Biomedical subjects

N Maehashi

Publications and source records attributed to N Maehashi.

10 recordsLinked to original sources

PubMed1991

The role of myocarditis and myocardial fibrosis in dilated cardiomyopathy. Analysis of 28 necropsy cases.

The hearts of 28 necropsy cases with DCM and 10 control cases were analysed to elucidate the role of myocarditis and fibrosis in dilated cardiomyopathy (DCM). The extent of fibrosis and myocyte diameter were measured in the transverse sections of the left ventricle. The degree and pattern of fibrosis varied widely from case to case. The DCM cases were then classified into 3 groups: 1) Group Ia, 8 cases with mild diffuse fibrosis; 2) Group Ib, 9 cases with severe diffuse fibrosis and 3) Group II, 11 cases with segmental fibrosis. Myocardial fibrosis and hypertrophy were significantly more prominent in Groups Ib and II than in the control group (p less than 0.01), but no differences were observed between Group Ia and the control group. Thus, it is reasonable to attribute the chronic CHF and LV dilatation in Groups Ib and II to the extensive myocardial fibrosis. In contrast, it is not reasonable to attribute the chronic CHF and LV dilatation in Group Ia to myocardial fibrosis. Focal lymphoid cell infiltration was graded to assess inflammatory changes. Group II showed more prominent inflammatory changes than the other 2 groups (p less than 0.05). Thus, it is possible that myocarditis is an etiologic factor for DCM with a segmental pattern of fibrosis.

Adolescent↗

PubMed1988

[Comparison of regional contractile dynamics and pathological findings of the left ventricular wall in patients with hypertrophic cardiomyopathy].

To investigate the relationship between regional contractile dynamics and regional myocardial lesions of the left ventricular wall in patients with hypertrophic cardiomyopathy (HCM), autopsy findings of 11 patients were compared with their ante mortem echocardiographic findings. The regional systolic wall thickenings (%RWT) of the interventricular septum (IVS) and left ventricular posterior wall (LVPW) obtained using M-mode echocardiography were converted into % normalized RWT (%NRWT) by the averaged %RWT in 15 normal subjects. The %NRWT was compared with the wall thickness obtained by echocardiography and/or autopsy, and histological findings, such as the myocardial fibrosis ratio, disarray area ratio, and mean myocyte diameter. 1. There were no significant correlations among wall thickness of the left ventricle, the myocardial fibrosis ratio, the disarray area ratio, and the mean myocyte diameter of each segment. 2. The %NRWT in 22 segments of the 11 patients with HCM was not significantly related to the echocardiographic wall thickness at end-systole, the autopsy wall thickness, the mean myocyte diameter and the disarray area ratio, but that correlated significantly with the echocardiographically-determined wall thickness at end-diastole (r = -0.53, p less than 0.02), and with the myocardial fibrosis ratios (r = -0.59, p less than 0.005). 3. The %NRWT in the IVS was significantly less than that in the LVPW. The %NRWT in all segments of the LVPW was significantly related to the myocardial fibrosis ratios (r = -0.80, p less than 0.005), but was not related to the wall thicknesses or the disarray area ratios.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

[Pathogenesis of dilated cardiomyopathy: a study based on comparison of the clinical features with other related conditions].

To investigate the pathogenesis and pathophysiology of dilated cardiomyopathy (DCM), we studied 28 patients with DCM by echocardiography and endomyocardial biopsy, and compared their findings with those of 34 patients including eight with myocarditis, seven with alcoholics, 12 with hypertensives and seven patients with hypertrophic cardiomyopathy. All 12 patients in the hypertensive group had congestive heart failure without accompanying high blood pressure, and prominent dilatation and uniform wall motion abnormality of the left ventricle observed echocardiographically on admission. After medical management, both heart failure and the echocardiographic abnormalities gradually resolved. Those in the alcoholic group had larger left ventricles and uniform wall motion abnormality compared to those in the other groups. The myocarditis and hypertrophic cardiomyopathy groups had smaller left ventricles, non-uniform wall motion and larger % myocardial fibrosis. Both ventricles in the hypertrophic cardiomyopathy group were thicker than those of the other three groups. Each patient with DCM had individual echocardiographic abnormalities, which could be categorized as two subsets depending on the degree of left ventricular dilatation and uniformity of the wall motion. The one was characterized by a prominently dilated left ventricle and uniform wall motion abnormality similar to the alcoholic group, and the other had less marked left ventricular dilatation and heterogeneous wall motion abnormality similar to the myocarditis group. From these findings, it was suggested that there are common factors to specific myocardial disease in the pathogenesis and pathophysiology of DCM, and thus, DCM might include many subsets of different etiologies.

Adult↗

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↗

PubMed1987

[A trial diagnosis of latent dilated cardiomyopathy].

To diagnose latent dilated cardiomyopathy (latent DCM), we performed loading echocardiography with Angiotensin II and ergometer exercise in 41 patients. Twenty-one patients were suspected of having latent DCM because of histories, of heart failure of myocarditis; 10 patients had DCM; and 10 normal persons served as controls. On angiotensin II loading, cardiac function deteriorated in the DCM group, but it was maintained in the normal controls. Nine patients in the latent DCM group showed the same pattern as normals (L1-group), and 12 did as the DCM group (L2-group). Although % fractional shortening, end-diastolic and end-systolic dimensions of the left ventricle did not differ between the L1 and L2-groups, the A/R, the ratio of the pulsed Doppler echocardiogram at the left ventricular inflow tract, was larger and the exercise change of the % fractional shortening and exercise tolerance were less in the L2-group than in the L1-group. Furthermore, the biopsy findings of the L2-group were similar to those of the DCM group in terms of myocardial degeneration, myocardial hypertrophy and interstitial fibrosis. Thus, patients in the L2-group were thought to have a risk for DCM, and were cases of latent DCM. Angiotensin II loading is thought to be useful for diagnosing such cases.

Angiotensin II↗

PubMed1986

[Mitral valve prolapse with myocardial disarrangement and familial hypertrophic cardiomyopathy: a case report].

This is a report of a patient with mitral valve prolapse (MVP) and myocardial abnormalities on endomyocardial biopsy in whose relatives hypertrophic cardiomyopathy (HCM) was identified. A 19-year-old woman was admitted to our hospital for evaluation of a heart murmur. A systolic ejection murmur was audible in the third intercostal space at the left sternal border, and a standard 12-lead electrocardiogram showed ST-T wave changes in leads II, III and aVF. Echocardiography revealed prolapse of the anterior leaflet of the mitral valve, but no left ventricular hypertrophy. Endomyocardial biopsy disclosed mild hypertrophy and disarrangement of the myocardium. The family study revealed asymmetrical septal hypertrophy in her mother, who had no history of hypertension. Her younger sister had mild hypertrophy of the interventricular septum on echocardiography, and her histopathological findings suggested a diagnosis of HCM. This case was clinically regarded as MVP, but development of left ventricular hypertrophy as noted in her mother may occur in the future.

Adolescent↗

PubMed1986

[Severity and non-uniformity of regional wall motion in dilated cardiomyopathy evaluated by two-dimensional echocardiography].

A two and a half year follow-up study of segmental left ventricular wall motion was performed by two-dimensional echocardiography for 26 patients with dilated cardiomyopathy (DCM). Segmental analysis of left ventricular wall motion abnormalities (WMA) was performed using 11 segments obtained by short- and long-axis views of the left ventricle. Wall motion in each segment was classified and assigned a numerical score as normal (0), hypokinetic (1), severely hypokinetic (2), and akinetic or dyskinetic (3). Based on this categorization, a wall motion abnormality index (WMAI) was derived as an overall assessment of left ventricular asynergy. The intersegmental standard deviation of the wall motion abnormality score was used as an index of left ventricular asynergy (non-uniformity index: NUI). During the follow-up period, the wall motion abnormality index increased in all of the 26 patients (from 1.23 to 1.82, p less than 0.001), but the non-uniformity index did not change (from 0.72 to 0.73). When comparing the non-uniformity index among three groups classified according to the grade of wall motion abnormality, both at the initial and during follow-up studies, the moderate wall motion abnormality group (1.0 less than or equal to WMAI less than 2.0) had larger non-uniformity indexes (0.83, 0.84) than the other groups, and the severe non-uniformity index (greater than or equal to 0.9) was observed solely in the moderate group. In the follow-up study, these 26 patients were categorized in two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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

[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

[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↗