Search PubMed⌕ Search

Biomedical subjects

G Shimizu

Publications and source records attributed to G Shimizu.

16 recordsLinked to original sources
PubMed1992

Prominent negative T waves with QT prolongation indicate reperfusion injury and myocardial stunning.

To observe the clinical course after reperfusion and recovery from myocardial stunning of the left ventricular anterior wall, we prospectively reviewed and analyzed cardiac enzymes, ECG changes, echocardiograms, and cineangiograms in 8 patients with the acute ischemic syndrome who fulfilled the following criteria: 1) no history of previous myocardial infarction, 2) repeated and/or prolonged episodes of chest pain, 3) critical stenosis of the left anterior descending artery with wall motion abnormalities, 4) successful emergency percutaneous transluminal coronary angioplasty, and 5) normal wall motion on repeat cineangiography 4 to 8 weeks later. Creatine kinase (CK) and/or its cardiac isoenzyme (CK-MB) were minimally elevated in all cases. Wall motion was normalized with the reduction of end-systolic volume (end-diastolic volume: from 139 +/- 25 to 140 +/- 37 ml, ns, end-systolic volume: from 68 +/- 16 to 39 +/- 13 ml, p < 0.001, ejection fraction: from 51 +/- 6 to 71 +/- 6%, p < 0.001). Serial echocardiograms showed normalization of wall motion within 4 to 28 days. T wave inversion in the left precordial leads developed 30 min to 5 hours after the cessation of chest pain or successful reperfusion, and prominent negative T waves (1.6 +/- 0.6 mV) with QT prolongation (0.56 +/- 0.08 sec) in V3 or V4 reached their peak values within one to 5 days. ECG abnormalities resolved after 21 to 95 days. These ECG findings may indicate reperfusion injury and the presence of myocardial stunning in the anterior wall of the left ventricle.

Aged↗
PubMed1991

Left ventricular midwall mechanics in systemic arterial hypertension. Myocardial function is depressed in pressure-overload hypertrophy.

BACKGROUND: Left ventricular (LV) midwall geometry has been described conventionally as the sum of the chamber radius and half of the wall thickness; this convention is based on the assumption of uniform transmural thickening during systole. However, theoretical considerations and experimental data indicate that the inner half (inner shell) of the LV wall thickens more than the outer half (outer shell). Thus, an end-diastolic circumferential midwall fiber exhibits a relative migration toward the epicardium during systole. As a result, the conventional method provides an overestimate of the extent of the midwall fiber shortening. METHODS AND RESULTS: We developed an ellipsoidal model with a concentric two-shell geometry (nonuniform thickening) to assess midwall fiber length transients throughout the cardiac cycle. This modified midwall method was used in the analysis of LV cineangiograms from 15 patients with systemic arterial hypertension and 14 normal subjects. Study groups were classified according to LV mass index (LVMI): 14 normal subjects (group I), eight hypertensive patients with a normal LVMI (group II), and seven hypertensive patients with an increased LVMI (group III). There were no significant differences in LV end-diastolic pressure or volume among the three groups; the ejection fraction was slightly greater in group II (70 +/- 5%) than in groups I (65 +/- 8%) and III (66 +/- 4%), but this trend did not achieve statistical significance. Values for endocardial and conventional midwall fractional shortening (FS) were also similar in the three groups. By contrast, FS by the concentric two-shell geometry (modified midwall method) in group III (16 +/- 2%) was significantly less than that seen in groups I and II (21 +/- 4% and 21 +/- 5%, respectively; both p less than 0.05). This difference achieves greater importance when it is recognized that mean systolic circumferential stress was lower in group III (151 +/- 22 g/cm2) than in groups I and II (244 +/- 37 g/cm2 and 213 +/- 38 g/cm2, respectively; both p less than 0.01). The midwall stress-shortening coordinates in six of the seven group III patients were outside the 95% confidence limits for the normal (group I) subjects. Thus, despite a normal ejection fraction, systolic function is subnormal in hypertensive patients with LV hypertrophy. CONCLUSIONS: Chamber dynamics provide an overestimate of myocardial function, especially when LV wall thickness is increased. This is due to a relatively greater contribution of inner shell thickening in pressure-overload hypertrophy.

Cardiomegaly↗
PubMed1991

Clinical assessment of left ventricular systolic function by force-length and stress-shortening relationships.

Left ventricular (LV) systolic function was assessed in patients with hypertensive heart disease (HHD, n = 30), hypertrophic cardiomyopathy (HCM, n = 27), dilated cardiomyopathy (DCM, n = 25), volume overload heart (VOH, n = 31) and normal subjects (NS, n = 32) in the two-dimensional framework of force-length (end-systolic stress-end-systolic volume index) and stress-shortening (mid-systolic stress-ejection fraction). Quadratic discriminant analysis revealed that the ellipses of confidence of HHD and normal subjects were in the same place with regard to both force-length and stress-shortening, while all other groups were well-discriminated. Three subgroups of patients, those with DCM with mild heart failure and those with VOH (with and without heart failure), were easily distinguishable on the basis of stress-shortening, but not on the basis of force-length measurements. It is concluded that LV systolic function and afterload are maintained within the normal range under pressure and volume overload until symptoms of heart failure appear via the mechanism of compensatory hypertrophy. Stress-shortening appears to be a more useful parameter than force-length for the analysis of LV systolic function in clinical practice.

Adult↗
PubMed1990

Spectrum of restrictive cardiomyopathy: report of the national survey in Japan.

This report describes clinical profiles and echocardiographic, hemodynamic, and histologic findings in 26 cases of idiopathic RCM based on the diagnostic criteria of (1) heart failure resulting from a stiff left ventricle, (2) normal LV size and systolic function, (3) absence of LV hypertrophy, and (4) cause or association unknown. There were 14 male and 12 female patients ranging in age from 5 to 63 years. Ten patients died during the mean follow-up period of 145 months, and five died of heart failure after 10 years. Three had a family history of HCM. Thromboembolism was observed in eight. Echocardiograms showed normal LV wall thickness and contraction. Hemodynamic characteristics included elevated biventricular filling pressures and a pulmonary wedge pressure that was usually higher than the right atrial pressure. Equalization of biventricular filling pressures was seen, however, in almost all patients with severe tricuspid regurgitation (seven of eight). The square root sign was seen in 50% in RV diastolic pressure tracings and 28% in LV tracings. This sign was observed in patients with elevated filling pressures. Interstitial fibrosis (22 of 23), endocardial thickening (13 of 23), and myofibrillar hypertrophy (10 of 23) were common histologic findings. Severe myocardial fiber disarray consistent with HCM was seen in four patients.

Adolescent↗
PubMed1990

Square root sign of left ventricular diastolic pressure curve in atrial septal defect.

The square root (dip and plateau) sign was observed in 7 of 21 adult patients with atrial septal defect (ASD). This study evaluated left ventricular (LV) diastolic filling dynamics and hemodynamic findings in 7 patients (Group 1) with, and 14 patients (Group 2) without the square root sign; 10 normal subjects (Group 3) served as controls. No significant differences were observed in LV end-diastolic and end-systolic volumes, ejection fraction, or left to right shunt. In Group 1, 77% of LV filling was completed in the first half of diastole; this percentage was 49% and 53% in Groups 2 and 3, respectively (both p less than 0.01 versus Group 1). Early diastolic filling velocity (at 20% of diastole) in Group 1 was significantly greater, and late diastolic filling velocity (at 80% and 90% of diastole) was reduced in Group 1 compared to those in Groups 2 and 3 (all p less than 0.05). The average values for right and left ventricular end-diastolic pressures were significantly higher in Group 1 (11 +/- 2 and 10 +/- 4 mmHg, p less than 0.05) than Group 2 (7 +/- 2 and 7 +/- 2 mmHg, p less than 0.05). It is suggested that a constrictive pathophysiology due to 4 chambers interaction or right ventricular constraint may play a role in the genesis of the square root sign in ASD.

Adolescent↗
PubMed1990

An assessment of left ventricular systolic function in pressure and volume overload heart with two shell compartment model of ellipsoid revolution.

Left ventricular (LV) midwall mechanics were evaluated in normal, pressure overload due to hypertension, and volume overload hearts due to aortic (AR) and mitral regurgitations (MR) using a 2 shell compartment model of ellipsoid revolution. While ejection fraction (EF) was in the normal range, midwall fractional shortening (MFS) was depressed with low end-diastolic and end-systolic stress in hypertrophied hearts with pressure overload. Not only LV volumes but also LV systolic pressure and wall thickness were increased in AR. LV end-diastolic pressure was elevated, and EF and MFS were reduced in patients with AR and congestive heart failure (CHF). In patients with MR and CHF, pulmonary capillary wedge pressure was elevated, LV volumes were enlarged and end-systolic stress was high, but LV wall thickness and MFS remained in the normal range. It is concluded from this observation that: 1) myocardial contractility is already depressed with normal systolic function in hypertrophied ventricle with pressure overload. 2) AR can be considered to be the disease of both pressure and volume overload, and symptoms of CHF are the result of depressed myocardial contractility. 3) MR is the disease of pure volume overload. Myocardial contractility is well preserved even with the presence of severe CHF in MR.

Adult↗
PubMed1988

Depressed myocardial contractility in mitral stenosis--an analysis by force-length and stress-shortening relationships.

To determine whether low ejection fraction (EF) in mitral stenosis (MS) is the result of depressed contractility or is mediated by other factors, left ventricular (LV) function was analyzed by force-length and stress-shortening relationships. Thirty patients without heart disease served as normal controls (Group 1). Forty-three patients with MS were divided into 2 subgroups: Group 2 (n = 19) had EF within one standard deviation of the mean of Group 1, and Group 3 (n = 24) had EF below it. Normal EF (Group 2) was associated with low preload (end-diastolic stress) and low afterload (end-systolic stress), and preload and afterload were in the normal range in patients with low EF (Group 3). A significant negative correlation was observed in the whole group of patients with MS between EF and end-systolic stress (Y = -0.14X + 72.8, r = -0.61, p less than 0.001), and a positive correlation between end-systolic stress and volume (Y = 1.39X + 65.4, r = 0.45, p less than 0.01). These observations suggest that systolic shortening and end-systolic volume of the left ventricle are in part governed by afterload in this disease. It is concluded that low EF of MS is not mediated by reduced preload or inappropriately elevated afterload, and contractility of the ventricle is mildly depressed in MS.

Adult↗
PubMed1988

Optimal timing for valve replacement in chronic aortic regurgitation: analysis based on the myocardial contractility and postoperative prognosis.

Left ventricular (LV) function was evaluated considering force-velocity and stress-shortening relationships in 14 asymptomatic (Group 1), 18 symptomatic patients (Group 2), and 53 normal subjects (Group 3) to determine the optimal time for valve replacement in patients with chronic aortic regurgitation (AR). Valve replacement was recommended for all Group 2 patients and for one patient in Group 1, who had sustained ventricular tachycardia. There was one operative death and five deaths remote from surgery; one patient in Group 1 died suddenly of undetermined cause, and four patients in Group 2 died of congestive heart failure (CHF). The LV end-systolic volume index (ESVI) was greater than 100 ml/m2 in the five patients whose death was unrelated to surgery (remote deaths). ESVI was less than 50 ml/m2 in all but two patients in Group 1, and more than 40 ml/m2 in all cases in Group 2. The index of preload, end-diastolic stress (sigma ed), was increased in Groups 1 and 2 as compared with Group 3. A significant positive correlation was observed between end-systolic stress (sigma es) and ESVI (r = 0.71, p less than 0.001) in patients with AR, and this linear line was not as steep as that of Group 3. Afterload (sigma es) and ejection fraction (EF) in Group 1 were within normal range, afterload was normal but EF was reduced in mildly symptomatic patients in Group 2, and severely symptomatic patients had markedly reduced EF and elevated afterload. There was a close correlation between ESVI and end-diastolic volume index (EDVI), and this was expressed as an exponential curve (Y = 21.69e0.006x, r = 0.88, p less than 0.001). This indicates that the rate of shortening of the muscle fiber deteriorates exponentially with enlargement of the ventricle. These observations suggest that in AR patients: 1) afterload and contractility of the ventricle remain normal in the majority of asymptomatic patients by means of compensatory hypertrophy and preload elevation (preload reserve), 2) deterioration of contractility seems to be the factor initiating CHF, and 3) progression of CHF is due to further deterioration of contractility in addition to elevation of afterload (afterload mismatch). It is concluded that careful observations are necessary when ESVI exceeds 50 ml/m2 in asymptomatic patients. Valve replacement is recommended when such patients develop symptoms of CHF, or either when EF falls to less than 50% or ESVI exceeds 100 ml/m2, even if patients remain asymptomatic.

Aortic Valve↗
PubMed1987

Functional and histopathologic correlation in patients with dilated cardiomyopathy: an integrated evaluation by multivariate analysis.

To correlate left ventricular function and histologic features in patients with dilated cardiomyopathy, precise indexes of hemodynamics and semiquantitative histologic data were combined for multivariate analysis. Right endomyocardial biopsy was performed at the time of cardiac catheterization. Five hemodynamic indexes were used for functional assessment: ejection fraction, ratio of end-systolic stress to volume index, end-diastolic stress, time constant (T) of left ventricular pressure fall, and end-systolic stress. Six histologic findings (disarray of myofibers, hypertrophy of myofibers, scarcity of myofibrils, nuclear changes of myofibers, vacuolization of myofibers and proliferation of collagen fibers) were graded from (-) to (4+). Each finding was assigned to category (-) or (+) according to the absence or presence of significant abnormality. Ordinary statistical analysis revealed that, although ejection fraction was lower in category (+) for proliferation of collagen fibers, ratio of end-systolic to volume index was reduced for category (+) of hypertrophy of myofibers. A significant correlation was present between hypertrophy of myofibers and proliferation of collagen fibers by Spearman rank correlation. When principal component analysis was applied to the hemodynamic data, two principal components could be extracted. Fisher's discriminant analysis could clearly differentiate two categories (-) and (+) in the semiquantitative histologic finding of proliferation of collagen fibers. The analysis indicated that contractility was reduced with elevated afterload in that category (+). Thus, proliferation of collagen fibers may play a pivotal role in deteriorating contractility in patients with dilated cardiomyopathy.

Cardiomyopathy, Dilated↗
PubMed1987

Right ventricular pacing reduces the rate of left ventricular relaxation and filling.

Right ventricular pacing alters left ventricular synchrony and loading conditions, each of which may independently influence left ventricular relaxation. Addition of a properly timed atrial contraction by using sequential atrioventricular (AV) pacing minimizes changes in left ventricular loading conditions, but ventricular asynchrony persists. To separate the effects of altered loading from those of asynchrony, the effects of right ventricular pacing and sequential AV pacing on the rate of isovolumic pressure decline (relaxation time constant), myocardial (segment) lengthening rate and chamber (minor axis dimension) filling rate were examined. In 12 open chest anesthetized dogs, left ventricular pressure (micromanometer) and either left ventricular free wall segment length transients (n = 6) or minor axis dimension transients (n = 6) were measured during right atrial, right ventricular and sequential AV pacing; length and dimension were measured using ultrasonic crystals. Compared with right atrial pacing, right ventricular pacing produced a decrease in systolic pressure, a reduction in fractional shortening, a prolongation of the relaxation time constant (23.5 +/- 0.7 to 29.8 +/- 0.8 ms, p less than 0.05), slower peak segment lengthening rate (6.2 +/- 0.6 to 4.6 +/- 0.8 s-1, p less than 0.05) and a slower rate of increase in chamber dimension (3.5 +/- 0.1 to 2.7 +/- 0.1 s-1, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Evaluation of left ventricular contractility in hypertrophic cardiomyopathy from end-systolic pressure-volume relation.

To evaluate myocardial contractility in hypertrophic cardiomyopathy (HC), we obtained the end-systolic pressure-volume relation (ESPVR) and the end-systolic stress-volume relation (ESSVR) by changing loading conditions with Angiotensin II. The left ventricular (LV) stress-shortening relation was also analyzed in order to assess myocardial contractility. LV end-systolic pressure, end-systolic volume, end-systolic stress, and ejection fraction were obtained at rest and during Angiotensin II infusion with simultaneous recordings of pressure and volume in 9 patients with hypertrophic cardiomyopathy and 9 normal subjects (N). The slopes of ESPVR, Emax, showed no significant difference (HC: 3.1 +/- 2.3 vs N: 2.6 +/- 1.4 mmHg/ml, ns). The slopes of ESSVR were statistically similar (HC: 5.2 +/- 2.1 vs N: 6.0 +/- 2.8 g/cm2 ml, ns). The slopes of end-systolic stress-ejection fraction relation were also in the same range in both groups (HC: -0.09 +/- 0.05 vs N: -0.10 +/- 0.05, ns). From these two different analyses of LV contractility, we conclude that myocardial contractility is normal in hypertrophic cardiomyopathy and not supernormal, at both chamber and muscle levels. Considering the increased muscle mass in hypertrophic cardiomyopathy (HC: 134 +/- 46 vs N: 74 +/- 19 g/m2, p less than 0.01), the presence of increased numbers of contractile units does not result in enhanced overall chamber contractility.

Adult↗
PubMed1987

Phase-plane analysis of left ventricular chamber filling and midwall fiber lengthening in patients with left ventricular hypertrophy.

Echocardiographic measurements of the left ventricle were used to define rates of circumferential fiber lengthening at the endocardium and midwall in 12 normal subjects and six patients with concentric left ventricular hypertrophy (wall thickness 11 to 16 mm). There was no difference in chamber size and systolic shortening in the two groups, but peak normalized lengthening rate [endocardial (+) VCF] was less than normal in the group with hypertrophy (4.8 +/- 1.4 and 3.1 +/- 0.9 sec-1, respectively, p less than .05). These results were contrasted with midwall (+) VCF data derived from two models that take into account nonuniform thickening across the left ventricular wall. Both models assume a constant left ventricular mass. The first allows changes in long axis and muscle cross-sectional area; the second assumes a constant cross-sectional area. Peak midwall (+) VCF with the first model was 2.1 +/- 0.5 sec-1 in the normal group and 1.4 +/- 0.3 sec-1 in the group with hypertrophy (p less than .01); with the second model peak midwall VCF was 2.8 +/- 0.6 and 1.4 +/- 0.4 sec-1 (p less than .01) in the two groups. The time to peak VCF and the dimension at the instant of peak (+) VCF were similar in the two groups. Phase-plane plots of length and velocity (dimension vs dD/dt) allow visual inspection and quantification of the relationships between instantaneous dimension, rate of change of dimension, and time in normal and hypertrophic hearts. These plots indicate abnormal filling of the left ventricular chamber and lengthening of midwall fibers in left ventricular hypertrophy.

Cardiomegaly↗
PubMed1986

Effects of intravenous injection of isosorbide dinitrate on the cardiovascular system.

An assessment of the acute hemodynamic effect of intravenous isosorbide dinitrate (ISDN) was performed with a Mikro-tip angiocatheter in 10 patients during the diagnostic cardiac catheterization. Both left ventricular (LV) systolic pressure (SP) and end-diastolic pressure (EDP) were decreased by 2 mg of ISDN. Cardiac index, stroke work index and heart rate did not change significantly, and neither systemic vascular resistance nor pulmonary arteriolar resistance was reduced. Isovolumic phase and ejection phase indices of contractility were not altered. End-diastolic stress, an accurate index of preload, was reduced significantly (47.0 +/- 27.6 to 28.7 +/- 24.6 g/cm2, p less than 0.01), and mid-systolic stress, an index of afterload, was also reduced (371 +/- 102 to 332 +/- 85 g/cm2, p less than 0.05). No undesirable side effects were noted during this study. We concluded that bolus intravenous (IV) ISDN safely reduced both preload and afterload. As 2 mg of IV ISDN had no significant change on SVR, a larger dose of ISDN bolus injection might be needed for a significant arterial vasodilating effect. Bolus IV ISDN seems to be very effective in cases in which rapid reduction of LV filling pressure is mandatory.

Adult↗
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↗