Teruhisa Tanabe

Evaluation of pericardial effusion with computed tomography.

Evaluation of pericardial effusion was attempted with computed tomography in 11 patients. The volume and distribution of pericardial fluid were assessed with satisfactory resolution and the nature of the fluid was estimated by the difference in x-ray transparency (CT numbers). The volume of pericardial fluid calculated by tomographic methods ranged from 25 ml. to 585 ml. and agreed well with the surgically drained fluid volume. The CT numbers of the pericardial effusion due to renal or heart failure, acute viral pericarditis, hypothyroidism, and hemopericardium were +12 to +13, +20, +28 to +30, and +26 to +40, respectively. Therefore the volume and gross nature of the pericardial fluid could be estimated noninvasively with computed tomography.

Co-localization of von Willebrand factor with platelet thrombi, tissue factor and platelets with fibrin, and consistent presence of inflammatory cells in coronary thrombi obtained by an aspiration device from patients with acute myocardial infarction.

Summary.  Background: Detailed histochemical analysis of coronary thrombi obtained freshly from acute phase of myocardial infarction patients may provide information necessary to understand the mechanism of coronary occlusive thrombus formation. Methods and Results: Coronary thrombi causing myocardial infarction were obtained from 10 consecutive patients of myocardial infarction in the acute phase, using a newly developed aspiration catheter. All the fixed specimens of coronary thrombi, by hematoxylin and eosin staining, were found to contain three major constituents, namely, platelets, densely packed fibrin and inflammatory cells, including polymorphonuclear and mononuclear cells, although their distribution in each specimen is totally heterogeneous. Immunohistochemical staining revealed the prominent presence of von Willebrand factor (VWF) at the sites of platelet accumulation, presence of tissue factor and platelets at the sites of deposition of fibrin fibrils. It also revealed the presence of CD16‐, CD45‐ and CD34‐positive cells, yet the functional roles of these cells have still to be elucidated. There are weak positive correlation between the number of inflammatory cells involved in the unit area of coronary thrombi specimen and the time of collection of the specimens after the onset of chest pain. Conclusions: In spite of various limitations, our results contain information suggesting the possible role of VWF in platelet‐thrombus formation, possible important role played by tissue factor and activated platelets in the formation of fibrin fibrils, and the positive relationship between inflammatory cells migration and the formation of occlusive thrombi in human coronary arteries.

Impact of vascular remodeling on the coronary plaque compositions: An investigation with in vivo tissue characterization using integrated backscatter-intravascular ultrasound

Recent studies have indicated that positive remodeling is strongly associated with development of acute coronary syndrome (ACS). The aim of this study was to compare plaque composition of vascular remodeling patterns by an established in vivo tissue characterization method using integrated backscatter (IB)-intravascular ultrasound (IVUS). The study population consisted of 41 consecutive patients who received IVUS prior to percutaneous coronary intervention. Remodeling index (RI) was calculated as the external elastic membrane (EEM) area at the minimal lumen area (MLA) site divided by average EEM area at the proximal and distal reference sites. The patients were divided into two groups based on RI: positive remodeling (PR) defined as RI>1 and non-PR as RI<or=1. A total of 21 areas centered at MLA per lesion site were evaluated by IB-IVUS at 1mm intervals. The occupancy rate of four tissue types within atherosclerotic plaques was compared between the two groups. Percent lipid volume in the PR group (n=20) was significantly greater than the non-PR group (n=21) (40.5+/-14.8% vs. 26.4+/-15.9%, p<0.001). In contrast, % fibrous volume in the PR group was significantly lower than the non-PR group (49.9+/-9.4% vs. 56.1+/-9.6%, p=0.042). Percent dense fibrous volume and % calcified volume were slightly but significantly lower in the PR group compared with the non-PR group (dense fibrous: 6.8+/-5.0% vs. 11.6+/-8.4%, p=0.034, calcified: 2.6+/-2.0% vs. 5.1+/-4.4%, p=0.026). In conclusions, PR lesions contain more lipid-rich and less hard plaque components compared with non-PR lesions, which may account for the higher incidence of ACS and plaque vulnerability.

Sudden cardiac arrest recorded during Holter monitoring: Prevalence, antecedent electrical events, and outcomes

BACKGROUND Causative arrhythmias of sudden cardiac arrest (SCA) are changing in this age of improved coronary care. OBJECTIVE The purpose of this study was to examine the frequency of terminal arrhythmias and the electrical events prior to SCA. METHODS We analyzed 24-hour Holter recordings of 132 patients enrolled from 41 institutions who either died (n = 88) or had an aborted death (n = 44). The Holter recordings were obtained for diagnosing and evaluating diseases and arrhythmias in those without any episodes suggestive of SCA. RESULTS In 97 patients (73%), SCA was associated with ventricular tachyarrhythmias and in 35 (27%) with bradyarrhythmias. The bradyarrhythmia-related SCA patients were older than those with a tachyarrhythmia-related SCA (70 ± 13 years vs. 58 ± 19 years, P < .001). The most common arrhythmia for a tachyarrhythmia-related SCA was ventricular tachycardia degenerating to ventricular fibrillation (45%). The bradyarrhythmia-related SCA was caused by asystole (74%) or AV block (26%). Spontaneous conversion was observed in 37 patients (38%) with ventricular tachyarrhythmias. Of those, 62% of the patients experienced symptoms including syncope, chest pain, or convulsion. Multivariate logistic analysis revealed that independent predictors of mortality for tachyarrhythmia-related SCAs were advanced age (odds ratio 1.04, 95% confidence interval 1.02-1.08) and ST elevation within the hour before SCA (odds ratio 3.54, 95% confidence interval 1.07-13.5). In contrast, the presence of preceding torsades de pointes was associated with spontaneous conversion (odds ratio 0.20, 95% confidence interval 0.05-0.66). CONCLUSION The most frequent cause of SCA remains ventricular tachyarrhythmias. Advanced age and ST elevation before SCA are risk factors for mortality in tachyarrhythmia-related SCAs.

Comparative Study of Nifekalant Versus Amiodarone for Shock-Resistant Ventricular Fibrillation in Out-of-Hospital Cardiopulmonary Arrest Patients

Background: In Japan, intravenous nifekalant (NIF) was often used for direct current cardioversion-resistant ventricular fibrillation (VF), until the use of intravenous amiodarone (AMD) was approved in 2007. The defibrillatory efficacy of NIF and AMD has thus far not been compared for resuscitation. Methods and Results: Between August 2007 and April 2009, 403 consecutive out-of-hospital patients with cardiopulmonary arrest were transferred to the Emergency Medical Service of Tokai University. Of these, 30 patients with first defibrillation failure or VF recurrence were enrolled for this NIF/AMD study. The final defibrillation success (and hospital survival rate) was 67% (10/15) in the AMD and 47% (7/15) in the NIF group. The discharge survival rate was 53% (8/15) in the AMD and 21% (4/15) in the NIF group (P = 0.06). Notably, all 4 survivors in the NIF group could take up normal daily life again, whereas this was restricted to only 2 patients from the 11 survivors in the AMD group. The difference is probably partly attributable to longer time from AMD administration to defibrillation success compared with NIF. In the cases of defibrillation failure, VF continued in 4/8 by NIF, however, asystole or pulseless electrical activity occurred in 4/5 patients by AMD. Conclusions: AMD may be borderline superior over NIF to facilitate defibrillation in out-of-hospital patients with cardiopulmonary arrest. However, from the view point of preservation of brain function, NIF is not inferior to AMD for CPR.

Year-long upregulation of connexin43 in rabbit hearts by heavy ion irradiation

A previous study from our laboratory has shown that a single targeted heavy ion irradiation (THIR; 15 Gy) to rabbit hearts increases connexin43 (Cx43) expression for 2 wk in association with an improvement of conduction, a decrease of the spatial inhomogeneity of repolarization, and a reduction of vulnerability to ventricular arrhythmias after myocardial infarction. This study investigated the time- and dose-dependent effects of THIR (5-15 Gy) on Cx43 expression in normal rabbit hearts (n = 45). Five rabbits without THIR were used as controls. A significant upregulation of Cx43 protein and mRNA in the ventricular myocardium was recognized by immunohistochemistry, Western blotting, and real-time PCR from 2 wk up to 1 yr after a single THIR at 15 Gy. THIR > or =10 Gy caused a significant dose-dependent increase of Cx43 protein and mRNA 2 wk after THIR. Anterior, lateral, and posterior free wall of the left ventricle, interventricular septum, and right ventricular free wall were affected similarly by THIR in terms of Cx43 upregulation. The radiation-induced increase of immunolabeled Cx43 was observed not only at the intercalated disk region but also at the lateral surface of ventricular myocytes. The increase of immunoreactive Cx43 protein was predominant in the membrane fraction insoluble in Triton X-100, that is the Cx43 in the sarcolemma. In vivo examinations of the rabbits 1 yr after THIR (15 Gy) revealed no significant changes in ECGs and echocardiograms (left ventricular dimensions, contractility, and diastolic function), indicating no apparent late radiation injury. A single application of THIR causes upregulation and altered cellular distribution of Cx43 in the ventricles lasting for at least 1 yr. This long-lasting remodeling effect on gap junctions may open the pathway to novel therapy against life threatening ventricular arrhythmias in structural heart disease.

Shear-induced von Willebrand factor-mediated platelet surface translocation of the CD40 ligand

BACKGROUND Platelets, which can adhere to damaged vascular surfaces and release bioactive substances upon activation, may play important roles in regulating local inflammatory responses. We focused on the surface translocation of CD40 ligand (CD40L) molecules when the platelets are exposed to a high shear stress. METHOD Blood specimens were obtained from eight apparently healthy adult donors. The number of CD40L molecules appearing on the surface of platelets after exposure of platelet-rich plasma to a shear rate of 10,800 s(-1) was determined by quantitative flow cytometry. RESULTS The number of anti-CD40L IgG molecules bound per platelet increased from 15+/-80/platelet before to 355+/-122/platelet after exposure of the platelets to a shear rate of 10,800 s(-1) (p<0.01), but not after their exposure to the relatively low shear rate of 1200 s(-1). This shear-induced platelet surface translocation of CD40L, mediated by the von Willebrand factor (VWF)-GP Ibalpha interaction, was enhanced in the presence of a low concentration of epinephrine (100 nM), which by itself, however, could not cause platelet activation. Our results demonstrate that fluid force induces the appearance of CD40L on the surface of platelets, and also that this phenomenon is enhanced in the presence of a low concentration of epinephrine, corresponding to that released by sympathetic stimulation.

Evaluation of a nine-lead Holter monitor for identifying and localizing ischemia and coronary artery disease detected by quantitative thallium-201 tomography

We devised a nine-lead Holter monitor system with a lead-switching technique to record electrocardiograms from multiple sites in the anterior and the posterior or lateral chest. Leads CM1 to CM6, high lateral (HL), low lateral (LL), and low posterior chest (LB) were used. The sensitivity, specificity, and predictive accuracy of this system for identifying specific regions of myocardial ischemia and coronary artery disease were investigated in 130 patients with coronary artery disease. Anterolateral leads (CM4 to CM6, HL, and LL) showed high sensitivity for detecting anterior and lateral ischemia (69% to 100%) but low specificity (4% to 44%) compared with tomographic results. The specificity of these leads for identifying single-vessel disease was low (6% to 47%) although some leads showed high sensitivity (69% to 100%). In contrast, the LB lead exhibited high sensitivity and specificity for detecting inferior ischemia (70% and 95%, respectively) and right coronary artery (RCA) disease (74% and 93%, respectively). Consequently, ST depressions in the LB lead (anode) are specific for identifying inferior ischemia and RCA disease, whereas those in the anterior and lateral chest leads do not identify the ischemic region or the obstructed coronary artery.

Effects of bunazosin, a selective α1-blocking agent, and propranolol used alone and in combination on canine ventricular refractoriness and its dispersion during myocardial ischemia

The individual and combined effects of bunazosin, a selective alpha 1-adrenergic blocking agent, and propranolol on ventricular refractoriness and its dispersion were assessed in 33 chloralose-anesthetized, sympathectomized, and vagotomized dogs 2-3 h after occlusion of the obtuse marginal branches of the circumflex artery. The refractory period was measured in eight sites of the ischemic zone, two sites of the border zone, and two sites of the normal zone with S1-S2 extrastimulus methods. In group 1 dogs (n = 9), coronary artery ligation significantly shortened refractoriness in the ischemic zone (p = 0.023-0.001 in each site). Intravenous (i.v.) administration of a low dose of bunazosin at 0.1 mg/kg significantly blunted the shortening of refractoriness in the ischemic zone (p = 0.026-0.002 in each site), although the values did not reach those observed in the nonischemic zones (both the border and normal zones), where refractoriness remained unchanged. In group 2 dogs (n = 11), a higher dose of i.v. bunazosin, 0.5 mg/kg, significantly blunted the shortening of the refractory period within the ischemic zone (from 149 +/- 14 to 175 +/- 8 ms; mean +/- SD, p < 0.001) and reached the levels of the nonischemic zones (border zone 175 +/- 15 ms, normal zone 170 +/- 14 ms), resulting in a dispersion reduction in refractoriness between the ischemic and nonischemic zones. This dispersion tended to increase again with i.v. administration of 0.2 mg/kg propranolol (ischemic vs. border zone p = 0.034; ischemic vs. normal zone p = 0.089).(ABSTRACT TRUNCATED AT 250 WORDS)

Two Cases in Which Myocardial Injury Could Be Only Evaluated by Nuclear Medicine Studies on Electric Shock Patients Whose Electrocardiogram and Myocardial Enzyme Levels Were Normal

Heart injury due to electric shock is currently diagnosed based on electrocardiogram (ECG) changes or elevated levels of myocardial enzymes or both. However, the rate at which ECG detects abnormalities is very low; thus, the estimated rate of the diagnosis of myocardial damage due to electric shock is lower than the actual rate. The method of nuclear medicine study of the heart is superior with regard to evaluating transient ischemia, such as angina pectoris, in patients whose ECG and myocardial enzyme levels are normal. Therefore, we attempted to diagnose transient myocardial damage in electric shock patients by using nuclear medicine study of the heart.