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Biomedical subjects

G Shimizu

Publications and source records attributed to G Shimizu.

28 records · Page 2Linked to original sources
PubMed1986

[The natural history of dilated cardiomyopathy and pathophysiology of congestive heart failure].

To clarify the natural history and mechanisms of compensation and decompensation in dilated cardiomyopathy (DCM), the hemodynamic and follow-up data of 52 patients who underwent cardiac catheterization between April 1976 and July 1984 were evaluated. The symptoms of the majority of 42 patients who were in severe congestive heart failure (CHF) (New York Heart Association Functional Class IV) on admission were improved. Two were in Class I, 22 in Class I, 22 in Class III, only six remaining in Class IV at the times of their catheterizations one to two months post admission. The patients were categorized as compensated (Class I and II) and decompensated (Class III and IV), and their data were compared with those of 30 normal subjects. Cardiac status was evaluated at the end of August 1984, and the mean follow-up period was 44 months. The hemodynamic and angiographic characteristics of DCM consisted of an enlarged and poorly contracting left ventricle, with an increased left ventricular (LV) muscle mass, low LV systolic pressure, reduced cardiac output, and elevated systemic vascular resistance. LV volume was larger, and the ejection fraction (EF) was more reduced in the decompensated group in association with elevated preload and afterload. Preload and afterload were within the normal range in the compensated group. LV wall thickness tended to decrease in the decompensated group, and the LV muscle masses did not differ between these two groups. There was a significant inverse correlation between afterload and EF (r = -0.57, p less than 0.01) in DCM. There were five sudden deaths and five CHF deaths, and cardiac symptoms improved in the majority of the survivors. One, two and five year survival rates were 91.2%, 79.8%, and 72.5%, respectively. No hemodynamic variables could be available to predict the prognosis except for the LV end-diastolic pressure and stress. It is concluded that the absence of adequate compensatory hypertrophy and the inappropriate elevation of afterload, or so-called "afterload mismatch" plays an important role in the development of CHF, in addition to depressed contractility in DCM. Persistent elevation of preload despite vigorous medical treatment indicates a poor prognosis. No other hemodynamic variables were good indicators of prognosis.

Blood Pressure↗
PubMed1985

Left ventricular chamber filling and midwall fiber lengthening in patients with left ventricular hypertrophy: overestimation of fiber velocities by conventional midwall measurements.

Observations that the inner (subendocardial) half of the left ventricular wall contributes more to total left ventricular wall thickening than the outer (subepicardial) half may have important implications in the analysis of myocardial fiber length transients. Accordingly, we measured endocardial and midwall shortening and lengthening rates in normal and hypertrophic heart and compared the results obtained with conventional methods of measurement with those obtained with a modified model that does not depend on use of conventional assumptions about the midwall. This modified (two-shell) cylindrical model) method considers the substantial contribution of inner wall thickening and thus does not require the assumption of a theoretical midwall fiber that remains at the midwall throughout the cardiac cycle. Echocardiographic data from six normal subjects and six patients with concentric left ventricular hypertrophy (LVH) were examined; left ventricular wall thickness ranged from 8 to 10 mm in normal subjects and from 11 to 16 mm in the patients with LVH. By design, the standard measurements of left ventricular size (diastolic and systolic dimensions) and systolic function (fractional shortening and endocardial fiber shortening velocities) were equal in the two groups. Endocardial, conventional midwall, and modified midwall methods all indicate reduced fiber lengthening rates in patients with LVH; peak fiber lengthening rates for normal and LVH groups were 4.5 +/- 0.7 vs 3.1 +/- 0.8 sec-1 (p less than .02) at the endocardium, 2.3 +/- 0.4 vs 1.6 +/- 0.4 sec-1 (p less than .02) at the midwall (conventional method), and 2.1 +/- 0.3 vs 1.4 +/- 0.3 sec-1 (p less than .01) at the midwall (modified method).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiomegaly↗
PubMed1984

Mechanisms of compensation and decompensation in dilated cardiomyopathy.

Left ventricular (LV) function was evaluated in 32 patients with dilated cardiomyopathy (DC) who underwent cardiac catheterization during the past 6 years (group 4), and the results were compared with the data of 30 normal subjects (group 1). The patients were divided into mildly (group 2, 12 patients) and severely symptomatic subgroups (group 3, 20 patients). DC was characterized by dilated and poorly contracting left ventricle with increased muscle mass, reduced cardiac output and elevated systemic vascular resistance. LV volume was larger, ejection fraction was lower, and end-diastolic and end-systolic stresses were higher in group 3 than in groups 1 and 2. No significant differences were seen in LV muscle mass and wall thickness between groups 2 and 3. A significant inverse correlation was seen between ejection fraction and end-systolic stress in patients with DC (Y = -0.05x + 48.7, r = 0.57, p less than 0.01). The slope of the correlation line between end-systolic stress and volume in DC (Y = 1.20x + 135, r = 0.52, p less than 0.02) was less steep than that of normal subjects (Y = 3.68x + 40, r = 0.64, p less than 0.001). These observations indicate that the primary problem of DC is depressed contractility.(ABSTRACT TRUNCATED AT 250 WORDS)

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

[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↗