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S Toh

Publications and source records attributed to S Toh.

49 records · Page 3Linked to original sources
PubMed1987

[Relationships between segmental left ventricular wall motion abnormalities and pathological findings in patients with dilated cardiomyopathy].

Relationships between segmental left ventricular wall motion abnormalities and myocardial fibrosis at autopsy were examined in 12 patients who died of dilated cardiomyopathy. In each case, wall motion abnormalities were assessed by two-dimensional echocardiograms for 11 segments, and semiquantitatively evaluated as normokinesis (N) to hypokinesis (H), severe hypokinesis (SH) or akinesis (A). From the necropsy specimens, the myocardial fibrosis ratio was histologically quantitated using a point-counting method in each segment corresponding to the echocardiographic segment. Wall motion abnormalities and the fibrosis ratio correlated significantly in a total of 132 segments of the 12 patients, but there were some discordances. The cases were then categorized in uniform and non-uniform groups based on the patterns of myocardial fibrosis. Wall motion abnormalities correlated much better with the fibrosis ratio in a total of 44 segments among four cases with non-uniform fibrosis, whereas no significant correlation was found in a total of 88 segments in eight cases with uniform fibrosis. The latter group had more severe segmental wall motion abnormalities in the interventricular septum than in the left ventricular free wall; and in the apical portion rather than in the basal portion, although no significant difference was observed in the fibrosis ratio among these regions. Patients with non-uniform fibrosis had higher incidences of chest pain and sudden deaths and a significantly larger left ventricular end-diastolic dimension on M-mode echocardiogram as compared to those with uniform fibrosis. Pathologically, in the former group, the heart was heavier, the mean left ventricular fibrosis ratio was significantly higher, and there was a greater incidence of infiltration of the myocardium by mononuclear cells, but there was no difference in the mean left ventricular wall thickness. These results suggest that myocardial fibrosis mainly contributes to the wall motion abnormalities in cases with non-uniform fibrosis which may be caused by chronic myocarditis, but not in cases with uniform fibrosis. In the latter group, other factors such as reduced contractility of the myocardial cells or lack of a compensatory mechanism for wall stress seem to play important roles in causing left ventricular wall motion abnormalities.

Adult↗
PubMed1986

[Malignant familial cardiomyopathy with sudden death, typical asymmetric septal hypertrophy and dilated cardiomyopathy-like features].

Twenty-one members of a family were traced for three generations including the propositus, who had typical dilated cardiomyopathy (DCM)-like features. Clinical, radiological, electrocardiographic and echocardiographic examinations were performed for 13 of 16 still living. Five of 21 members died including three of sudden death. Among living 16 members, five had congestive heart failure, greater than grade III of the NYHA, and cardiomegaly on chest radiography in five. Left ventricular hypertrophy, abnormal Q waves, and ST-T changes were observed on electrocardiography in two, five and eight members, respectively. Echocardiography revealed asymmetric septal hypertrophy (ASH) in four, two of whom had systolic anterior motion (SAM) of the mitral valve. Two had features simulating DCM, and five had mitral valve prolapse. Among six patients with ASH or features simulating DCM, four had cardiac catheterization, coronary angiography and endomyocardial biopsy. None had significant coronary stenosis, but all had high left ventricular end-diastolic pressure (LVEDP) (23 +/- 7 mmHg). Endomyocardial biopsy showed moderate myocardial cellular hypertrophy, interstitial myocardial fibrosis, nuclear changes and myocardial disarrangement, with features characteristic of HCM. In this family with malignant HCM, patients had various clinical features including typical HCM, simulated DCM, DCM coexisted with mitral valve prolapse, and sudden death occurred frequently.

Adolescent↗
PubMed1985

Study on the mitral valve prolapse. I. Incidence in Kobe University students. II. Follow up study.

Incidence of mitral valve prolapse (MVP) in 4517 students of Kobe University, and clinical features in cases with MVP were studied. MVP was detected in 42 cases by two-dimensional echocardiography, and the prevalence of MVP was 0.93 percent (42 of 4517 cases). Among 42 cases with MVP, apparent mitral regurgitation (MR) was noted in one case with severe MVP, ventricular tachycardia was detected in one and ST-T wave abnormalities were detected in 10 respectively. In another follow up study of our hospital, 14 of 85 patients followed more than one year were noted to be deterioration in echocardiographic parameters. Eight of 14 patients had severe prolapse with severe MR, but remaining 6 had mild or moderate prolapse with mild or absent of MR. However, ST-T wave abnormalities, serious arrhythmias, and low response of %FS increase on exercise were found in high incidence in 6 of mild or moderate prolapse as well as in severe prolapse. So these follow up results suggested that not only students with severe MVP but also students with mild or moderate MVP with ST-T wave changes or VPC found in university medical examination must be followed up carefully.

Adolescent↗
PubMed1985

[Hypertensive heart disease simulating dilated cardiomyopathy].

Echocardiography was performed for 246 patients with hypertension. Among the 246 patients, echocardiographic features simulating dilated cardiomyopathy (DCM) were observed in 12. These patients had past history of hypertension and prominent left ventricular dilatation with reduced left ventricular contractility, but no left ventricular wall thickening. To elucidate the mechanism producing DCM-like features in patients with hypertension, the clinical and echocardiographic findings of the 12 hypertensive patients (HT-DCM) were compared with those of 50 hypertensive patients without dilated left ventricles and of 31 patients with DCM. On admission, all patients with HT-DCM had congestive heart failure (CHF) without high blood pressure and their echocardiograms revealed the abnormal findings described above. There were no differences of the clinical and echocardiographic findings on admission between HT-DCM and DCM. Following medical treatment, relatively early improvement of CHF was noted in all patients with HT-DCM; the LV dimension decreased and diffuse wall motion abnormality improved steadily with gradual elevation of blood pressure during the follow-up periods. The LV function of most patients with HT-DCM improved markedly but never reached normal levels. There were no significant differences the right ventricular endomyocardial biopsy findings of between DCM and HT-DCM. It was suggested the DCM-like features in these cases are caused, not only by hypertension, but by other factors, as well.

Adult↗
PubMed1985

[Hypertrophic cardiomyopathy with progressive left ventricular hypertrophy: a case report].

A 64-year-old man was hospitalized in March 1983 for recurrent episodes of dyspnea and palpitation despite medical treatment. At 48 years of age (1967), hypertension was diagnosed, but well controlled by propranolol. At the age of 59 years (1979), his first episode of dyspnea and palpitation was noted, with electrocardiographic (ECG) evidence of left ventricular hypertrophy (LVH), and abnormal Q waves in leads III and a VF. The echocardiogram, however, showed mild LVH with neither asymmetric septal hypertrophy (ASH) nor systolic anterior movement (SAM). On admission (1983), his blood pressure was 130/70 mmHg, and a grade III systolic murmur was heard along the left sternal border and over the apex. On ECG, the left precordial voltage (Sv1 + Rv5) was diminished and the depth of the Q wave in lead III increased compared with that of 1978. On echocardiography, we observed prominent septal hypertrophy (IVST: 20 mm) with ASH (IVST/PWT = 2.0), SAM, an enlarged left atrium, and a diminished left ventricular (LV) cavity. Left ventricular catheterization showed a pressure gradient of 90 mmHg between the LV apex and outflow tract and histological examination of the bi-ventricular endomyocardial biopsy material showed markedly hypertrophied and mildly disarranged myocardial fibers with bizarre nuclei. We considered that this was an interesting case in which ASH and SAM developed in the progression of LVH during the follow-up period.

Cardiac Catheterization↗
PubMed1985

[Regional right ventricular hypertrophy in hypertrophic cardiomyopathy and hypertension].

The mode of right ventricular hypertrophy was assessed by two-dimensional echocardiography (2DE) for 24 patients with hypertrophic cardiomyopathy (HCM), and the results were compared with those of 51 patients with hypertension (HT). The patients with HT were categorized in four groups depending on the thickness of the interventricular septum (IVST) and left ventricular posterior wall (PWT): HT-ASH with both left ventricular hypertrophy (LVH) (IVST greater than or equal to 13 mm) and asymmetric septal hypertrophy (ASH) (IVST/PWT greater than or equal to 1.3), severe HT with LVH and without ASH, and mild HT without LVH and ASH. Anterior wall thickness (AWT), posterior wall thickness (PWT), and diaphragmatic wall thickness (DWT) of the right ventricle were obtained from 2DE in the parasternal long-axis view, the short-axis view and subxiphoid view, respectively. These were recorded on video tape, and the measurements were made on the stop frames. Right ventricular hypertrophy (RVH) was estimated by the maximal right ventricular wall thickness (max RVWT), and the ratio of the maximal and minimal thickness (max RVWT/min RVWT) was calculated to evaluate asymmetrical hypertrophy (AH) of the right ventricle (RV). The incidence of RVH (Max RVWT greater than or equal to 5 mm) and asymmetrical hypertrophy (AH) (max RVWT/min RVWT greater than or equal to 1.3) of the RV in HCM, HT-ASH and mild HT were 67% and 41%, 57% and 45%, and 15% and 11%, respectively. The incidence of RVH with AH was more frequent in patients with HCM as well as HT with ASH than in patients with HT without ASH.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Volume↗
PubMed1985

[Regional left ventricular function in dilated cardiomyopathy: observation of regional left ventricular wall motion before and during dobutamine administration].

To investigate left ventricular function and the prognosis of patients with dilated cardiomyopathy (DCM), regional wall motion of the left ventricle of 38 patients with DCM was observed before and during dobutamine infusion (8 micrograms/kg X min) by two-dimensional echocardiography (2DE). The left ventricle was divided into 11 segments and the severity of wall motion abnormality (WMA) was classified into 4 grades, i.e. akinesis or dyskinesis (A), severe hypokinesis (SH), hypokinesis (H) and normokinesis (N), and numerical scores were assigned to each grade of WMA as follow; A: 3, SH: 2, H: 1, and N: 0. In the 38 patients with DCM, the number of segments with WMA was 8.3 +/- 2.9 (mean +/- SD). Among 418 segments in the 38 patients, we observed A in 71 segments, SH in 104 segments, H in 140 segments, and N in 103 segments. The WMA was not uniform in the left ventricle, and severe WMA was observed in the apex (WMA score: 2.0 +/- 1.0), while the grades of WMA in the lateral and posterior walls were mild (WMA score: 0.8 +/- 1.1) compared with those of other segments. The total sums of the WMA scores in 11 segments for each patient (TWMAS) were significantly greater in patients with severe heart failure (New York Heart Association [NYHA] functional class III or IV) than in patients with mild heart failure (NYHA class I or II) (22.0 +/- 5.2 and 9.9 +/- 4.9, p less than 0.001). TWMAS correlated with the cardiac index (CI) (r = -0.58, p less than 0.005) and pulmonary capillary pressure (PCP) (r = 0.68, p less than 0.001). In 242 segments of 22 patients, whose regional wall motion was observed before and during dobutamine administration, wall motion was improved by one grade in 82 of 170 segments with WMA before dobutamine infusion; i.e. regional wall motion changed from A to SH in six segments, from SH to H in 31 segments, and from H to N in 45 segments with dobutamine administration. According to the change in grade of TWMAS induced by dobutamine administration, 22 patients with DCM were classified into two groups: a good response group (% change of TWMAS greater than or equal to 40%), and a poor response group (% change of TWMAS less than 40%). The poor response group had ventricular tachycardia more frequently, more severe heart failure, lower CI and higher PCP than the good response group.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1984

Clinical significance of left ventricular hypertrophy in dilated cardiomyopathy: an echocardiographic follow-up of 50 patients.

To evaluate the significance of left ventricular (LV) hypertrophy in patients with dilated cardiomyopathy (DCM), 50 patients seen between 1976 and 1983 were studied echocardiographically. We categorized the patients as four groups according to the degree of LV dilatation or hypertrophy. Group consisted of 17 patients with mild to moderate LV dilatation without hypertrophy (LV end-systolic I dimension: Ds less than 60 mm, LV wall thickness at end-systole: WTs less than 15 mm). Group II, 12 with mild to moderate LV dilatation and hypertrophy (Ds less than 60 mm, WTs greater than or equal to 15 mm). Group III, eight with marked LV dilatation and hypertrophy (Ds greater than or equal to 60 mm, WTs greater than or equal to 15 mm), and Group IV, 13 with marked LV dilatation without hypertrophy (Ds greater than or equal to 60 mm, WTs less than 15 mm). Twenty patients had LV hypertrophy and 30 patients were without LV hypertrophy at the start of this study. New York Heart Association functional classes, cardiothoracic ratio and ECG findings at the first study did not show any statistically significant differences among the four groups. During the prospective follow-up of 2.7 years in average, eight patients died of congestive heart failure including five of Group IV, and three of Group I who had progressive LV dilatation. Three patients of Group I, II and III died suddenly. Ambulatory ECGs showed life-threatening ventricular arrhythmias in all 32 patients studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

[Regional myocardial contraction in ischemic heart disease: evaluation of regional myocardial thickening by two-dimensional echocardiography].

There were many studies concerning the evaluation of regional wall motion in ischemic heart disease by left ventriculography (LVG) and two-dimensional echocardiography (2DE), but only a few observations on the regional myocardial thickening have been reported. In a survey of 48 cases of old myocardial infarction, we selected 21 cases with adequate 2DE images for the evaluation of regional wall motion and thickening. In all cases the 2DE examinations were performed within seven days before or after LVG examinations. The left ventricular wall on 2DE was divided into 11 segments and wall motion and thickening in each segment were graded to three classes, i.e. none, reduced and normal. The results on 2DE were then compared with the grade of wall motion of the corresponding segment on LVG. The sensitivity and specificity of 2DE wall motion were 50% and 89% in none, 59% and 48% in reduced, and 89% and 84% in normal, respectively. The sensitivity and specificity of 2DE myocardial thickening were 81% and 93% in none, 82% and 70% in reduced, and 92% in normal, respectively. These results indicated that the regional myocardial thickening by 2DE has a higher sensitivity and specificity. Therefore, observation of both myocardial thickening and wall motion will be necessary for the proper evaluation of regional myocardial contraction in ischemic heart disease.

Adult↗
PubMed1982

[Two-dimensional echocardiographic findings of patients with papillary muscle dysfunction].

Two-dimensional echocardiographic examination was performed to investigate pathophysiological mechanism of mitral regurgitation due to papillary muscle dysfunction in 6 patients with myocardial infarction (anterior : 3, inferior: 2 and subendocardial: 1) and 13 patients with dilated cardiomyopathy. The patients were divided into 2 groups; Group I was 9 with mitral valve prolapse and Group II was 10 without mitral valve prolapse (MVP). In Group I MVP was observed in the posterior leaflet in 6 and in both leaflets in the remainder. The apical four-chamber view of all patients in Group II showed that the point of mitral valve coaptation displaced toward the apex of the left ventricle during systole and the both mitral leaflets were convexed toward the left ventricle. Follow-up observation in a patient with dilated cardiomyopathy revealed that the heart was not enlarged (CTR 50%), no murmur was heard and mild anterior mitral leaflet prolapse was observed in 1979, but, in 1981, CTR became 63%, and a grade IV systolic murmur suggesting mitral regurgitation was noted. Two-dimensional echocardiography revealed that mitral leaflets became convex toward the left ventricle and coaptation point of the mitral closure shifted to the apex of the left ventricle below the level of mitral annulus. Thus, the transition to Group II from Group I was suggested. Echocardiographic measurements revealed that left ventricular end-diastolic dimension was 71 +/- 11 mm in Group I and 74 +/- 10 mm in Group II, left ventricular end-systolic dimension was 61 +/- 11 mm in Group I and 62 +/- 11 mm in Group II, and anterio-posterior mitral ring dimension was 31 +/- 3 mm in Group I and 35 +/- 3 mm in Group II (p less than 0.05). In conclusion, it was suggested that two mechanisms of mitral regurgitation are present in papillary muscle dysfunction; 1) mitral valve prolapse and 2) shift of mitral coaptation point toward the apex of the left ventricle associated with marked dilatation of the mitral annulus.

Adult↗
PubMedDate not supplied

Techniques for reducing anterior knee symptoms after anterior cruciate ligament reconstruction using a bone-patellar tendon-bone autograft.

Seventy-five patients underwent unilateral anterior cruciate ligament reconstruction with an ipsilateral bone-patellar tendon-bone autograft at our institution. The graft was harvested using a two-transverse-incision technique, and patellar and tibial bony defects were repaired with cored bone grafts collected by reaming the femoral socket and the tibial socket or tunnel. We evaluated the incidence of anterior knee pain, donor site tenderness, and sensory disturbance after use of these procedures. We also analyzed the correlation between anterior knee pain and age, sex, bone plug length, range of motion, postoperative stability, patellar tendon shortening, infrapatellar nerve injury, and the size of the patellar defect. Thirteen patients reported anterior knee pain. Donor site tenderness was detected in 10 patients and was located on the inferior pole of the patella, the tibial tubercle, or both. Sensory disturbance was found over the infrapatellar nerve area in 13 patients. Statistical analysis showed that anterior instability (side-to-side difference of >3 mm) and residual patellar bony defect (depth >2 mm) were risk factors for anterior knee pain. The results of our study suggest that cored cancellous bone grafting for complete restoration of the donor site bony defects and the two-transverse-incision technique to preserve the infrapatellar branch of the saphenous nerve contribute to prevention of anterior knee symptoms.

Adolescent↗
PubMedDate not supplied

Graft incorporation within the tibial bone tunnel after anterior cruciate ligament reconstruction with bone-patellar tendon-bone autograft.

We described histologic changes in patellar tendon autografts that occur over time within the tibial tunnel in specimens harvested from patients undergoing revision anterior cruciate ligament reconstruction. Ten patients, averaging 21.2 years of age, were divided into two groups based on the time period between their original and revision surgery: early revision (less than 1 year, four patients) and late revision (more than 1 year, six patients). Among the early revision group, the tendon within the tunnel showed increased cellularity and random collagen bundles. A specimen from the shortest early revision case revealed a normal original bone-tendon junction, whereas others showed an obscured structure. Between the tendon and the tunnel wall, granulation tissue was seen and the bone-tendon junction was still immature. In the late revision group, the tendon appeared similar to normal ligament. The original bone-tendon junction was not seen, and the tendon continued completely to the tunnel wall with Sharpey-like fibers. Observations in the early revision group suggest that tendon remodeling and bone-tendon integration continue for at least several months after transplantation. The original bone-tendon junction appears to have shifted to the proximal patellar tendon-tunnel wall junction with time. These findings are in agreement with prior animal studies.

Adolescent↗