected by PDE coincided well in timing with a regurgitant murmur recorded on the phonocardiogram (PCG) except one patient. In four of five pts with provocative MR, abnormal Doppler signals indicating MR were detected even at rest and these coincided temporally with a newly developed regurgitant murmur by provocation. Phase of MR detected by PDE was not synchronous with prolapse of the mitral leaflets examined by TDE in five out of 23 pts, suggesting that MR does not necessarily occur in accordance with mitral prolapse. Regurgitant flow patterns examined by PDE in 30 pts including 10 pts of MR due to other etiology were either a widely dispersed dot pattern or a narrow banded reverse flow pattern. Pts with a loud systolic regurgitant murmur (Levine 3/6 or greater) tended to show a widely dispersed dot pattern, and pts with a soft systolic regurgitant murmur (less than Levine 2/6) showed a narrow banded reverse flow pattern. In conclusion, PDE seems to be more sensitive than PCG for the detection of MR in MVP, and PDE may serve to the qualitative as well as quantitative evaluation of MR in MVP.

[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)

[Pulsed Doppler echocardiographic observation of right and left ventricular inflow velocity patterns in various types of arrhythmia, with special reference to the mechanism of atrioventricular regurgitation].

To investigate the possibility for detection of atrio-ventricular (A-V) regurgitation in arrhythmias non-invasively, we recorded velocity patterns of blood flow at the inflow tract of the right (RVI) and left ventricles (LVI), and at the outflow tract of the left ventricle (LVO) by pulsed Doppler echocardiography in 32 patients with various types of arrhythmia. They were six cases with supraventricular premature contraction (SVPC), 13 with ventricular premature contraction (VPC), two with second degree A-V block, five with complete A-V block and six with artificial right ventricular pacemaker. The following results were obtained. In SVPC, peak velocity of the preceding early diastolic flow of RVI and LVI was related to the coupling interval. A crucial ectopic atrial contraction occurring at the early diastole augmented right or left ventricular filling by summation of the two kinds of ventricular filling. Peak velocity of the early diastolic flow at RVI and LVI was decreased after SVPC compared with that of normal sinus rhythm. A reverse flow was not observed in RVI or LVI velocity pattern in these cases. In VPC, peak velocity of the preceding early diastolic flow at RVI and LVI was related to the coupling interval. An effective early diastolic flow was not observed when coupling interval was short. A systolic A-V reverse flow was detected in six of eight cases of VPC with compensatory pause. In these six cases, M-mode and two-dimensional echograms showed patterns of tricuspid and/or mitral valve prolapse and systolic "bulging" of the left ventricular posterior wall. Peak velocity of the blood flow at LVO was decreased in VPCs with short coupling intervals, but it was increased markedly in the next beat after compensatory pause (post-extrasystolic potentiation). Velocity pattern of a blood flow at RVI and LVI showed two types of reverse flow patterns in all cases with complete A-V block or with artificial right ventricular pacemaker; a) systolic reverse flow in beats with P wave superimposed on QRS complex or ST segment, and b) diastolic reverse flow in beats with markedly prolonged P-R intervals. Diastolic tricuspid regurgitation was demonstrated by contrast echography at the level of the tricuspid valve orifice, and diastolic mitral regurgitation by left cineventriculography. The clinical implication of pulsed Doppler echocardiography to detect A-V regurgitation during systole and diastole was discussed in various types of arrhythmia.

[Mode of production of the splitting of the second heart sound in post-extrasystolic beats].

The changes in left and right ventricular systolic time intervals (LV- and RVSTIs) and split interval of the second heart sound (IIA-IIP interval) associated with post-extrasystolic potentiation were studied in 48 patients including 37 without a significant intracardiac shunt or valvular regurgitation or pulmonary hypertension, 7 with aortic stenosis (AS) and 4 with hypertrophic obstructive cardiomyopathy (HOCM). In 19 out of 37 patients mentioned above, LV- and RVSTIs were measured from carotid pulse and pulmonary arterial pulse waves, and IIA-IIP interval of post-extrasystolic beat with a compensatory pause was compared to that of the preceding sinus beat. In the other 29 patients including AS and HOCM, LVSTI, total electromechanical systole of the right ventricle (Q-IIP) and IIA-IIP interval were compared. There was no significant difference in the coupling index [(compensatory pause-coupling interval)/preceding RR interval X 100(%)] among three groups. The following results were obtained: In all patients without HOCM, post-extrasystolic beats showed wider IIA-IIP interval than the control beats independent upon the diseased entity and severity of cardiac function. In pts with HOCM, a IIA-IIP interval was shortened in post-extrasystolic beats. A IIA-IIP interval at post-extrasystolic beats was prolonged in proportion to the augmentation of coupling index. However, this finding was no longer observed in cases with the coupling index of more than 80%. LVSTI: In patients without HOCM, almost no change or prolongation of left ventricular ejection time (LVET) and shortening of left ventricular preejection period (LPEP) were observed in post-extrasystolic beats. The degree of changes in LVET and LPEP was greater in patients with the abnormal left-sided PEP/ET than in patients with the normal PEP/ET. The degree of changes in LPEP was always greater than that in LVET, therefore, total electromechanical systole of the left ventricle (Q-IIA) was shortened in all patients. In HOCM, a marked prolongation of LVET and a shortening of LPEP were observed. The degree of changes in LVET was greater than that in LPEP, therefore, Q-IIA was prolonged in all patients. RVSTI: Prolongation of right ventricular ejection time (RVET) and shortening of right ventricular preejection period (RPEP) were observed in all patients in post-extrasystolic beats. The degree of changes in RVET and RPEP was increased in patients with the increased right-sided PEP/ET. The degree of changes in RVET was greater than or equal to that in LPEP, therefore, Q-IIP showed slight prolongation or no change.(ABSTRACT TRUNCATED AT 400 WORDS)

Structure of the TCR expressed on a gastritogenic T cell clone, II-6, and frequent appearance of similar clonotypes in mice bearing autoimmune gastritis.

A parietal cell-specific Th1 clone, II-6, which was established from a BALB/c mouse bearing post-thymectomy autoimmune gastritis (AIG), recognizes a peptide of the alpha subunit (alpha891-905) of H+/K+-ATPase and induces gastritis in nu/nu BALB/c mice by adoptive cell transfer. In the present study, the primary structure of the TCR of II-6 was determined as Valpha10-Jalpha c5a-Calpha and Vbeta14-Jbeta2.3-Cbeta2 by cDNA cloning. Using PCR with specific primers, we defined the use of this II-6 TCR in nu/nu mice with transferred II-6 cells and in mice that spontaneously developed AIG by thymectomy on day 3 after birth (d3-Tx). II-6 TCR mRNAs were detected in the gastric mucosa of all of the nu/nu mice, suggesting that II-6 cells indeed home to the gastric mucosa and thereby were directly involved in the destruction of target parietal cells. TCR beta chain mRNAs encoding CDR3 region sequences almost identical with that of II-6 were also found in the gastric mucosa in 43% (six of 14 mice tested) of the d3-Tx AIG mice at 4-12 weeks old by nested RT-PCR. Such a frequent appearance of similar clonotypes in independent individuals suggests that T cells bearing II-6-like TCR including the II-6 itself might be directly involved in, although not essential for, the pathogenesis of AIG in 3d-Tx mice.