Biomedical subjects
Publications and source records attributed to S Kusachi.
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BACKGROUND: Iodine-123 metaiodobenzylguanidine (123I-MIBG) concentrates in adrenergic neurons and has been developed for evaluation of the sympathetic nervous system. Recent studies have demonstrated that the normal heart is clearly visualized by 123I-MIBG cardiac scintigraphy, whereas abnormal 123I-MIBG myocardial uptake and washout have been demonstrated in patients after myocardial infarction and in patients with congestive cardiomyopathy, long QT syndrome, and ventricular tachycardia. HYPOTHESIS: Based on evidence from recent studies, it can be hypothesized that 123I-MIBG uptake is related to histopathologic changes in the myocardium. METHODS: The relation of 123I-MIBG uptake to the histologic findings for the heart was studied in 24 patients with dilated cardiomyopathy (DCM). The study group did not include patients with complicating disorders that primarily affect the adrenergic nervous system. The 123I-MIBG uptake was visually assigned one of four grades using the two criteria of the mean score for six regional uptake grades (mean score) and the global score obtained by visual evaluation of the entire image (global score). The 123I-MIBG uptake score was also determined for the region at which the biopsy specimen was obtained (biopsy region score). The histologic findings were evaluated by assigning one of four grades for each of the following five factors: myocyte hypertrophy, myocardial fibrotic change, myocyte degeneration and necrosis, mononuclear cell infiltration, and myocyte disarray. The sum for all grades was defined as the total score, and the global score was also assigned to the overall histologic findings. RESULTS: All of the global, mean, and biopsy region scores for 123I-MIBG uptake correlated significantly with the global and total scores for the histologic findings. Among the histologic factors, myocyte degeneration showed score correlated with all global, mean, and biopsy region scores for the uptake. Myocyte hypertrophy was associated weakly with the 123I-MIBG uptake scores. CONCLUSION: These results indicate that 123I-MIBG uptake imaging is associated with histopathologic abnormalities in patients with DCM.
OBJECTIVE: To examine the hypothesis that tenascin, an extracellular matrix glycoprotein, contributes to fibrotic changes in dilated cardiomyopathy. METHODS: The localisation of tenascin in biopsy specimens of the hearts obtained from eight patients with dilated cardiomyopathy was examined using staining by the avidin-biotin-peroxidase complex method. RESULTS: (1) Perimysium and endomysium. Although positive staining for tenascin was observed in the enlarged perimysium and endomysium in all patients, moderately intense staining was characteristically observed near the replacement fibrotic lesions. In the narrow perimysium and endomysium of the myocardium not containing replacement fibrotic lesions, tenascin was not present, as in the control specimens. (2) Replacement fibrotic lesions. Non-homogeneous positive staining for tenascin was detected in all replacement fibrotic lesions examined. Intense tenascin deposition was observed in the peripheral portion of the replacement fibrotic lesions. The tenascin staining observed in the small replacement fibrotic lesions was more intense than that in the large lesions. CONCLUSIONS: Tenascin contributes to the development of the fibrotic changes seen in the dilated cardiomyopathic heart. Its characteristic location, specifically the distribution along the margin of the fibrosis, suggests that fibrotic change is a continuous process in hearts with dilated cardiomyopathy.
BACKGROUND: The healing process, which affects ventricular remodeling, is an important factor in the prognosis of myocardial infarction. We hypothesized that laminin and type IV collagen contribute to extracellular matrix assembly in healing after myocardial infarction. We examined sequential changes in these two components after experimental myocardial infarction in rats. 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 laminin and type IV collagen was performed by the avidin-biotin-peroxidase method. RESULTS: Laminin: On day 3, laminin initially appeared in a wavy fashion in the granulation tissue of the infarct peripheral zone and was not restricted to the cell membrane; the staining distribution in the peripheral zone then gradually increased, reaching a maximum on days 7-11. The distribution progressed from the peripheral zone to the outer lesion of the central zone of the infarct for 1-2 days, and reached the center point after 2 weeks. The extent of the staining distribution gradually decreased after reaching this maximum, but the staining did not completely disappear. Type IV Collagen: Changes in type IV collagen were essentially the same as those in laminin. A wavy staining pattern of type IV collagen appeared in the infarct peripheral zone from day 3, reached its maximum extent on days 7-11, and decreased gradually thereafter. The distribution progressed from the peripheral zone to the outer lesion of the central zone for 1-2 days, reaching the center point after 2 weeks. CONCLUSIONS: Laminin and type IV collagen contribute to extracellular matrix formation in the infarct zone relatively early after myocardial infarction.
A few studies have indicated that adenosine terminated triggered-activity idiopathic ventricular tachycardia, but all involved a small number of cases. The effects of adenosine triphosphate (ATP) on wide QRS tachycardia have thus not yet been completely clarified. This retrospective study was performed to evaluate the therapeutic and diagnostic utility of ATP in wide QRS tachycardia. A total of 18 patients with wide QRS tachycardia (QRS width > 120 msec, rate > or = 150 beats/min) were evaluated. ATP, 20-40 mg, was administered intravenously. An electrophysiological study and treadmill stress test were performed in all patients to elucidate the mechanism of the tachycardia. ATP terminated tachycardia or induced atrio-ventricular block in all 6 patients who had supraventricular tachycardia, but it had no effect on preexcited atrial fibrillation or pre-excited atrial flutter. Ventricular tachycardia was terminated by ATP in 5 of the 10 patients. In 4 of these 5 patients, the focus of the tachycardia was the right ventricular outflow tract. No entrainment phenomenon was demonstrated by electrophysiological study with induction of the tachycardia by stress test or isoproterenol infusion, suggesting the contribution of triggered activity to the tachycardia. In the remaining patient with complete right bundle branch block type tachycardia with right axis deviation, the mechanism of ventricular tachycardia could not be determined. In the 5 patients in whom ATP failed to terminate ventricular tachycardia, the reentry mechanism was suggested by the presence of entrainment phenomenon depicted on electrophysiological study. In summary, this study suggests that ATP terminates supraventricular wide QRS tachycardia and ventricular tachycardia due to triggered-activity, but that it has no effect on pre-excited atrial fibrillation or flutter or on ventricular tachycardia due to a reentry mechanism. These findings add to the mounting evidence regarding the therapeutic and diagnostic utility of ATP in wide QRS tachycardia.
Fibrotic change is one of the characteristic features of the heart with idiopathic dilated cardiomyopathy (DCM), but the extracellular matrix components have not been fully clarified. Fibronectin, laminin, and types IV, I and III collagen staining using the avidin-biotin-peroxidase complex method was conducted to study the localization of extracellular matrix components in biopsy specimens obtained from 7 patients with DCM. Fibronectin was observed in the endomysium and perimysium, co-existent with types I and III collagen; it was also distributed nonhomogeneously in the replacement fibrotic lesions. The staining intensity in a section varied substantially from location to location. Laminin surrounded the myocytes and was distributed in the endomysium localized together with type IV collagen, but it was not found in the perimysium. Weak but positive staining was observed in replacement fibrotic lesions in 2 patients. Similarly to laminin, type IV collagen staining was observed around the myocytes and in the endomysium. It was also observed in replacement fibrotic lesions in 4 patients either with or without laminin. Type I collagen, localized together with type III collagen, was distributed in both the endomysium and perimysium. It was also distributed nonhomogeneously in the replacement fibrotic lesions. Similar staining to type I collagen was seen for type III collagen. In summary, all examined components were observed in the fibrotic lesions with no primary deficit of any examined component being demonstrated. The variability of staining intensity and positive fibronectin staining suggests that the phases of fibrotic changes differed substantially from location to location.
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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)
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.
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)
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.
BACKGROUND: The effects of reperfusion on time-dependent alteration of type I collagen have not been examined. OBJECTIVES: We compared the sequential changes in the appearance and distribution of type I collagen in reperfused infarct rat hearts to those in non-reperfused hearts. METHODS: Using an experimental rat model of infarction, we performed immunohistochemical staining with a polyclonal antibody to type I collagen by the avidin-biotin-peroxidase method. Reperfusion was established after 2-h coronary ligation that produced complete necrosis of myocytes. RESULTS: In reperfused hearts, type I collagen appeared in the peripheral zone of the infarct at day 2, which was 1 day earlier than in non-reperfused hearts. The extent of distribution of type I collagen in reperfused hearts was comparable to that observed approximately 1 day later in non-reperfused hearts. CONCLUSION: Reperfusion can accelerate collagen matrix formation compared with that in non-reperfused hearts after acute myocardial infarction.
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.
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.
A total of 51 patients with hypertrophic cardiomyopathy (HCM) were followed for at least 3 years (mean follow-up period 6.5 years) by serial M-mode and two-dimensional echocardiography. An increase of the left ventricular diastolic dimension (LVDd) to > or = 55 mm with a decrease in the left ventricular ejection fraction (LVEF) to < 55% was observed in eight (15.7%) patients (progressive disease group). In five of these eight patients, the LVDd was > or = 60 mm and the LVEF was < 40%. Ventricular enlargement was closely related to mortality and death due to congestive heart failure occurred in three of these patients. No deaths occurred among the 37 patients without significant progression of ventricular enlargement (nonprogressive group). The annual changes of LVEF and LVDd in the progressive disease group were larger than in the nonprogressive group (LVEF -0.18 +/- 1.45 vs. -2.46 +/- 1.47 %/year; LVDd 0.22 +/- 0.81 vs. 1.43 +/- 0.77 mm/year). An increment in LVDs occurred earlier than the enlargement of the LVDd. Therefore, close attention to the LVDs seems to be important to detect early left ventricular morphological changes in HCM. In summary, this study indicates that HCM patients include a subgroup with symptoms resembling dilated cardiomyopathy, in whom the left ventricle enlarges with hypofunction and in whom there is high mortality due to congestive heart failure.
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.