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Biomedical subjects

N Fukuda

Publications and source records attributed to N Fukuda.

At least 343 records · Page 19Linked to original sources

[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.

Arrhythmias, Cardiac↗

[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)

Animals↗

[Evaluation of left ventricular function in patients with atrial septal defect by exercise echocardiography].

In order to evaluate left ventricular function in atrial septal defect (ASD), 12 cases with ASD, 18 postoperative cases of ASD and 27 normal controls were examined by means of exercise echocardiography using supine bicycle ergometer (50 watts and 3 min). M-mode echocardiograms and left ventricular (LV) short-axis views by two-dimensional echocardiography were subjected to the observation. M-mode echocardiographic studies: ASD group showed an increased stroke dimension (SD) during exercise mainly due to a marked increase of left ventricular end-diastolic dimension ( LVDd ) and a slight decrease of left ventricular end-systolic dimension ( LVDs ). Postoperative ASD group showed an increased SD during exercise mainly due to a marked decrease of LVDs and a slight decrease of LVDd . On the other hand, in normal control group exercise increased SD only by a significant decrease of LVDs . Right ventricular dimension was decreased during exercise in ASD group, but did not change significantly in postoperative ASD and normal control groups. During exercise in ASD group, peak velocity of circumferential fiber shortening (VCF) was increased most markedly, and negative peak VCF was decreased most strikingly. Eight of 12 patients with ASD who showed abnormal interventricular septal motion demonstrated remarkable improvement of the motion during exercise. Two-dimensional echocardiographic studies: Left ventricular short-axis views demonstrated that the shape of the left ventricular cavity changed from flattened to more circular configuration during exercise at end- and early-diastole in ASD group. The shape of the left ventricular cavity at late-systole did not change significantly during exercise in this group. In postoperative ASD group, the left ventricular short-axis view demonstrated circular configuration of the left ventricle at end-diastole both in rest and during exercise. The shape of the left ventricular cavity did not change by exercise. It was concluded that in ASD group cardiac output is increased during exercise by decreasing a left to right shunt at the atrial level and increasing left ventricular filling rate. Therefore, the left ventricular function was found to be good in ASD.

Adolescent↗

[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.

Adolescent↗

[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)

Adolescent↗

[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)

Adult↗

[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)

Adult↗

[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)

Adult↗

Rotor's syndrome: a study on variations in pigment metabolism with age.

The effects of aging on the pigment metabolism in Rotor's syndrome were investigated in six cases examined at least twice at an average interval of 10.5 +/- 6.5 years and additional four cases examined only once. No significant increase was found in the total (TB) or direct (DB) bilirubin in serum. However, indirect bilirubin increased significantly from 1.21 +/- 0.72 mg/dl to 2.28 +/- 1.00 mg/dl (p less than 0.05) and DB/TB ratio (% Direct) decreased significantly from 77.3 +/- 6.6% to 64.4 +/- 8.7% (p less than 0.05). BSP retentions at 45 minutes increased significantly from 26.8 +/- 10.9% to 45.3 +/- 14.9% (p less than 0.05). A significant positive correlation between the values of BSP retained at 45 minutes and the age was also observed (p less than 0.01). These results suggest that the pigment metabolism in Rotor's syndrome deteriorates with the age.

Adolescent↗

Effect of a test meal, duodenal acidification, and tetragastrin on the plasma concentration of beta-endorphin-like immunoreactivity in man.

The effects of various test materials on plasma beta-endorphin-like immunoreactivity (beta-EpLI) were investigated in man using a specific radioimmunoassay developed by the authors. Plasma beta-EpLI was determined after extraction by the acid/acetone method (recovery 73 +/- 5%). The intraassay and interassay coefficients of variation were 5.0% and 7.6%, respectively. The plasma concentrations of human beta-EpLI in normal subjects were 11.6 +/- 4.0 pmol/l for men (n = 23) and 10.7 +/- 4.8 pmol/l for women (n = 27). Ingestion of a test meal (150 g of Campbell's condensed meat soup) resulted in a biphasic rise in plasma beta-EpLI from the basal level of 4.4 +/- 1.0 pmol/l to 29.2 +/- 1.9 pmol/l after 5 min and 24.8 +/- 6.7 pmol/l after 90 min. Intraduodenal infusion of 115 ml of 0.1 M HCl over 10 min increased the plasma beta-EpLI level from 8.7 +/- 0.5 pmol/l to 15.5 +/- 0.4 pmol/l at 10 min after the start of infusion, but the level rapidly returned to the initial value after the end of the infusion. Intramuscular injection of 4 micrograms/kg body weight of tetragastrin markedly stimulated gastric acid output and beta-EpLI release, but pretreatment with 10 mg of histamine H2 receptor antagonist inhibited the gastric acid output and plasma beta-EpLI release induced by tetragastrin. These results indicate that beta-EpLI release is stimulated by ingestion of meat soup, duodenal acidification and tetragastrin administration. It is suggested that gastric acid participates, at least in part, in postprandial release of beta-EpLI, probably from the gastrointestinal tract.

Adult↗

Purification and properties of thermostable beta-xylosidase from immature stalks of Saccharum officinarum L. (sugar cane).

Thermostable beta-xylosidase was purified from immature sugar cane stalks to an electrophoretically homogeneous form by ammonium sulfate fractionation, ion-exchange chromatography on DEAE-cellulose and P-cellulose columns, heat treatment (70 degrees C, 20 min) and gel filtration on a Sephadex G-100 column. The purification was about 165-fold in specific activity with a high recovery of 43%. The apparent molecular weight of the enzyme, as determined by gel filtration, was 62,000. In SDS-polyacrylamide gel electrophoresis, the purified enzyme was homogeneous and consisted of only one polypeptide, having a molecular weight of approximately 62,000. The optimum temperature and pH were found to be 75 degrees C and 4.85, respectively. The enzyme was thermostable and especially stable in the presence of D-xylose. The enzyme retained full activity after incubation at 70 degrees C for 60 min in the presence of 0.1% D-xylose and when heated at 75 degrees C in the presence of 1% D-xylose, the enzyme was stable up to 30 min. Among the various sugars tested, D-xylose was found to be most effective stabilizer. The Km and Vmax values were 2.05 mM and 20.4 mumol/mg/min, respectively. The substrate specificity of purified sugar cane beta-xylosidase was investigated with 16 substrates. It was not able to hydrolyze any p-nitrophenyl glycopyranosides, larch wood xylan, or sugar cane except for p- and o-nitrophenyl-beta-D-xylopyranosides. The enzyme hydrolyzed p-nitrophenyl-beta-D-xylopyranoside more rapidly than o-nitrophenyl-beta-D-xylopyranoside. The hydrolysis of p-nitrophenyl-beta-D-xylopyranoside was markedly inhibited by AgNO3, HgCl2, and D-xylose. Competitive inhibition was shown to occur with both HgCl2 and D-xylose. AgNO3 was found to be a non-competitive inhibitor. The enzyme lost 20% of its activity by photo-oxidation in the presence of methylen blue for 8 h. By polyacrylamide disc gel electrophoresis, the enzyme was found to contain carbohydrate. The enzyme was then hydrolyzed and the carbohydrate content found to be 13.5%, the constituent sugars being arabinose and galactose.

Amino Acids↗

[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.

Adult↗