[Uncommon forms of subaortic stenosis].
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Aortic Stenosis, Subvalvular↗
Biomedical subjects
R Okada
Publications and source records attributed to R Okada.
Local treatment with antithrombotic drugs can prevent thrombus formation: an angioscopic and angiographic study.
OBJECTIVES: This study was designed to evaluate the efficacy of local versus systemic treatment of thrombosis with various antithrombotic drugs. BACKGROUND: Local use of low dose antithrombotic drugs has been proposed as being effective and safe. METHODS: Heparin (30 U/kg), an antithrombin agent (argatroban, 0.05 mg/kg body weight) or a defibrinogenating drug (batroxobin, 0.05 U/kg) was locally infused into one side of the canine iliac artery after injury by balloon inflation. The other side was injured as a control. The efficacy of systemic delivery of high dose (heparin [300 U/kg] and argatroban [0.5 mg/kg]) and low dose drugs was also assessed. RESULTS: Sixty minutes after local treatment in 22 dogs, no thrombotic stenosis was observed by angiography in locally treated arteries (p < 0.005 vs. mean thrombotic stenosis of 27% in control segments for heparin, 25.3% in control segments for argatroban and 32% in control segments for batroxobin). Angioscopy demonstrated the same trend. In locally treated arteries, thrombus weight was significantly lower in the treated than control side. In the systemic high dose group (n = 10), angiographic thrombotic stenosis was < 5% after high dose drug delivery (p < 0.05 vs. control segments, 37.4% for heparin, 43% for argatroban). In another 10 dogs, low dose systemic delivery was not effective in inhibiting thrombus formation. Activated partial thromboplastin time and fibrinogen levels did not change with local treatment. CONCLUSIONS: Compared with systemic administration of antithrombotic drugs, local treatment is a safer and more effective method of preventing thrombosis.
Angiography↗
Corticosteroid therapy for ventricular tachycardia in children with silent lymphocytic myocarditis.
OBJECTIVE: The objective of our study was to describe the efficacy of corticosteroids for ventricular tachycardia in four children with structurally normal hearts in whom endomyocardial biopsy revealed histologic changes of lymphocytic myocarditis. PATIENTS: The four patients had unexplained ventricular tachycardia. Three dysrhythmias were sustained, and one was inducible by exercise. Patient ages ranged from 4 months to 12 years. Three of the four patients had no symptoms. In two of them, ventricular tachycardia was identified by mass screening for heart disease. Two patients received oral steroids and two received pulse steroid therapy. RESULTS: In all four patients, significant underlying diseases were not found by noninvasive evaluation. Right ventricular endomyocardial biopsy revealed abnormal histologic findings of chronic lymphocytic myocarditis in all patients. Steroid therapy was effective in all four patients, two of whom received methylprednisolone pulse therapy. CONCLUSIONS: We conclude that unexplained ventricular tachycardia may be the only manifestation of clinically silent myocarditis. Steroid therapy should therefore be considered if conventional antiarrhythmic medication is not effective and histologic findings confirm the presence of lymphocytic myocarditis.
Adolescent↗
Reduced vasoreactivity and thrombogenicity with pulsed laser angioplasty: comparison with balloon angioplasty.
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Angioplasty, Balloon↗
Causal association between major histocompatibility complex and myocardial infarction in NZW x BXSB F1 mice.
The NZW x BXSB F1 male mice that a model for systemic lupus erythematosus (SLE) develop myocardial infarction. To determine whether the gene(s) linked to the major histocompatibility complex (MHC) of NZW mice are involved in myocardial infarction, we developed an H-2-congenic NZW.H-2d strain and compared the incidence of myocardial infarction in NZW x BXSB F1 (H-2z/b) male mice to that in NZW. H-2d x BXSB F1 male mice (H-2d/b). H-2z/b heterozygous F1 male mice showed a higher incidence of myocardial infarction than H-2d/b F1 male mice. This observation suggests that the myocardial infarction seen in SLE may be related to MHC.
Animals↗
[Immunohistochemical study of the endomyocardial biopsy of systemic lupus erythematosus].
The mechanisms of cardiac involvement in systemic lupus erythematosus (SLE) were studied using immunohistochemical staining of endomyocardial biopsy specimens from 14 patients with SLE and normal coronary arteriograms. All 14 specimens showed mild interstitial edema, 11 showed mild cardiac fibrosis, and another two cases showed moderate cardiac fibrosis with myocardial derangements. Four specimens showed moderate cell infiltration in the interstitium. Area of fibrosis, diameter of myocardium and area of interstitial edema were increased in the SLE patients compared to the control cases. Immunofluorescence showed IgG and fibrinogen deposition in the membrane of cardiac myocytes and in the interstitium. Immunohistochemistry found no B lymphocytes in any of the seven SLE cases. T lymphocytes were observed in all seven SLE cases, and OKT 8 lymphocytes were increased significantly in the interstitial tissue as compared with OKT 4 lymphocytes. At endomyocardial biopsy, all 14 patients were receiving corticosteroid therapy and had low activity disease. The results suggest that cardiac tissue damage was associated with immunological abnormalities and might progress silently under conditions in which the disease activity was suppressed by corticosteroid therapy.
Adult↗
Long-term outcome of operative treatment of focal atrial tachycardia.
BACKGROUND: This study examined the long-term clinical outcome of patients with focal atrial tachycardia who were treated surgically. Focal atrial tachycardia is a relatively rare arrhythmia that is often difficult to control with conventional medical therapy. Therapeutic modalities are not well defined because of the scarcity of long-term data of treated patients, including pathologic findings. STUDY DESIGN: Nine patients, six men and three women, ranging in age from 16 to 50 years (mean of 34 +/- 14 years), underwent operative treatment for focal atrial tachycardia. The average rate of tachycardia was 167 +/- 22 beats per minute. All patients were treated with antiarrhythmic drugs (mean 2.9 drugs per patient). Concomitant operative procedures were performed upon four patients, including division of the accessory atrioventricular pathway for the Wolff-Parkinson-White syndrome in two patients, plication of the right atrium for idiopathic right atrial dilatation in one patient, and a closure of the atrial septal defect in one patient. Focal ablation was performed in all instances. RESULTS: There was no early or late death nor postoperative complications. Atrial tachycardia disappeared and there were no episodes of recurrent tachycardia postoperatively during the mean follow-up period of 67 +/- 38 months. Histopathologic findings from four patients revealed a sinus node-like structure, diffuse chronic epimyocarditis, focal myocarditis, and fascicular disarray lesions. CONCLUSIONS: Excellent long-term result were obtained in patients with focal atrial tachycardia who were treated operatively. Early operative intervention is preferable before the occurrence of impaired ventricular function. From the histopathologic findings, operative therapy should be selected in patients with diffuse atrial lesions.
Adolescent↗
Spontaneous non-traumatic rupture of the thoracic aorta.
Spontaneous non-traumatic rupture of the aorta is a very rare condition that requires immediate surgery. However, correct preoperative diagnosis is difficult or impossible to establish. We report a case of spontaneous aortic rupture which was successfully treated by emergency surgical exploration following a transesophageal echographic diagnosis of hemopericardium. This case, as well as other reports, suggests that hemopericardium along with symptoms which suggest aortic dissection or rupture (e.g., acute chest or back pain) should raise a strong suspicion of spontaneous aortic rupture even in the absence of intimal flap or aortic dilatation, and the emergency surgery may be life-saving.
Aorta, Thoracic↗
Antithrombin and thrombolytic effects of a new antithrombin agent: angioscopic and angiographic comparison with heparin or batroxobin.
The antithrombotic effect of three different types of antithrombotic agents (antithrombin:argatroban, heparin, defibrinogenating agent:batroxobin) were evaluated in canine coronary and iliac arteries. An occlusive thrombus was produced by balloon injury. One of the three agents was infused intravenously at 1 hour after thrombus formation (heparin 250 U/kg, argatroban 0.5 mg/kg, batroxobin 0.5 U/kg) and the effect of thrombus size reduction was evaluated. On the contralateral side of the iliac artery, the preventive effect of these agents on thrombus formation was evaluated after balloon injury. In the iliac artery, angioscopic percent area obstruction by the thrombus before and 60 minutes after treatment reduced from 69% to 32% in the argatroban group, and from 64% to 51% in the batroxobin group (P < 0.0001 and P < 0.05, respectively). No significant change was observed in the heparin group. Angiography demonstrated the same trend. The percent area stenosis with thrombus at 60 minutes following balloon injury was 0.75% in the argatroban group, 18.9% in the heparin group (P < 0.05 vs argatroban), and 12.9% in the batroxobin group. Thrombus size at the treated site was smaller than that at the control site in all three groups (P < 0.05 vs control). In the coronary artery, angioscopic percent area obstruction by the thrombus before and 60 minutes after treatment reduced from 84% to 53% in the argatroban group, and from 86% to 68% in the batroxobin group (P < 0.0001 and P < 0.05, respectively). No significant change was observed in the heparin group. Angiography also demonstrated the same trend. The activated partial thromboplastin time (APTT) was prolonged to 189% of the control value with argatroban and to 1253% of the value with heparin (P < 0.0001). Fibrinogen was markedly reduced with batroxobin. These results showed that both the antithrombin agent and the defibrinogenating agent have a preventive effect on thrombus formation and the effect on thrombus size reduction, without marked prolongation of the APTT.
Angiography↗
Surgical treatment of ventricular tachycardia after surgical repair of tetralogy of Fallot. Relation between intraoperative mapping and histological findings.
BACKGROUND: The mechanism of ventricular tachycardia (VT) after correction of tetralogy of Fallot (TF) is poorly understood. The purpose of this study was to examine the histopathology of the arrhythmogenic area detected by intraoperative mapping. METHODS AND RESULTS: The patients were three men who underwent radical surgery for TF at age 3, 3, or 5 years, respectively. VT developed at 8, 9, or 11 years, respectively, after surgery, and shock developed during VT in every case. The ECG revealed monomorphic VT in two cases and polymorphic VT in one case. Induction of VT resulted in a wide left-axis deviation-pattern QRS with cycle lengths varying between 260 and 330 milliseconds. The VT origin was identified at the right ventricular outflow tract (RVOT). A radical operation was performed with the patient under cardiopulmonary bypass. On epicardial mapping, delayed activation of the RVOT was recorded during sinus rhythm, and clockwise circus movement of the macroreentry current during VT on the right ventricular free wall was documented in each case. The VTs were treated successfully by surgical resection and cryoablation of the myocardium. In every patient, histology of the myocardial specimens showed degeneration, adiposis, fibrosis, inflammatory cell infiltration, and scattered myocyte islets. These lesions corresponded anatomically to the area of myocardium in which delayed activation was evident during epicardial mapping. CONCLUSIONS: The results of this study indicate that patients with VT after radical correction of the TF have abnormal histopathological findings at the site of the prior right ventriculotomy scar. These lesions were noted within the region of delayed activation found during epicardial mapping and were found to be a part of the reentrant circuit.
Adult↗
[Cardiac pathology of sudden death].
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Adolescent↗
[Emotional stress and cardiac sudden death].
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Animals↗
[Pathology of congenital heart disease in adulthood].
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Adolescent↗
Preventive effect of betamipron on nephrotoxicity and uptake of carbapenems in rabbit renal cortex.
The preventive effect of betamipron (N-benzoyl-3-propionic acid: BP) on the renal uptake and nephrotoxicity of carbapenems (panipenem and imipenem) was studied in rabbits. Panipenem, a new carbapenem antibiotic, induced nephrotoxicity at a dose of 200 mg/kg, i.v., but this was less severe than that caused by a single dose of imipenem or cephaloridine. Along with the significant reduction of nephrotoxicity, the uptake of these carbapenems in the renal cortex was remarkably inhibited by simultaneous treatment with BP (200 mg/kg, i.v.). These results suggest that BP reduces the nephrotoxicity of carbapenems through inhibiting the active transport of carbapenems in the renal cortex. Because of the low toxicity of BP (LD50 in the rat, more than 3,000 mg/kg, i.v.), it was concluded that BP might be a good candidate for reducing the nephrotoxicity induced by panipenem or imipenem.
Alanine↗
Mesothelioma in the atrioventricular node. Case report.
A patient with complete atrioventricular block and an implanted permanent pacemaker died of colon cancer at the age of 64 years. At autopsy, a cardiac tumor in the region of the atrioventricular node (mesothelioma of the atrioventricular node) was found. The origin of this type of tumor is controversial. Histochemical findings suggested that the tumor in this case was of endodermal origin.
Atrioventricular Node↗
A case of arrhythmogenic right ventricular dysplasia with atrial flutter.
A 57-year-old male who had arrhythmogenic right ventricular dysplasia (ARVD) with recurrent atrial flutter (AF) is reported. The patient had more frequent episodes of AF than of ventricular arrhythmias. Magnetic resonance imaging, echocardiography and right ventriculography revealed dilatation of the right ventricle and endomyocardial biopsy specimens from the right ventricle showed findings which were compatible with ARVD. The left ventricular specimen, however, also revealed a loss of myocytes and interstitial fibroelastic changes. The present case demonstrates an overlap of post-inflammatory or primary endomyocardial fibroelastic changes with ARVD.
Aged↗
Apoptosis in acute and chronic myocarditis.
Programmed cell death or apoptosis plays a major role in the modification of morphologic and functional maturity in various normal organ systems. However, it is also related to certain diseases. We conducted a pathological study of the apoptosis of cardiomyocytes in six cases with myocarditis (three of acute myocarditis and three of chronic or persistent myocarditis) using histochemical methods. In normal hearts obtained from autopsy cases, apoptosis was seen in endocardial cells. There was no apoptosis in myocardial cells, except for a few in myocytes with two nuclei. In myocarditis, although the myocytes of all cases with acute myocarditis did not show apoptosis, one of the three cases with chronic or persistent myocarditis showed many apoptotic myocytes. Apoptosis may be one of the mechanisms causing myocyte damage in myocarditis.
Acute Disease↗
An autopsy case of hypertrophic cardiomyopathy with pathological findings suggesting chronic myocarditis.
Myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM) may play an important role in the function and/or dimensions of the left ventricle. We present an autopsied case of HCM followed for 10 years. A 68-year-woman with HCM underwent trans-aortic myectomy of the interventricular septum in 1979. A significant amount of round cell infiltration, myocardial fibrosis and disarray were observed in the resected specimen. She experienced repeated admissions due to diabetes mellitus and congestive heart failure, and died of renal failure in 1989. An autopsy revealed extensive myocardial fibrosis and significant cell infiltration in the ventricular myocardium. The infiltrating cells were almost all lymphocytes, and the ratio of CD4 to CD8 was 3.8. This ratio was different from that of typical viral myocarditis. This case suggests that there may be an undefined inflammatory process causing fibrosis in HCM, in addition to the ischemia due to intramural small coronary artery stenosis.
Aged↗