Biomedical subjects

F Ohmori

Publications and source records attributed to F Ohmori.

At least 55 records · Page 3Linked to original sources

PubMed1986

Clinical study on cardiac sarcoidosis.

Forty-one patients with sarcoidosis were investigated for cardiac involvement. The results are summarized as follows: The focal left ventricular perfusion defect was found on the TMPS's of 5 out of 41 patients with sarcoidosis. The defect disappeared in four of these five patients over a 3-year period, but remained in the patient with fatal myocardial sarcoidosis. A decreased left ventricular ejection fraction was found in 14 out of 41 patients with sarcoidosis, and in 3 out of 5 patients with the left ventricular perfusion defect. Echocardiographic examination did not reveal left ventricular wall dysfunction at the site of the left ventricular perfusion defect, except in one patient with fatal myocardial sarcoidosis. Holter ECG's showed such abnormalities as CRBBB, heart blocks, PVC, and PSC in 13 out of 32 patients with sarcoidosis. SACE activity was elevated in all three patients with the left ventricular perfusion defect that were examined, and it could be correlated with changes in the left ventricular perfusion defect in one of them.

Adult↗

PubMed1986

[Greetings at the beginning of 1986].

Explore the source record for details and available documents.

Humans↗

PubMed1986

[Asymmetric septal hypertrophy of sporadic form with abnormal thallium perfusion and myocardial enzymes].

Asymmetric septal hypertrophy with abnormal thallium scintigram and elevated cardiac enzymes were observed in five patients and were studied with special reference to the clinical significance of their clinicopathological features. They were not familial cardiomyopathy patients. Two of the five patients (Cases 1 and 2) exhibited the clinical features characteristic of hypertrophic cardiomyopathy without abnormal thallium perfusion and serum cardiac enzyme levels. A right endomyocardial biopsy for Case 1 disclosed myocardial fibrosis in addition to hypertrophy and disarray of myocardial fibers. The left ventricular cavities of two other patients (Cases 4 and 5) tended to be dilated with signs of impaired systolic function and asymmetric septal hypertrophy. A regional area of reduced thickness was observed in the medial portion of the left ventricular posterior wall of Case 4. The remaining case (Case 3) exhibited left ventricular dilatation and reduced left ventricular systolic function, disproportionate hypertrophy, and had clinical signs of congestive heart failure. Necropsy disclosed massive fibrosis and diffuse disarray of myocardial fibers. Some patients with familial hypertrophic cardiomyopathy progress to exhibit clinical features of dilated cardiomyopathy in the terminal stages, and have massive fibrosis of the myocardium histologically. Thallium scintigraphic abnormalities and elevated serum levels of cardiac enzymes, especially the LDH1 isoenzyme, in patients with hypertrophic cardiomyopathy may be a meaningful indicator of such progression in its early stages. The five patients in the present study exhibited a variety of clinical and histological features which may comprise a spectrum of clinical conditions during the progression from hypertrophic cardiomyopathy to a condition like dilated cardiomyopathy, similar to that in familial patients. This progression and the factors promoting it should be studied further in the near future.

Adult↗

PubMed1986