[Cleaning and sterilization of the upper gastrointestinal endoscope].
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Biomedical subjects
Publications and source records attributed to T Oki.
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The clinical significance of the mode of left ventricular (LV) diastolic filling in hypertrophic cardiomyopathy was studied by the LV inflow velocity patterns (LVIF) of pulsed Doppler echocardiography and LV early diastolic filling rates (V2) of radionuclide (RI) angiography. The relationship between the deceleration time (DT) obtained from LVIF and the V2 was evaluated in 34 patients with nonobstructive hypertrophic cardiomyopathy (HCM) and in nine with obstructive hypertrophic cardiomyopathy (HOCM), and the results were compared with those of 10 patients with dilated cardiomyopathy (DCM), of two with restrictive cardiomyopathy (RCM), and of 19 normal subjects. HCM was subdivided into the following groups according to V1-DT relationships: Group 1 with prolonged DT and decreased V1, Group 2 with normal or short DT and normal V1, and Group 3 with normal or short DT and decreased V1. There were significant negative correlations between V2 and DT in Groups 1 and 2 of HCM, normal and HOCM. However, there were significant positive correlations in Group 3 of HCM, DCM and RCM. Nearly all patients in Group 3 had decreased LV ejection fraction and % fractional shortening, distinct B-B' step formation of the mitral valve echogram, and huge A wave of the apexcardiogram. These findings suggested that the LV rapid filling interval gradually became shorter because the LV contraction is decreased as myocardial fibrosis develops in HCM, and that we must pay attention to the diagnosis of such abnormalities, similar to those of DCM or RCM.
A case of primary pericardial malignant mesothelioma was presented, which initially had a relatively large quantity of pericardial fluid, followed by constrictive pericarditis. The patient was a 43-year-old woman whose chief complaint was dyspnea and admitted to our hospital in March, 1984. Because of a relatively large quantity of pericardial fluid was observed. In April, drainage of the fluid and pericardiotomy were performed with marked relief of symptoms. She was discharged, but her dyspnea recurred in August, and she was readmitted. After the second admission, the chest radiograph showed a cardiothoracic ratio of 62%, and her electrocardiogram showed low voltage. A pericardial knock was recorded, and the timing of this sound coincided with that of the peak of the early distolic wave of the mitral flow velocity pattern. A jugular pulse tracing showed a deep and sharp y descent. The diastolic pressure curve of the right ventricle revealed a dip and plateau pattern. The echocardiographic finding was characterized by abnormal systolic motion and an early diastolic dip of the interventricular septum, multiple abnormal echoes and thickening of the pericardium, and an abnormal mass echo in the left atrial cavity. Based on the above examinations, pericardiotomy was performed, but the tumor was not entirely resected. The histological diagnosis was malignant mesothelioma.
The effect of sublingual nifedipine on left ventricular (LV) function was assessed by analyzing LV inflow velocity patterns using pulsed Doppler echocardiography (PDE) and radioisotope (RI) angiography in 23 patients with hypertrophic cardiomyopathy (HCM), 13 with hypertensive heart disease (HHD) and 24 with ischemic heart disease (IHD). The results were as follows: LV inflow velocity pattern and M-mode echocardiography after the administration of nifedipine (Study-I). The deceleration time (DT) of the diastolic rapid filling wave was shortened after nifedipine in HCM and HHD, but not in IHD. The acceleration time (AT) of the diastolic rapid filling wave and the A/D ratio (amplitude of an atrial contraction wave/amplitude of a diastolic rapid filling wave) were not significantly changed in all groups. Peak negative Vcf was significantly improved after nifedipine in HCM, but unchanged in the other groups. Fractional shortening and peak Vcf did not change in all groups. LV inflow velocity pattern and RI angiography after nifedipine (Study-II). The mean LV rapid filling rate (V1) based on the LV volume curve by multi-gated blood pool scans increased during nifedipine in HCM and HHD, but other diastolic indices, such as the peak filling rate and 1/3 filling fraction, were unchanged. The DT-V1 relationship during nifedipine shifted toward the right and downward in HCM and HHD. In IHD, however, this relationship shifted toward the left and downward in cases with reduced LV function (V1 less than 1.0 EDC/sec), but toward the right and downward in patients whose LV function was maintained (V1 greater than or equal to 1.0 EDC/sec). Nifedipine therapy was associated with an improved LV filling in nearly all cases of HCM and HHD, and in some cases of IHD. PDE and RI angiography are useful for evaluating LV diastolic function during sublingual nifedipine in various heart diseases.
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.
To investigate the mechanism of an apical mid-diastolic rumble in hypertrophic cardiomyopathy (HCM), we recorded left ventricular (LV) inflow velocity patterns using pulsed Doppler echocardiography and apexcardiography for 10 HCM patients with rumble and 20 HCM patients without rumble. Controls consist of 17 normal subjects, three patients with complete atrioventricular block and two patients with artificial right ventricular pacemakers. The LV inflow velocity profiles were analyzed in terms of acceleration time (AT) and deceleration time (DT) of the rapid filling wave, and the ratio of peak velocity of the atrial contraction wave to that of the rapid filling wave (A/D ratio). The results were as follows: The apical mid-diastolic murmur in HCM had a crescendo-decrescendo character mainly of medium frequency, and increased in intensity after the inhalation of amyl nitrite. All patients with rumble had asymmetric septal hypertrophy and the five of these had LV outflow obstruction. In six of the 10 patients with rumble, mild mitral regurgitation was detected. In HCM with rumble, the AT tended to be shorter than that of HCM without rumble, but it was significantly longer than the AT of normal subjects. In HCM with rumble, the DT was significantly shorter than that of HCM without rumble, but it was significantly longer than the DT of normal subjects. There was no significant difference in the A/D ratio between the HCM with rumble and the normal subjects, but the A/H ratio of the apexcardiogram was significantly increased in HCM with rumble as compared with those of HCM without rumble and of the normal subjects. The LV dimension was significantly decreased in HCM with rumble as compared with those of HCM without rumble and the normal subjects. Peak negative VCF was significantly decreased in HCM with rumble as compared with that of HCM without rumble. But there was no significant difference in this parameter between HCM with rumble and the normal subjects. In simultaneous recordings of apical mid-diastolic rumble and LV inflow velocity patterns, the rumble appeared to start after the beginning of the diastolic rapid filling wave and to stop before or at the end of the diastolic rapid filling wave. In patients with complete atrioventricular block and with artificial right ventricular pacemakers, the apical mid-diastolic rumble appeared when the P wave was during the rapid filling phase of the left ventricle.(ABSTRACT TRUNCATED AT 400 WORDS)
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.
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The mechanism of an early diastolic posterior motion of the interventricular septum (IVS) was investigated by means of M-mode, two-dimensional and pulsed Doppler echocardiographies in 53 patients with pure mitral stenosis (MS). Velocity patterns of the blood flow at the inflow tract of the left ventricle (LVIT) were classified into three types as previously reported (cf. Fig.3). The results obtained were as follows: The mitral valve orifice area (MVA) was significantly smaller in patients with type III of the LVIT flow velocity pattern than in patients with type I (p less than 0.001). An amplitude ("a") of the posterior IVS motion in systole (P1) was significantly diminished in type III (4.2 +/- 1.1 mm) than in type I (6.6 +/- 1.5 mm) (p less than 0.001). An amplitude ("b") of the posterior IVS motion in early diastole (P3) showed a significant increase in type III (7.5 +/- 1.2 mm) than in type I (5.2 +/- 1.5 mm) (p less than 0.001). Difference of the amplitude between P1 and P3 ("a-b") was significantly greater in type III (-3.4 +/- 1.1 mm) than in type I (1.4 +/- 0.9 mm) (p less than 0.0001). MVA was correlated statistically with "a" (r = 0.58, p less than 0.001), "b" (r = -0.38, p less than 0.01) and "a-b" (r = 0.80, p less than 0.0001). Deformity of the left ventricular cavity due to the flattened IVS in early diastole was observed in severe MS with an augmented septal P3 dip. A case of severe MS with type III velocity pattern and an augmented P3 dip showed type II velocity pattern and a decreased P3 dip after the attack of acute myocardial infarction. These findings suggested a close relationship between type III of the LVIT flow velocity pattern and the prominent septal P3 dip. The importance of diastolic suction of the left ventricle in producing an early diastolic posterior motion of IVS (P3) was discussed.
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)
Systolic and diastolic motions of the interventricular septum (IVS), especially of its lower portion at the level of the chordae tendineae, were evaluated by M-mode echocardiography in normal subjects and in patients with various cardiac disorders. The following conclusions were derived from this study. In normal subjects, downward motion of the IVS exhibited three patterns; namely, P1, between the onset of electrical depolarization and the onset of the second heart sound; P2, between the onset of the second heart sound and the E point of the anterior mitral leaflet; and P3, between the E point of the anterior mitral leaflet and the end of the left ventricular rapid filling phase, during each cardiac cycle. The systolic IVS pattern (P1) of atrial septal defect was classified as follows: Normal type: nearly normal posterior motion during ventricular systole, Flat type: flat motion during ventricular systole, Paradoxical (early systolic) type: anterior motion during the first half of ventricular systole, followed by normal posterior motion, Paradoxical (pansystolic) type: anterior motion during ventricular systole. In atrial septal defect, the right ventricular dimension was markedly increased in the flat and paradoxical (pansystolic) types compared with those of the normal and paradoxical (early systolic) types. Marked downward IVS motion (P2) was observed in cor pulmonale with paradoxical pulse, pulmonary hypertension, Ebstein's anomaly, pulmonic insufficiency, atrial septal defect, funnel chest, tricuspid insufficiency and constrictive pericarditis. In cor pulmonale with paradoxical pulse, the deep downward motion (P2) was observed more distinctly during inspiration compared to expiration, and right ventricular inflow velocity pattern was characterized by an apparent increase in peak flow in velocity of the diastolic rapid filling wave during inspiration. Two interesting findings were a deep "y" trough of the jugular pulse tracing and prominent P2 in funnel chest. Therefore, it was likely that exaggerated P2 seemed to be direct evidence of a marked increase in right ventricular rapid filling in the presence of normal or decreased left ventricular rapid filling. The augmented septal dip of P3 was observed in cases with the third heart sound as in normal subjects, and those with mitral insufficiency, and ventricular septal defect, constrictive pericarditis and mitral stenosis. We theorized that exaggerated P3 results from the "sucking action" secondary to increased left ventricular rapid filling velocity in cases with the third heart sound or constrictive pericarditis.(ABSTRACT TRUNCATED AT 400 WORDS)
Relationship between various parameters of the left ventricular inflow velocity patterns by pulsed Doppler echocardiography and the early diastolic mean filling rate (V1) by multi-gated blood pool scans was evaluated. The materials consist of 26 patients with hypertrophic cardiomyopathy (HCM), 24 with old myocardial infarction (MI), seven with hypertensive heart disease (HHD), seven with dilated cardiomyopathy (DCM), seven with ischemic heart disease (IHD), and 16 normal subjects (N). The results were as follows: 1. Acceleration time (AT) and deceleration time (DT) were significantly prolonged in HCM (120 +/- 20 msec, 147 +/- 23 msec), MI (102 +/- 17 msec, 124 +/- 21 msec), HHD (105 +/- 11 msec, 141 +/- 17 msec) and IHD (111 +/- 16 msec, 122 +/- 20 msec) compared with those of normals (89 +/- 20 msec, 106 +/- 18 msec). 2. V1 was significantly decreased in HCM (1.14 +/- 0.28 sec-1), MI (0.68 +/- 0.24 sec-1), HHD (0.73 +/- 0.12 sec-1), DCM (0.67 +/- 0.30 sec-1) and IHD (1.03 +/- 0.29 sec-1) compared with that of normals (1.48 +/- 0.28 sec-1). 3. There were significant negative correlations between V1 and AT or DT in HCM, IHD with slightly impaired diastolic filling and normals. However, there were significant positive correlations between V1 and AT or DT in MI and DCM. These findings suggested that left ventricular diastolic filling is impaired in both HCM and MI, and that DT-V1 relationship is useful for differentiating HCM characterized by the "chamber stiffness" from MI characterized by the "myocardial stiffness".
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)
The effects of various new anthracycline antibiotics on DNA and RNA synthesis were studied using DNA polymerase I (EC 2.7.7.7), RNA polymerase (EC 2.7.7.6) obtained from Escherichia coli and reverse transcriptase obtained from avian myeloblastosis virus. Aclacinomycin A, its analogues, baumycins A1 and A2, adriamycin and daunomycin showed potent inhibitory effects on these polymerases, with calf thymus DNA as template, with IC50 values of 10-30 microM. With poly(rA) x d(pT)10 as template for reverse transcriptase, aclacinomycin A and daunomycin showed IC50 values higher than 500 microM. Baumycins B1, B2, C1, and C2 showed high IC50 values on three polymerases. Addition of excess template DNA to the reaction mixture reversed the inhibitory effect of anthracyclines. Addition of calf thymus DNA to anthracyclines caused a bathochromic and hypochromic change in the visible spectrum. Apparent binding constant for aclacinomycin A, its analogues, and adriamycin were in the range of (1-2) X 10(6) M-1. Aclacinomycin A and adriamycin also bind to heat denatured DNA, but not strongly to yeast RNA. From these results, the structure-activity relationships of new anthracyclines on DNA binding and polymerase reactions are discussed.
Two patients with cleft palate, clubfoot, congenital scoliosis, and arthrogryposis multiplex congenita showed increased numbers of lipid droplets in biopsied muscle fibers. There was little abnormality in the mitochondrial morphology of the muscle and the results of blood chemistry including carnitine concentrations. Accumulation of large lipid droplets, increased amount of glycogen and a decreased number of mitochondria were observed in chondrocytes from the biopsied iliac crest cartilage of these patients. It was suggested that the present cases might belong to a previously unknown clinico-pathological entity of myopathies.
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.
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)