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Biomedical subjects

S Kusachi

Publications and source records attributed to S Kusachi.

At least 19 recordsLinked to original sources

Q-wave regression unrelated to patency of infarct-related artery or left ventricular ejection fraction or volume after anterior wall acute myocardial infarction treated with or without reperfusion therapy.

We examined the relation of Q-wave regression to left ventricular (LV) indexes in acute anterior wall myocardial infarction (AMI) in relation to reperfusion therapy. A total of 94 patients with their first anterior wall AMI (segment 6 or 7 occlusion according to the American Heart Association classification) were examined. The follow-up period with 12-lead electrocardiograms ranged from 6 to 60 months (mean 24 +/- 18). An abnormal Q wave was defined as > 40 ms and > 25% of the R-wave amplitude. Q-wave regression was defined as Q-wave disappearance and r-wave regression > 0.1 mV in > or = 1 lead. Contingency tables with the chi-square test and analysis of variance were used for assessment of the relation between Q-wave regression and angiographic and clinical indexes. Q-wave regression in > or = 1 lead was found in 77% of the patients. The incidence of Q-wave regression in patients with patent infarct-related artery (81%) was not significantly different from that in those with an occluded lesion (67%). Q-wave regression appeared within 1 month in 60% of patients with a patent infarct-related artery but in 25% of those with an occluded lesion. No difference in the incidence of Q-wave regression was seen between patients with lesions at segments 6 (81%) and 7 (70%), or between those with (75%) and without (77%) collateral circulation. Q-wave regression did not correlate with LV ejection fraction, LV end-diastolic or end-systolic volumes, or regional wall motion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Sequential changes in the distribution of type I and III collagens in the infarct zone: immunohistochemical study of experimental myocardial infarction in the rat.

AIM: Ventricular remodeling following acute myocardial infarction is an important factor in prognosis. The healing process, involving changes in type I and III collagens, is one of the major factors in remodelling. We therefore examined sequential changes in type I and III collagens after experimental myocardial infarction. MATERIALS AND METHODS: Hearts were excised from 1 day to 10 weeks after permanent left coronary ligation in rats. Immunohistochemical staining with a polyclonal antibody to each collagen was performed by the avidin-biotin-peroxidase method. RESULTS: Type I collagen initially appeared in the peripheral zone of the infarct from 3 days after ligation, the extent of staining gradually increasing until it reached a maximal level on days 21-28, after which the distribution remained unchanged. Type III collagen appeared in the peripheral zone of the infarct from 3 days after ligation; the extent of staining reached the maximal level after 11-28 days, after which a slight decrease in the distribution was observed, although the staining did not entirely disappear. CONCLUSIONS: Type I collagen was a major factor in collagen matrix formation, especially in the relatively late phase. Type III collagen, however, contributed particularly to collagen matrix formation in the relatively early phase. This study improves current understanding of the time-dependent alterations in type I and III collagens involved in the healing process after coronary artery occlusion.

Animals

Changes in extracellular matrix components in cardiomyopathic Syrian hamster, BIO 14.6.

We examined changes in the distribution of extracellular matrix components in the myocardium of cardiomyopathic Syrian hamsters (BIO 14.6). Fibronectin, laminin, and type IV collagen, and type I and III collagens were immunohistochemically stained by the avidin-biotin-peroxidase complex method, using a polyclonal antibody for each component. Hearts obtained from 4 stages of BIO 14.6 cardiomyopathy were examined. Peri- and endomysial fibrosis increased as the disease progressed. Replacement and meshwork (perimysial fibrosis penetrating the intercellular space) fibrotic lesions appeared beginning in the 2nd stage, ie, the fibrotic and healing stage. All of the components examined, ie, fibronectin, laminin and type IV collagen, and type I and III collagens, were present in various fibrotic lesions and played a significant role in fibrotic changes throughout all of the stages of the disease. No primary deficit of any of these components was seen. An increased distribution of fibronectin was observed in both the enlarged peri-and endomysial spaces beginning in the initial stage, ie, the necrotic stage, when myocyte hypertrophy was inconspicuous, and distribution throughout the myocardium increased further as the disease progressed. Laminin and type IV collagen in the fibrotic lesions were not restricted to the myocyte membrane. Type III collagen was distributed in replacement and meshwork fibrotic lesions, and the extent of its distribution increased in proportion to that of type I collagen. The continuous increases in the distribution of fibronectin, laminin and type III collagen indicate that fibrotic changes occurred continuously in this model.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

[Preventive effect of pravastatin on restenosis following coronary angioplasty: prospective randomized trial].

This study investigated the preventive effect of pravastatin on restenosis following successful transluminal coronary angiography (PTCA) in 109 consecutive patients. Patients were randomly and prospectively assigned to the pravastatin group (group P, n = 57) or the control group (group C, n = 52). The former received 10 mg/day pravastatin from the day of PTCA for 3 months. Restenosis was defined as a > or = 50% diameter stenosis at follow-up angiography with a > or = 15% reduction in luminal diameter compared to post-PTCA. The effect of pravastatin was analyzed in association with 7 clinical and 15 angiographic factors. Follow-up rate, serum lipid levels (total cholesterol, triglyceride, and HDL-cholesterol), and clinical and angiographic backgrounds except age and angularity of the lesions were not significantly different between the two groups at PTCA. Three months later, total cholesterol decreased from 222.3 +/- 35.1 to 179.2 +/- 31.2 mg/dl in group P, but was unchanged in group C (from 226.0 +/- 33.7 to 211.7 +/- 30.9 mg/dl). The restenosis rate was not different between the two groups (35.6 vs 35.7% per patient, 32.0 vs 33.3% per lesion). Moreover, no relationship between restenosis rate and serum total cholesterol level at follow-up angiography was observed. Multivariate analysis, including 7 clinical and 15 angiographic factors, found neither pravastatin administration nor serum lipid levels were significantly correlated with decreased luminal diameter. Pravastatin (10 mg/day) did not reduce the incidence of restenosis after PTCA when administered from the day of PTCA for 3 months.

Aged

Prediction of isolated first diagonal branch occlusion by 12-lead electrocardiography: ST segment shift in leads I and aVL.

OBJECTIVES: This study was performed to determine electrocardiographic (ECG) features that could distinguish first diagonal branch occlusion from left anterior descending coronary artery occlusion. BACKGROUND: The ECG findings associated with first diagonal branch obstruction have not previously been compared with those of left anterior descending coronary artery obstruction. METHODS: The ECG findings in 34 patients with isolated diagonal branch occlusion (group 9) were compared with those in 20 patients with occlusion at site 6 (group 6) and 20 with occlusion at site 7 (group 7), according to American Heart Association classification. This study had a power > 80% to detect a 50% difference between groups at a probability value of 0.05. RESULTS: ST segment elevation was observed in leads I and aVL for all group 9 patients, in 80% (p < 0.05) of group 6 patients for lead I and 90% for lead aVL and in 50% (p < 0.01) of group 7 patients for lead I and 55% (p < 0.01) for lead aVL. Similarly, there was a higher incidence of abnormal Q waves and inverted T waves in leads I and aVL in group 9 than in groups 6 and 7. In contrast, group 9 showed a significantly lower incidence of ST segment elevation (3.4%), abnormal Q waves (3.0%) and inverted T waves (0%) in lead V1 than group 6 (80%, 40% and 90%, respectively) and group 7 (75%, 60% and 70%, respectively) (p < 0.01 for each). Multivariate analysis revealed that abnormalities in leads I and aVL, combined with a normal lead V1 (and V6), provided good criteria for distinguishing isolated diagonal branch occlusion from left anterior descending coronary artery occlusion. CONCLUSIONS: Isolated diagonal branch occlusion more frequently caused ECG abnormalities in leads I and aVL and less frequently caused changes in the precordial leads compared with left anterior descending coronary artery obstruction, indicating that leads I and aVL represent myocardium perfused by the diagonal branch.

Adult

Silent zone on Lorenz plots of the ventricular response before termination of paroxysmal atrial fibrillation--report of a case.

An ambulatory 24 h Holter electrocardiogram was recorded during paroxysmal atrial fibrillation in a 67-year-old man. His paroxysmal atrial fibrillation terminated spontaneously approximately 12 h after the start of recording. The RR variability of this Holter recording was studied using Lorenz plots, frequency domain analysis, and time domain analysis. A silent zone appeared on the Lorenz plots beginning a few hours before the termination of his attack. The coefficient of variance (CV) and the power of the high-frequency component of RR variability (HF) gradually increased toward the termination. The silent zone was closely related to the functional refractory period of the atrioventricular node estimated from the Lorenz plots, and the functional refractory period was significantly correlated with the CV and HF power of RR variability. This case suggests that a silent zone on Lorenz plots reflects increased parasympathetic tone. In addition, such a silent zone may be useful for predicting the course of paroxysmal atrial fibrillation and for evaluating the role of the autonomic nervous system in this condition.

Aged

Effects of emergency coronary angioplasty on left ventricular volume after acute myocardial infarction compared with intracoronary thrombolysis.

BACKGROUND: The effects of emergency coronary angioplasty on left ventricular remodeling have not been fully evaluated. We compared the effects of emergency coronary angioplasty on left ventricular volume with those of intracoronary thrombolysis in patients suffering from their first acute myocardial infarction (AMI). METHODS: A total of 51 patients who had a culprit lesion at site No 6 of the American Heart Association (AHA) classification were analyzed. Patients with re-obstruction of the culprit lesion after reperfusion were excluded from the study. The coronary angioplasty and the thrombolysis groups consisted of 28 and 23 patients, respectively. Left ventricular volume was measured by left ventriculography at 4 weeks after infarction. RESULTS: Clinical and angiographic background factors showed no significant differences between these two groups. The left ventricular end-systolic volume index was significantly smaller in the angioplasty group than in the thrombolysis group (31 +/- 14 versus 45 +/- 14 ml/m2, P < 0.01). Similarly, the left ventricular end-diastolic volume index was significantly smaller in the angioplasty group (64 +/- 13 versus 82 +/- 13 ml/m2, P < 0.01). Conversely, the left ventricular ejection fraction was larger in the angioplasty group than in the thrombolysis group (54 +/- 13 versus 45 +/- 13%, P < 0.05). Multivariate analysis revealed that the selection of coronary angioplasty was one of the factors significantly associated with a decrease in left ventricular end-systolic and end-diastolic volume. CONCLUSION: These results suggest that emergency coronary angioplasty produces better left ventricular remodeling than intracoronary thrombolysis after AMI.

Adult

Auto-antibody against adenine nucleotide translocator in dilated cardiomyopathy and myocarditis--incidence and relation to cardiac function and morphology.

Using an enzyme-linked immunosorbent assay, we measured anti-adenine nucleotide translocater (ANT) antibody in control subjects and in patients with dilated cardiomyopathy (DCM), myocarditis, and other heart disease. Analysis with sodium dodecyl sulfate-polyacrylamide gel electrophoresis, Western blotting, and immunoabsorption tests confirmed accurate purification of the ANT protein and correct measurement of anti-ANT auto-antibody. Anti-ANT antibody was detected in 6 of 37 cases (16%) of DCM and in 5 of 12 cases (42%) of myocarditis. This antibody was not positive in other heart diseases or in apparently healthy controls. There were no differences between anti-ANT autoantibody-positive and -negative DCM or myocarditis patients in any of the cardiac parameters examined (left ventricular ejection fraction, LVEF; left ventricular end-diastolic dimension, LVDd; and cardiothoracic ratio, CTR). Moreover, in patients who were positive for anti-ANT auto-antibody, no positive correlations were found between the parameters and anti-ANT antibody titers in either DCM or myocarditis. Although these results indicate that the detection of anti-ANT antibody was achieved at a high specificity and could have certain diagnostic value in DCM and myocarditis, there was no statistically significant relationship between the cardiac parameters (LVEF, LVDd, and CTR) and anti-ANT antibody titers in either DCM or myocarditis. Some compensatory mechanism of ventricular function may mask the effects of the anti-ANT auto-antibody or alternatively, this auto-antibody may have mimic effects on the pathogenesis and/or progression of DCM and myocarditis.

Adult

Histological abnormalities in a biopsy specimen obtained from the left ventricle without reduced function in a patient with right ventricular dysplasia.

Left ventricular histological examination was performed in a patient with right ventricular (RV) dysplasia. Although the left ventricle (LV) appeared to have a normal shape and function, the LV biopsy specimen revealed apparent myocyte hypertrophy and substantial fibrotic changes without fatty infiltration. It was not clear whether these considerable histological changes were part of right ventricular dysplasia or not. The present case indicates that even with normal LV shape and function in patients with right ventricular dysplasia, histological examination of LV may provide additional information on its pathogenesis and prognosis.

Aged

Effects of reperfusion on left ventricular ejection fraction and volume after acute myocardial infarction.

The effects of reperfusion on left ventricular (LV) function and volume were studied in patients with evolving acute myocardial infarction (AMI). We analyzed the LV ejection fraction and volume in patients who had been admitted within 24 h of the onset of their first AMI with culprit lesion of #6, #7 and #1 (American Heart Association classification). Sixty-five patients (Re group) received successful reperfusion therapy within 6 h after the AMI. The other 60 patients (Oc group), who were admitted from 6 to 24 h after the AMI, received conservative therapy. Patients with re-obstruction of the culprit lesion after reperfusion therapy were excluded from the Re group. Patients with spontaneous recanalization following conservative therapy were excluded from the Oc group. The LV ejection fraction (LVEF), LV end-systolic volume index (LVESVI), and LV end-diastolic volume index (LVEDVI) were measured using a modified Dodge's formula by left ventriculography performed 4 weeks after the AMI. LVEF in the Re group was significantly greater than in the Oc group (57 +/- 12 vs 49 +/- 11%) (mean +/- SD, p less than 0.01). LVESVI in the Re group was significantly smaller than in the Oc group (30 +/- 13 vs 38 +/- 16 ml/m2, p less than 0.01). Although LVEDVI was not significantly different between the 2 groups, in patients with a responsible coronary lesion of segment #6, LVEDVI in the Re group was significantly smaller than in the Oc group (67 +/- 14 vs 77 +/- 18 ml/m2, p less than 0.05). Although LVEF and LV volume correlated in both groups, the correlation was weak (r = 0.40-0.42), suggesting that LV volume was not dependent solely on LV functional recovery. The incidence of ventricular aneurysm in the Re group was significantly lower than in the Oc group (15.4 vs 45.0%, p less than 0.01). Multivariate analysis selected reperfusion of the responsible coronary artery as one of the factors significantly associated with a reduction of LVEDVI, LVESVI, an improvement of LVEF, and a decrease in the rate of aneurysm formation. In summary, our results indicated that reperfusion improved EF, reduced LV volume, and decreased the rate of aneurysm formation as compared to non-reperfusion, which suggests that reperfusion therapy is beneficial for both functional recovery and ventricular remodeling.

Adult

Emergency coronary angioplasty for acute myocardial infarction--factors affecting acute restenosis in catheterization laboratory and reocclusion during hospitalization.

A total of 107 consecutive patients with acute myocardial infarction underwent emergency coronary angioplasty (PTCA). Restoration of blood flow with TIMI grade III was established by emergency PTCA in 101 patients (94.4%). "Acute restenosis" was defined as a lesion that, when dilated to less than 50%, narrowed again to more than 75% luminar reduction 5 min after the balloon inflation. Acute restenosis occurred in 39 patients (39%). Multivariate analysis selected 3 factors associated significantly with an increased rate of acute restenosis: (1) dissection, (2) small balloon/artery diameter ratio and (3) low systolic blood pressure during PTCA. Reocclusion, which was defined as a total reobstruction of the lesion during hospitalization following emergency PTCA, was examined by predischarge coronary angiography. Acute restenosis correlated significantly with an increase in reocclusion rate. The incidence of documented reocclusion was 12%. Residual stenosis, multivessel disease and irregular dilation correlated significantly with an increased rate of reocclusion. The in-hospital and postdischarge mortalities were 5.6% and 2.1%, respectively. In summary, emergency PTCA produced a high angiographic success rate. Use of adequate balloon size and sufficient dilation correlated significantly with angiographic outcome in emergency PTCA. Patients with acute restenosis, high residual stenosis, irregular dilation, and multivessel disease would have a relatively high risk of reocclusion.

Adult

NG-nitro-L-arginine attenuates flow debt repayment in the reactive hyperemic response of the open-chest dog coronary artery: contribution of endothelium-derived relaxing factor.

To test the hypothesis that the endothelium-derived relaxing factor (EDRF) contributes to coronary vasodilation induced by myocardial ischemia, we examined the effect of NG-nitro-L-arginine (a potent and selective inhibitor of EDRF release) on the coronary reactive hyperemic response in the open-chest dogs. Intracoronary infusion of NG-nitro-L-arginine at a coronary plasma concentration of 5 x 10(-5) M had no effect on hemodynamics and myocardial oxygen metabolism, but attenuated repayment of the flow debt by an average of 20.4% and 20.0% following coronary occlusion for 10 sec and 20 sec, respectively. Concomitant infusion of NG-nitro-L-arginine at the same concentration and 8-phenyltheophylline (a potent adenosine receptor blocker) at a coronary plasma concentration of 10(-5) M further attenuated flow debt repayment following 10 sec and 20 sec of coronary occlusion by 47.7 and 59.4%, respectively. These results indicate that EDRF plays a significant role in the coronary reactive hyperemic response and may cause vasodilation independently of adenosine-mediated vasodilation following coronary occlusion.

Adenosine

[Managements of hospital MRSA infections in digestive tract surgery].

1444 cases if digestive tract surgery in our department were studied for the prevention of postoperative MRSA infections, during the period from September 1987 to February 1992. They were divided into nine stages each six months. There were no significant differences in incidence of postoperative MRSA infections, after some managements for hospital infection among each stage. We used the antibiotics as follows; the first generation of cefem families was used for the upper digestive tract operations and the second generation of cefem families was used for the lower digestive tract operation, and the incidence of postoperative MRSA infections were diminished significantly. This study showed that managements for hospital infections and appropriate selection of antibiotics for the purpose of postoperative prophylactic use are effective for the prevention of MRSA infections.

Cephalosporins

Improvement of left ventricular aneurysm after myocardial infarction: report of three cases.

We report on the disappearance of a left ventricular aneurysm after myocardial infarction in three cases. Coronary blood flow was restored by spontaneous recanalization in two cases and by angioplasty in one case. When the aneurysm was observed, the findings in these cases were (1) no or limited abnormal Q wave in surface electrocardiography, (2) total or subtotal stenosis of the proximal coronary artery without adequate distal filling through collaterals, (3) no ST shift in exercise electrocardiography, and (4) decreased but not absent thallium-201 uptake in myocardial scintigraphy. In Cases 1 and 2, respectively, 3 years and one year and 8 months after the myocardial infarction, an anginal episode occurred and the ventricular aneurysm disappeared. In Case 3, the aneurysm disappeared after coronary angioplasty. These cases suggest that even without a demonstration of reversible ischemic myocardium and/or severe stenosis without distal filling through collaterals, the myocardium presenting a ventricular aneurysm would be hibernating. These cases were also informative about the detection of hibernating myocardium.

Aged

Oxygen metabolism of the hypertrophic right ventricle in open chest dogs.

STUDY OBJECTIVE: The aim was to investigate oxygen metabolism of the hypertrophic right ventricle in anaesthetised open chest dogs. DESIGN: Right ventricular hypertrophy was induced by right ventricular pressure overload with banding the pulmonary artery for six months. Coronary blood flow and myocardial oxygen metabolism of the hypertrophic right ventricle were determined during control and after increasing right ventricular oxygen consumption, and compared with those of the normal right and left ventricles. SUBJECTS: Seven mongrel dogs with right ventricular hypertrophy and 21 normal dogs were used. All were anaesthetised with pentobarbitone sodium. MEASUREMENTS AND MAIN RESULTS: Oxygen extraction [(A-V)O2] of the hypertrophic right ventricular myocardium was greater than that of normal right ventricle in controls and almost identical to the (A-V)O2 of the normal left ventricle. It showed no increase when coronary blood flow and right ventricular oxygen consumption were raised in response to a further elevation of the right ventricular pressure and isoprenaline infusion. However, the right ventricular interventions which increased right ventricular oxygen consumption produced an elevation of (A-V)O2 of the right ventricle with an increase in right coronary blood flow. CONCLUSIONS: Higher oxygen extraction during control and no response of oxygen extraction of the hypertrophied right ventricle in response to stimuli which increase right ventricular oxygen consumption indicate that oxygen supply to the hypertrophic right ventricle is different from that of the normal right ventricle, and is more like that of the left ventricle.

Animals

Interaction between adenosine and beta-adrenoceptors.

Interaction between adenosine and isoproterenol (ISP) on myocardial inotropic action was studied in open-chest dog hearts. The local myocardial force and the left ventricular (LV) dP/dt were measured as indices of myocardial contractility. Isoproterenol [ISP, 9.47 microM (2 micrograms/ml)] was infused into the left circumflex coronary artery at rates of 0.05 ml/min (low dose ISP) or 0.2 ml/min (high dose ISP). Two mM adenosine or 0.5 mM N6-phenylisopropyl-adenosine (PIA) were infused into the coronary artery at rates of 0.2 (4 x 10(-7) mol/min), 0.5 (1 x 10(-6) mol/min) and 10 ml/min (2 x 10(-5) mol/min) in the presence of either a low or a high dose of ISP. Adenosine infusion at a rate of 0.2 ml/min did not modify myocardial contractility in the presence of the both doses of ISP. The larger doses of adenosine, 0.5 ml/min and 10 ml/min, decreased myocardial-developed tension and LVmax dP/dt dose-dependently. However, the dose of adenosine which affected myocardial contractility was inphysiologically high in comparison with the concentration in the ischemic myocardium. PIA, a potent agonist of adenosine A1-receptor, attenuated an increase in myocardial contractility in a dose-dependent manner which was caused by intracoronary ISP infusion. This indicates that A1-adenosine receptors exist, but a functional adenosine-catecholamine antagonism does not play a significant role in the canine left ventricle.

Adenosine

Association between high grade ventricular arrhythmia and extent of left ventricular hypertrophy in hypertrophic cardiomyopathy.

The association between the extent of left ventricular (LV) hypertrophy and severity of ventricular or atrial arrhythmias are examined. Two-dimensional echocardiography and 24-h Holter electrocardiography monitoring were performed in 60 patients with hypertrophic cardiomyopathy (HCM). According to the distribution of the LV hypertrophy, the patients were divided into three groups: 1. Apical hypertrophy (APH), 2. Septal hypertrophy, and 3. Extensive hypertrophy. Ventricular arrhythmias were found in 82% of the patients and supraventricular arrhythmias were detected in 70% of the patients. Lown grade III and IV arrhythmias occurred significantly more frequently in patients with extensive than with septal hypertrophy. Lown grade III to IV arrhythmias did not occur in patients with APH. Present results show a significant association between the extent of LV hypertrophy and the severity of ventricular arrhythmias in HCM.

Adult