Biomedical subjects

K Furubayashi

Publications and source records attributed to K Furubayashi.

10 recordsLinked to original sources

PubMed1984

Detection of left atrial thrombi in man using indium-111 labelled autologous platelets.

A scintigraphic technique using indium-111 labelled platelets to detect left atrial thrombi was used in 28 patients, 14 of whom had mitral valve disease and 14 combined valve disease. Imaging was performed in the anterior, right anterior oblique (45 degrees), and left lateral views on the day of injection and thereafter at one or two day intervals for a maximum of four days. When scintiphotos obtained in two or three views 72 or 96 hours after the platelet injection showed "hot spot areas" within the left atrial pool and indium-111 activity in these areas did not decrease with time they were interpreted as positive for thrombi. Of 28 patients, seven had positive platelet images by this criterion; of these, three underwent surgery and were found to have left atrial thrombi. One patient died, and a thrombus was found at necropsy. The remaining 21 patients had normal scintiphotos; of these, seven had no thrombi at operation and one had false negative images. The diagnostic accuracy of platelet scintigraphy by this criterion of positivity in the 12 patients in whom surgical or postmortem confirmation of thrombi could be obtained was 92%. These results indicate that this technique is a promising method for detecting active left atrial thrombi.

Adult↗

PubMed1984

Sequential changes of left ventricular function after cineangiography in normal heart and coronary artery disease.

To evaluate the effect of contrast material on left ventricular (LV) function, LV pressure and its first derivative were continuously monitored during and after LV cineangiography with Mikro-tip angiocatheters in 15 normal subjects (Group 1) and patients with coronary artery disease (CAD) without LV asynergy (Group 2, n = 10), with mild asynergy (Group 3, n = 12) and severe asynergy (Group 4, n = 13). In all 4 groups, systolic hypotension, decrease of negative dP/dt, and prolonged time constant of LV pressure fall (T) were observed in 30 seconds after dye injection, and all these parameters returned to the control value in 2 minutes. LV end-diastolic pressure (EDP) began to elevate at one minute, reached its peak at 2 minutes, and stayed elevated for 7 minutes. Although significant decrease in LV systolic pressure was seen, indexes of LV contractility, peak positive dP/dt and (dP/dt)/DP40, showed increase in all groups. No different directional changes of these parameters were observed among 4 groups. The degree of LVEDP elevation was parallel to the diastolic elastic stiffness constant (K) in Group 1 (r = 0.64, (p less than 0.05). It is concluded that systolic hypotension and prolonged relaxation are only transient, and elevation of LVEDP after the contrast material injection seems to be the effect of only acute volume overload.

Adult↗

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↗

PubMed1981

Hemodynamic characteristics of hypertrophic and congestive cardiomyopathies.

To elucidate the hemodynamics and mechanical properties of the myocardium in hypertrophic (HCM) and congestive cardiomyopathies (CCM), preload (end-diastolic stress), afterload (mid-systolic stress), contractility (peak positive dp/dt, (dp/dt)/DP40, ejection fraction), relaxation (peak negative dp/dt, time constant T), compliance (elastic stiffness constant, end-diastolic elastic stiffness), and performance (left ventricular minute work, left ventricular minute work/muscle mass) were determined in 19 patients with HCM, 11 with CCM, and 15 normal subjects. Preload was in the normal range in HCM even with elevated left ventricular end-diastolic pressure. In cases of CCM it was high only when congestive heart failure was present. Afterload was mildly elevated in CCM with heart failure, but only half the normal value in patients with HCM. The three indices of contractility were in the normal range in patients with HCM, and markedly reduced in those with CCM. Relaxation abnormalities were demonstrated in both HCM and CCM. The elastic stiffness constant was high in HCM and normal in CCM. End-diastolic stiffness was normal in HCM and high in CCM with heart failure. These observations suggest that chamber stiffness is markedly elevated in HCM, and stiffness of unit muscle is elevated in CCM when heart failure appears. Although left ventricular minute work was normal in HCM, minute work of unit muscle (left ventricular minute work/muscle mass) was markedly reduced. These observations indicate that the chief problem in CCM is contractile failure and that elevation of preload and muscle stiffness is associated with congestive heart failure in this disease. Although the conventional indices of contractility are in the normal range in HCM, the contractility of unit muscle is reduced, and hypertrophy seems to be a compensatory mechanism when the relations between afterload and ejection fraction and between preload and performance are considered.

Adult↗

PubMed1981

[Pathophysiology of hypertrophic and congestive cardiomyopathies: a guide of fundamental therapeutic approach (author's transl)].

A precise assessment of left ventricular (LV) function was performed in 20 patients with hypertrophic cardiomyopathy (HCM) and 14 patients with congestive cardiomyopathy (CCM) to elucidate the pathophysiology of these diseases, expecting to establish a fundamental therapeutic approach of them. Twenty-two patients who underwent cardiac catheterization and were found to have normal LV function served as normal control. LV preload, defined as LV end-diastolic stress, was normal in HCM, and it was elevated in patients with CCM and congestive heart failure (CHF). While an index of afterload, defined as mid-systolic stress, was markedly reduced in HCM, it was elevated in CCM and CHF. Although three indices of LV contractility including the rate of LV pressure rise divided by developed pressure of 40 mmHg ((dp/dt)/DP40), ejection fraction (EF) and LV minute work index, were all in a normal range in HCM, they were very low in CCM. This observation indicates that the systolic function of HCM is normal as a pump, and that it is markedly reduced in CCM. One index of LV relaxation, which was the peak rate of LV pressure fall (peak negative dp/dt) was reduced in both HCM and CCM, and the other index, which was the time constant of LV pressure fall (the time constant T) was prolonged in both of these diseases. An index of compliance, defined as diastolic elastic stiffness constant (K) was high in HCM and normal in CCM, and the other index, defined as end-diastolic elastic stiffness was normal in HCM and high in patients with CCM and CHF. This observation suggests that chamber compliance is low in HCM, and that muscle compliance begins to decline with the appearance of CHF in CCM. Although poor systolic function is evident in CCM, poor contractility or inadequate contraction of a unit muscle is also suspected in HCM since 1) normal EF was maintained with very low afterload, 2) LV end-systolic volume index was normal with very low end-systolic stress, and 3) LV unit muscle minute work about one half of normal value with normal preload. Several important therapeutic guidelines can be derived from this study: As CCM is a disease of reduced LV contractility, the main therapy for this disease is to enhance the contractility. Elevation of preload and afterload are associated with the appearance of CHF, and this coincides with New York Heart Association functional class III. Therefore, the indication of preload and/or afterload reducing agents, such as diuretics and vasodilators, is considered for such patients. Although preload and/or afterload reducing agents are well known to be contraindicated in obstructive type of HCM, since they increase the intracardiac pressure gradient, these agents must be used with great precaution in nonobstructive type, as they reduce preload suddenly, and life-threatening low cardiac output might take place. For the same reason, strenuous exercise must be prohibited in HCM...

Adolescent↗

PubMed1979