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Biomedical subjects

K Kaku

Publications and source records attributed to K Kaku.

At least 163 records · Page 9Linked to original sources
PubMed1982

Hypertrophic nonobstructive cardiomyopathy: a precise assessment of hemodynamic characteristics and clinical implications.

A precise assessment of left ventricular function was performed in 20 patients with hypertrophic nonobstructive cardiomyopathy to elucidate the basic pathophysiology, and the data were compared with those in 22 normal subjects. Whereas end-diastolic pressure was high in those with cardiomyopathy, a more accurate index of preload, end-diastolic stress, did not differ from normal value. Afterload was about half the normal value. Both isovolumic indexes [peak positive dP/dt and (dP/dt)/DP40] and ejection phase indexes of contractility (ejection fraction) were in the normal range; however, the end-systolic stress volume ratio was significantly reduced (43% of the normal value). Although the left ventricular minute work index was in the normal range, the unit muscle performance (minute work/mass) was very low (49%). An abnormality of left ventricular relaxation was demonstrated by low peak negative dP/dt (56%) and prolonged time constant T (191%), and a stiff left ventricle was demonstrated by a high diastolic elastic stiffness constant (129%). These observations suggest that the contraction of a unit muscle is inappropriate to produce an adequate contraction of the whole ventricle, and that hypertrophy might be an adaptive process to maintain normal systolic function by increasing mass and reducing afterload.

Adult↗
PubMed1982

Spontaneously acquired factor VIII inhibitor in a 7-year-old girl.

The youngest case with spontaneously acquired inhibitor to factor VIII is reported. A 7-year-old girl without any previous disorders presented with a hemarthrosis in the left knee and developed a rapidly expanding hematoma on the right arm, shoulder and chest after an initial infusion of factor VIII concentrate (1,000 units). Circulating antifactor VIII antibody was detected. Her coagulopathy was successfully managed with an additional massive infusion of factor VIII concentrate (7,500 units) and combination therapy of prednisolone and cyclophosphamide.

Autoantibodies↗
PubMed1982

[Midsystolic closure of the aortic valve in hypertrophic nonobstructive cardiomyopathy].

Midsystolic cessation of left ventricular contraction was documented in a patient with hypertrophic nonobstructive cardiomyopathy (HCM) associated with Cushing's syndrome (adrenal adenoma) without history of hypertension. The carotid pulse tracing showed a rapid upstroke with a prominent percussion wave which was rapidly decayed at midsystole followed by a tiny tidal wave. The decay of this percussion wave coincided in timing with midsystolic closure of the aortic valve in the echocardiogram. The left ventricle (LV) was symmetrically hypertrophied (wall thickness = 1.8 cm). The motion of the interventricular septum and LV posterior wall appeared trapezoid, and the contraction of these walls was normal in early-systole followed by the sudden cessation at midsystole till end-systole. Systolic anterior motion of the mitral valve was not observed. Cardiac catheterization revealed no pressure gradient in the LV even after the various provocative maneuvers. The left ventriculogram simultaneously recorded with LV pressure showed that LV ejection was completed at midsystole, when LV pressure fell from 98 to 83 mmHg. Mitral regurgitation was not observed. Midsystolic cessation of left ventricular contraction in this case is thought to be the cause of sudden interruption of forward aortic flow, resulting in a bifid carotid pulse and midsystolic closure of the aortic valve in the echocardiogram.

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↗
PubMed1982

[Evaluation of left ventricular function in patients with dilated cardiomyopathy by exercise echocardiography].

In order to evaluate left ventricular function of dilated cardiomyopathy, 24 patients and ten healthy subjects were studied by exercise echocardiography. The patients with dilated cardiomyopathy were classified into 3 groups according to the presence or absence of mitral regurgitation and the severity of left ventricular dilatation: Group I was consisted of five cases with mitral regurgitation. Group II was consisted of seven cases without mitral regurgitation who had marked left ventricular dilatation, where the left ventricular end-diastolic dimension index (DdI) was greater than 46 mm/m2 and left ventricular end-systolic dimension index (DsI) was greater than 40 mm/m2. Group III was consisted of 12 cases without mitral regurgitation who had moderate left ventricular dilatation, where the DdI was less than 46 mm/m2 or DsI was less than 40 mm/m2. The ergometer exercise tests were performed for 3 min at 25 watts in a supine position. There was no significant differences of exercise-induced increases in heart rate, elevations of systolic blood pressure and increases of rate pressure product, respectively, between healthy subjects and each group of dilated cardiomyopathy. In healthy subjects, both DdI and DsI were unchanged on exercise. In Group I, DdI was unchanged but DsI decreased (p less than 0.02), thus percent fractional shortening of the left ventricle (delta D) was increased (p less than 0.05). In Group II, both DdI and DsI were unchanged. In Group III, DdI was increased (p less than 0.05) while DsI was unchanged, thus delta D was increased (p less than 0.02). These results suggested that the left ventricle is able to respond to exercise by its further dilatation (increase of preload) in mild to moderate dilated cardiomyopathy (Group III). On the other hand, in cases with marked left ventricular dilatation (Group II), the further dilatation is not induced. The same was true in dilated cardiomyopathy with mitral regurgitation (Group I), where the left ventricle had almost the same size as in Group II, although changes in DsI and delta D were not evaluated precisely because of the associated regurgitation.

Blood Pressure↗
PubMed1981

Doublet-outlet right ventricle [S,D,L] with subaortic ventricular septal defect and pulmonary stenosis: successful repair using an intraventricular conduit.

An 18-year-old Japanese girl with double-outlet right ventricle (DORV) [S,D,L], subaortic ventricular septal defect and pulmonary stenosis was successfully treated under cardiopulmonary bypass by resection of the obstructing subpulmonic infundibulum, pulmonary valvulotomy and construction of an intraventricular conduit between the ventricular septal defect and the aorta. The postoperative course was uneventful, except for mild low-output syndrome, and she was discharged 7 weeks after surgery in good condition. She is at present free from all untoward cardiac symptoms.

Adolescent↗