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Introduction We previously reported that LP positive patients after percutaneous coronary intervention (PCI) had higher rate of re-hospitalization in the small-scale study (135 patients). In this study, we evaluated correlation between LP and later cardiac events leading to re-hospitalization more extensively in greater population. Methods and results A 24-h high-resolution (HR) ambulatory electrocardiogram (ECG) was performed in 421 patients that received PCI for the treatment of acute coronary syndrome (ACS) within 30 days. Various baseline characteristics and post-PCI ECG parameters including LP were examined for correlation with later re-hospitalization. LP was evaluated based on 3 different conditions, i.e., the worst, mean and best values, from 24-h signal-averaged QRS wave data. During the post-PCI follow-up period (611 ± 489.0 days), 90 patients were re-hospitalized due to cardiac events. Multivariate analysis identified only positive LP based on the worst value as an independent predictor for re-hospitalization with OR 2.26. Most of re-hospitalization cases (>75%) were predominantly attributed to ischemic events. LP positive population had significantly higher incidences of ischemic events as well as overall re-hospitalization compared to LP negative population. The predictive power of LP was decreased when it was combined with other variables. The receiver operating characteristic analysis determined the LP cut-off values consistent with the LP positive criteria previously reported and standardized. Conclusion The presence of LP in the 24-h HR ambulatory ECG post-PCI was an independent predictor for a risk of re-hospitalization due to ischemic cardiac events in ACS patients.

BACKGROUND Targeted external heavy ion irradiation (THIR) of rabbit hearts 2 weeks after myocardial infarction (MI) reduced the vulnerability of fatal ventricular tachyarrhythmias (VT/VF) in association with the increased connexin43 (Cx43). Increased Cx43 was maintained for at least 1 year in normal rabbits, but the long-term antiarrhythmic effects in the MI model are unknown. We investigated the propensity for late potentials and VT/VF inducibility. METHODS Intracoronary injection of microspheres was performed to induce nontransmural MI in anesthetized eight beagles. Four beagles were treated with THIR (12 C6+ , 15 Gy) 2 weeks later (MI + THIR group), and four without THIR served as controls (MI group). Signal-averaged electrocardiography, programmed electrical stimulation, immunohistochemical analysis, and echocardiograms were performed at 1 year. RESULTS Filtered QRS duration was exacerbated after MI and remained unchanged for 1 year in the MI group (118 ± 1.4 ms), but significantly returned toward baseline in the MI + THIR group (109 ± 6.9 ms). Similarly, root mean square voltage of the last 40 ms was exacerbated after MI, but recovered after THIR. VT/VF inducibility decreased to 25% in the MI + THIR group compared with 100% in the MI group. Immunostaining Cx43 expression in cardiac tissues significantly increased by 24-45% in the MI + THIR group. Left ventricular ejection fractions remained within the normal range in both groups. CONCLUSION A single exposure of the dog heart to 12 C irradiation attenuated vulnerability to ventricular arrhythmia after the induction of MI for at least 1 year through the modulation of Cx43 expression.

BACKGROUND Sleep-disordered breathing (SDB) is highly associated with arterial hypertension (HT). Sympathetic hypertonia increases the risk of sudden cardiac death in patients with sleep apnea. This study aims to noninvasively investigate the electrophysiological features in SDB patients with and without arterial HT. METHODS Fifty-three patients with SDB were classified into two groups: SDB group and SDB + HT group. Twenty subjects with arterial HT were enrolled as controls (HT group). To assess arrhythmogenic vulnerability, high-resolution 24-hour ambulatory electrocardiograms were obtained for analyzing continuous late potential (LP), T-wave amplitude variability (TAV), and heart rate variability (HRV). RESULTS A higher incidence of positive LP was observed in the SDB + HT (85%) group than that observed in the SDB (50%) and HT (20%) groups (P < 0.01). TAV was highest in the SDB + HT group (78 μV) compared with the SDB (61 μV) and HT groups (42 μV; P < 0.01). Positive LP and TAV values were observed at night in the SDB + HT and SDB groups. The low-frequency/high-frequency of the HRV analysis was highest in the SDB + HT (4.7) group compared with that in the SDB (2.9) and HT (2.9) groups (P = 0.01). CONCLUSION Nocturnal LP, TAV, and HRV examinations were useful to investigate arrhythmogenesis. SDB patients with arterial HT showed a high prevalence of depolarization and repolarization abnormalities and relative sympathetic hyperactivity. This suggests that an electrophysiological instability is more prevalent in SDB patients with arterial HT.

Background High-risk patients with Brugada syndrome (BrS) have inherent late potential (LP) fluctuations that might be explained by autonomic activity, electrolyte abnormality, and body temperature changes. However, the correlation between postural changes and LP determinates remains unknown. Methods Forty patients with BrS (38 men, 43.9 ± 13.5 years) and 15 controls (15 men, 42.4 ± 11.2 years) were enrolled. LP variations were investigated at five body positions using high-resolution ambulatory monitoring electrocardiography (HR-ambulatory ECG). The HR-ambulatory ECG was recorded for 3 hours and LP parameters (fQRSd, LAS40, and RMS40) were obtained for at least 15 minutes in each at the supine, left and right lateral decubitus, and prone and sitting positions. Results Determinate LP in the BrS group was significantly abnormal in all positions. Among the five body positions, positive LP were much more frequent in the supine and left and right lateral decubitus positions than in the prone and sitting positions and normalized in the last two positions in patients with BrS. RMS40 variance by postural change was significantly larger in the coved group than in the saddle back group. Determinate LP improved in the sitting position compared to the supine position in the coved group. Conclusions Positive LP findings normalized in the sitting position in patients in the coved BrS group with a resuscitation history, suggesting that depolarization instability might be related to the risk of fatal ventricular arrhythmia. Posture-induced LP variance should be examined using HR-ambulatory ECG analysis in patients with BrS.

Causative arrhythmias of sudden cardiac arrest (SCA) are changing in this age of improved coronary care.The purpose of this study was to examine the frequency of terminal arrhythmias and the electrical events prior to SCA.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.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).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.

Targeted external heavy ion irradiation (THIR) of rabbit hearts 2 weeks after myocardial infarction (MI) reduced the vulnerability of fatal ventricular tachyarrhythmias (VT/VF) in association with the increased connexin43 (Cx43). Increased Cx43 was maintained for at least 1 year in normal rabbits, but the long-term antiarrhythmic effects in the MI model are unknown. We investigated the propensity for late potentials and VT/VF inducibility.Intracoronary injection of microspheres was performed to induce nontransmural MI in anesthetized eight beagles. Four beagles were treated with THIR (Filtered QRS duration was exacerbated after MI and remained unchanged for 1 year in the MI group (118 ± 1.4 ms), but significantly returned toward baseline in the MI + THIR group (109 ± 6.9 ms). Similarly, root mean square voltage of the last 40 ms was exacerbated after MI, but recovered after THIR. VT/VF inducibility decreased to 25% in the MI + THIR group compared with 100% in the MI group. Immunostaining Cx43 expression in cardiac tissues significantly increased by 24-45% in the MI + THIR group. Left ventricular ejection fractions remained within the normal range in both groups.A single exposure of the dog heart to

The aim of this study was to investigate the significance of late potential (LP) after percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS).We enrolled 135 consecutive patients with ACS admitted to Tokai University Hospital from February to December 2012. Twenty-four hour high-resolution ambulatory electrocardiogram was performed between post-PCI procedure and hospital discharge. The patients were divided into the LP-positive (33 patients) and LP-negative (102 patients) groups, and the relationship between LP and re-hospitalization was prospectively investigated.The body mass index, serum creatinine, and creatine phosphokinase-MB were higher in the LP-positive group than in the LP-negative group (p0.05). The re-hospitalization rate was higher in the LP-positive group. (9 patients, 27.3% vs. 10 patients, 9.8%; p = 0.03). There were no significant differences in the occurrence of ventricular tachycardia or cardiac death between the groups. According to Kaplan-Maier analysis, proportion of re-hospitalization was significantly lower in the LP-positive group than in the LP-negative group (p = 0.01; average follow-up, 451.4 ± 25.9 days). The odds ratio of LP presence was 3.45 (highest among all variables; 95% confidence interval, 1.3-9.4; p0.01).Positive LP in patients with ACS after PCI may predict re-hospitalization.

Very late stent thrombosis (VLST) is a major unresolved problem of drug-eluting stent (DES) implants. However, its actual incidence with respect to the distribution of DES-target vessel and accuracy of adjudicating stent thrombosis according to the ARC definition has not been yet adequately evaluated. We studied 720 patients who had completed over 1 year from elective DES implantation. In this cohort, we extracted patients who present acute coronary syndrome (ACS) (n = 3, 0.4%). The timing of ACS events was 17, 19, and 24 months after DES implantation. At the time of presentation, VLST was strongly suspected as the initial diagnosis, however, coronary angiography (CAG) confirmed the different culprit lesion from DES and clearly no thrombus within the DES. According to ARC definition, three probable stent thromboses in this cohort before CAG, however, no stent thrombosis was confirmed after the CAG. Thus, no stent thrombosis was confirmed among this study population. In the very late phase after DES implantation, new onset ACS is not at all extraordinary occurrence in the target vessels of previous DES implantation. However, stent thrombosis is often assumed without angiographic confirmation. The clinical possibility that non-stent thrombosis is incidentally diagnosed with stent thrombosis without angiographic confirmation should be considered within the current accepted definition of stent thrombosis.

Background: Several studies have indicated that the clinical outcomes of sirolimus-eluting stents (SES) are significantly associated with longitudinal positioning of the stent relative to the underlying plaque distribution. Methods and Results: Optimal SES landing was determined using unique stepwise intravascular ultrasound (IVUS) criteria, mainly targeting the sites with plaque burden

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.

Background: A multicenter, randomized, placebo-controlled, double-blind trial was conducted with patients with persistent atrial fibrillation (AF) to determine the dose-response effects and safety of bepridil, using every-day transtelephonic monitorings. Methods and Results: A total of 90 patients were randomized to receive placebo, 100 mg/day and 200 mg/day of bepridil treatment for 12 weeks. After the treatment, those patients who converted to sinus rhythm was 3.4% in placebo, 37.5% in those who received 100 mg/day and 69.0% in those who received 200 mg/day, thus demonstrating a linear dose-response relationship for AF conversion. The conversion rate gradually reached a maximal value at ~6 weeks after initiation of bepridil. However, the AF recurrence rate was high (91.7% in those receiving 100 mg/day and 75.0% in those receiving 200 mg/day). Adverse events, presumably related to the drug, were also frequent: ventricular tachycardia in 2, QT prolongation in 4 and sinus bradycardia in 2 patients. In those patients treated with 200 mg/day group, 1 patient died suddenly because of ventricular tachycardia. Conclusions: This study demonstrated the dose response-relationships of bepridil for AF conversion to sinus rhythm. However, the high rate of AF recurrence and substantial drug-related adverse effects, including sudden death, raised caution about using bepridil to treat persistent AF. The balance between benefits and risks of the drug should be individualized. (Circ J 2009; 73: 1020-1027)

Background Final kissing balloon technique (KBT) is known to alter long-term clinical outcomes for treatment of bifurcated coronary lesions. However, determination of adequate diameters of the 2 balloons remains difficult because of lack of a working index. Methods and Results Twenty-one cases of left main (LM)-related bifurcated lesions, treated with CypherTM stents (single/crush stenting) and final KBT, were enrolled. The formula "R2 = D12 + D22" was used, adjusting balloon diameter (D1, D2) to the downstream branches, to predict the theoretical mean hugging balloon diameter (R) within the main portion. The degree and pattern of stent expansion in the LM and main branch (MB) segments was compared by volumetric intravascular ultrasound assessment. Stents in the LM segments expanded to a greater extent and more asymmetrically than in MB segments (average stent area: 13.2±3.1 mm2 vs 7.6±2.1 mm2, p

Sleep-disordered breathing (SDB) is highly associated with arterial hypertension (HT). Sympathetic hypertonia increases the risk of sudden cardiac death in patients with sleep apnea. This study aims to noninvasively investigate the electrophysiological features in SDB patients with and without arterial HT.Fifty-three patients with SDB were classified into two groups: SDB group and SDB + HT group. Twenty subjects with arterial HT were enrolled as controls (HT group). To assess arrhythmogenic vulnerability, high-resolution 24-hour ambulatory electrocardiograms were obtained for analyzing continuous late potential (LP), T-wave amplitude variability (TAV), and heart rate variability (HRV).A higher incidence of positive LP was observed in the SDB + HT (85%) group than that observed in the SDB (50%) and HT (20%) groups (P0.01). TAV was highest in the SDB + HT group (78 μV) compared with the SDB (61 μV) and HT groups (42 μV; P0.01). Positive LP and TAV values were observed at night in the SDB + HT and SDB groups. The low-frequency/high-frequency of the HRV analysis was highest in the SDB + HT (4.7) group compared with that in the SDB (2.9) and HT (2.9) groups (P = 0.01).Nocturnal LP, TAV, and HRV examinations were useful to investigate arrhythmogenesis. SDB patients with arterial HT showed a high prevalence of depolarization and repolarization abnormalities and relative sympathetic hyperactivity. This suggests that an electrophysiological instability is more prevalent in SDB patients with arterial HT.

Radiation has been shown to enhance intercellular communication in the skin and lungs through an increase of connexin43 (Cx43) expression. If analogous Cx43 up-regulation is induced in the diseased heart, it would provide a new perspective in radiation therapy for arrhythmias. The aim of the present study is to test this hypothesis.Non-transmural myocardial infarction (MI) was created in 24 rabbits by microsphere injection into the coronary arteries. Twenty-four rabbits without MI were used as controls. Targeted external heavy ion beam irradiation (THIR; 15 Gy) was applied 2 weeks after MI with an accelerator (HIMAC, Chiba, Japan).The THIR was associated with an increase of Cx43 mRNA and protein levels in the left ventricle in control as well as in MI rabbits. THIR also increased lateralization of Cx43, which was no longer colocalized with cadherins. In MI hearts, immunoreactive Cx43 signals were reduced in the peri-infarct zone, and the reduction was reversed by THIR. In-vivo epicardial potential mapping on the free wall (64 unipolar electrodes to cover 7 x 7 mm) in MI hearts revealed reduced conduction velocity, whereas dispersion of the activation-recovery interval (ARI) was increased compared with controls, and these changes were reversed by THIR. The vulnerability for ventricular tachyarrhythmias (VT/VF), which was estimated by programmed stimulation, was increased in MI hearts, and this increased vulnerability to arrhythmias was reversed by THIR.THIR increases Cx43 expression, improves the conductivity, decreases the spatial heterogeneity of repolarization, and reduces the vulnerability of rabbit hearts to ventricular arrhythmias after MI. THIR could have an antiarrhythmic potential through an improvement of electrical coupling.

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.

Background Because nifekalant hydrochloride (NIF) displayed a superior defibrillating effect on ventricular tachycardia/fibrillation (VT/VF) in cardiopulmonary arrest (CPA) patients, despite some QT prolongation, its effect on transmural dispersion of repolarization (TDR) in the left ventricle (LV) in an animal model of CPA was investigated. Methods and Results Eight beagle dogs were created with a myocardial infarction under anesthesia, and then VT/VF induction by continuous stimulation and cardiopulmonary resuscitation (CPR) were repeated. NIF (0.3 mg/kg) was administered under acidotic conditions (pH 7.26). The QTc interval measured by Y-lead ECG showed no significant prolongation before and after NIF. The activation recovery interval (ARI) measured by 64-lead LV surface mapping showed minimum ARI prolongation (40%) by NIF without maximum ARI prolongation, and as a result the ARI dispersion decreased by 67%. The repolarization time (RPT) with the plunge electrode showed 13-19% prolongation in the subendocardium and subepicardium with CPR, but NIF prolonged the RPT in the middle layer alone (17%), and as a result Plunge-TDR decreased by 82% (n=8, p

Background Platelets play an important role in myocardial infarction and ischemic stroke events, but whether platelet aggregability is related to early stage arteriosclerosis remains unclear. Methods We used a novel platelet counting system which makes it possible to detect spontaneous platelet aggregation, to evaluate the relationship between platelet aggregability and carotid artery arteriosclerosis in 125 outpatients with primary hypertension (46–73 years old: 65 men, 60 women). All subjects underwent carotid artery ultrasonography to determine whether plaque was present and to estimate intima-media thickness. Results Patients with carotid artery plaques (Plaque(+), n = 63) were older and had higher systolic blood pressures than patients without plaques (Plaque(−), n = 62), but no significant differences in sex, body mass index, diastolic blood pressure, plasma concentrations of glucose, total cholesterol, triglyceride, lipoprotein cholesterol, fibrinogen or the platelet count in whole blood were observed between Plaque(+) and Plaque(−) groups. Plaque(+) subjects showed greater spontaneous platelet aggregability and platelet aggregation induced by 2 μM or 0.5 μM of ADP or 0.3 μM of epinephrine than the Plaque(−) group. When age and systolic blood pressure were matched ( n = 52 in both groups), the Plaque(+) subjects exhibited greater platelet aggregability than the Plaque(−) subjects. Platelet aggregation induced by 2 μM of ADP showed statistical significant positive correlation coefficients with age, HbA1c and diastolic blood pressure. Conclusion Our results indicate that hypertensive patients with carotid artery plaque have increased platelet aggregability. A prospective study is recommended to clarify whether this increase in platelet aggregability promotes the progression of arteriosclerosis.

Background Spiral re-entry plays the principal role in the genesis of ventricular tachycardia and ventricular fibrillation (VT/VF). The specific IKr blocker, nifekakant (NIF) has, often in combination with lidocaine (LID), recently been used in Japan to prevent recurrent VT/VF, but the combined effects of these drugs on spiral re-entry had never been investigated. Methods and Results A ventricular epicardial sheet was obtained from 13 Langendorff-perfused rabbit hearts by means of a cryoprocedure, and epicardial excitations were analyzed with a high-resolution optical mapping system. Nifekakant (0.5 μmol/L) caused significant prolongation of action potential duration (APD) and LID (3 μmol/L) attenuated the APD prolongation without affecting the conduction velocity. VT were induced in 6 hearts by cross-field stimulation, and single- or double-loop spirals circulating around variable functional block lines were visualized during the VT. Nifekakant reduced VT cycle length and caused early termination in association with destabilization of the spiral dynamics (prolongation of functional block line, frequent local conduction block, and extensive meandering). These modifications of spiral-type re-entrant VT by NIF were prevented by addition of LID. Conclusions The effects of NIF on the spiral excitations are reversed by LID. This interaction should be taken into account when these drugs are used in combination to treat VT/VF. (Circ J 2005; 69: 576 - 584)

BACKGROUND: High‐risk patients with Brugada syndrome (BrS) have inherent late potential (LP) fluctuations that might be explained by autonomic activity, electrolyte abnormality, and body temperature changes. However, the correlation between postural changes and LP determinates remains unknown. METHODS: Forty patients with BrS (38 men, 43.9 ± 13.5 years) and 15 controls (15 men, 42.4 ± 11.2 years) were enrolled. LP variations were investigated at five body positions using high‐resolution ambulatory monitoring electrocardiography (HR‐ambulatory ECG). The HR‐ambulatory ECG was recorded for 3 hours and LP parameters (fQRSd, LAS40, and RMS40) were obtained for at least 15 minutes in each at the supine, left and right lateral decubitus, and prone and sitting positions. RESULTS: Determinate LP in the BrS group was significantly abnormal in all positions. Among the five body positions, positive LP were much more frequent in the supine and left and right lateral decubitus positions than in the prone and sitting positions and normalized in the last two positions in patients with BrS. RMS40 variance by postural change was significantly larger in the coved group than in the saddle back group. Determinate LP improved in the sitting position compared to the supine position in the coved group. CONCLUSIONS: Positive LP findings normalized in the sitting position in patients in the coved BrS group with a resuscitation history, suggesting that depolarization instability might be related to the risk of fatal ventricular arrhythmia. Posture‐induced LP variance should be examined using HR‐ambulatory ECG analysis in patients with BrS.

An estimated 50,000 patients have heart failure (HF) in Japan, and the left ventricular ejection fraction (LVEF) is the typical predictor of prognosis. The identification of a noninvasive marker to predict most high-risk patients is urgently needed. This study aimed to log the continuous ventricular late potential (LP) by using high-resolution ambulatory monitoring in patients with HF with non-sustained ventricular tachycardia, and determine the association between the LP variation and prognosis.The 90 hospitalized patients were classified into cardiogenic death (n = 10) and non-death (n = 80) groups. The LVEF, LP, and coefficient of variation (CV) of the filtered QRS (fQRS), and low-amplitude signal40 µV for the terminal QRS portion of (LAS40) of both groups were evaluated. The maximum fQRS over 24 h was defined as the maximum fQRS (Max-fQRS).The results were as follows: (1) cardiogenic death occurred in 32% (10/31 patients) with an LVEF ≤ 45% and a Max-fQRS ≤ 114 ms; (2) cardiogenic death occurred in 38% (10/26 patients) with a LAS40-CV ≥ 0.09; and (3) using LVEF, Max-fQRS, and LAS40-CV as the three predictors, the specificity and accuracy were 83% and 82%, respectively, with an odds ratio of 12.3.LAS40 variations and increases might be new risk indicators of prognosis.

Background: Although incidence of ventricular arrhythmias after partial left ventriculectomy (PLV) has been reported, there are no studies comparing incidence before and after PLV. Although operative scars may give rise to arrhythmias, improved energetic efficiency after PLV may decrease their incidence. Methods: Pre- and postoperative ventricular arrhythmias were monitored by Holter ECG and analyzed in 17 patients undergoing PLV in Curitiba, Brazil. Results: Although total 24-hour heart beat (THB) increased significantly (p = 0.018), ventricular premature contractions (VPCs) decreased markedly (p = 0.036), excluding one patient dying in low cardiac output (LOS) who had terminal arrhythmias increased multifold. In the remaining 16 patients, VPC pairs were also reduced significantly on the average (p = 0.038). In contrast, ventricular tachycardia (VT; more than three consecutive VPCs) disappeared in five patients, decreased in two patients, and newly occurred in four patients, with five patients showing no change; one of them developed a prolonged VT, successfully reversed by external cardioversion. Conclusions: Despite notable significant increase in THB immediately after PLV, PVC and PVC pairs were significantly decreased in contrast to VT, which disappeared in some patients and newly occurred in other patients, remaining constant on the average. Sustained VT occurring in a patient with all other arrhythmias suppressed may suggest a unique electrophysiological substrate, may justify prophylactic use of amiodarone or an implantable cardioverter-defibrillator, and may underscore the importance of further and extended studies.

The purpose of the study was to determine whether a new KATP channel opener, Y 26763 (Y), can influence the electrophysiological properties in the ischemic myocardium as well as to determine whether the blunting effect of the alpha 1-adrenoceptor antagonist bunazosin (BN) on an ischemia-induced shortening of repolarization time can be related to the KATP channel activity. The anterior descending branch of the left coronary artery was ligated four times for 5 minutes, separated by 15 minutes of reperfusion (stages 1-4) to test the dose-dependent effect of drugs on repolarization. Dogs received either vehicle (n = 9), Y (0.4, 2.0, and 4.0 micrograms/kg at stages 2, 3, and 4, respectively, with 0.4 microgram/kg/min drip infusion at each of stages 2-4, n = 7), BN (0.1 mg at each of stages 2-4, n = 8), or a combination of these two drugs (BN + Y, the same dose of BN and Y in groups BN and Y, respectively, n = 9). Drugs were administered into the left atrium. The monophasic action potential (MAP) and regional electrograms were recorded. The MAP90 and the duration of the slow deflections (DSD) of the regional electrogram were used as markers of repolarization. The Vmax of the MAP and the rapid deflections (DRD) of the regional electrogram were used as markers of conduction. Y augmented an ischemia-induced shortening of MAP90 and DSD in proportion to an increase in the dose given and the plasma concentration (P < .05-.01), especially at the epicardial site. BN and BN + Y blunted the ischemia-related shortening of MAP90 and DSD, causing a reduction in repolarization time dispersion between the ischemic and normal zones. There were no significant changes in the Vmax or DRD in the ischemic zone between periods before and after an increase in each drug dose in the four groups. None of the seven dogs developed ventricular tachycardia (VT)/ventricular fibrillation (VF) in the Y group, whereas two of the eight dogs in the BN group, three of the nine dogs in the BN + Y group, and three of the nine dogs in the control group developed VT/VF. These results suggest that the alpha 1-adrenergic blocker bunazosin blunts the shortening effect of KATP channel activator on repolarization time, and that the KATP channel opener Y may be antiarrhythmic, although the repolarization time dispersion during myocardial ischemia is increased.

Background: There are few reports on long-term convalescence with regard to cardiac injury caused by blunt chest trauma. Nuclear medicine study of the heart (NMSH) in the early stages of injury is reportedly superior to detect the correlation between injury and fatal arrhythmia. Therefore, we prospectively performed NMSH and Holter electrocardiogram (ECG) in the early and chronic stages for a cardiac injury patient, and we longitudinally examined the recovery process and the occurrence of fatal arrhythmia. Methods and Results: A total of 202 patients with blunt chest trauma were admitted to our hospital between April 2006 and January 2007. Of 65 patients who were diagnosed with cardiac injury by ECG, a myocardial enzyme, or cardiac ultrasonography, 11 were enrolled in this study because they agreed to outpatient visiting for regular examinations for 1 year. NMSH showed positive findings in 6 of the 11 patients in the acute period of < 1 month. Twelve months later, five patients improved but still exhibited protracted cardiac damage without complete recovery. Among the six patients in whom NMSH showed positive findings, Holter ECG indicated an abnormal finding in two patients in the acute period and in four patients in the chronic period, and detected one patient with a nonsustained ventricular tachycardia in the chronic period. Conclusion: Cardiac injuries may exacerbate cardiac functions and lead to fatal arrhythmia during the chronic period. Therefore, evaluating recovery for at least 12 months after myocardial damage is necessary to prevent sudden cardiac death.

We investigated the response of refractory periods and blood flow to blockade of α1- and β-adrenoceptors alone, or in combination on endocardium and epicardium, during myocardial ischemia. Dogs were anesthetized with α-chloralose and divided into bunazosin (an α1-blocking agent)-treated (0.1–0.2 mg/kg, IV, n = 14), propranolol-treated (0.2 mg/kg, IV, n = 12), and vehicle-control (n = 10) groups. The diagonal branches of the left anterior descending artery were ligated. The refractory period (ERP) and blood flow (RMBF) were determined by an S1-S2 extrastimulus method and a nonradioactive microsphere technique, respectively. The duration of regional electrograms (DRE) was measured in the endocardial and epicardial sites. Bunazosin alone reversed the ischemia-related shortening of ERPs at both the endocardial and epicardial sites, with a greater effect seen epicardially (P < .05). Subsequent administration of propranolol further prolonged ERPs in both sites, although the effect was greater in the epicardial surface (P < .05). Bunazosin reduced RMBF to a greater degree at the endocardial site than at the epicardial site in the ischemic zone (P < .01 and P < .05, respectively), but the magnitude of the reduction in RMBF and the difference in RMBF between sites were similar to the control group (P < .01). Propranolol alone and subsequent administration of bunazosin prolonged the ERP more at the epicardial site (P < .01) than at the endocardial sites in the ischemic zone. Propranolol produced no significant difference in RMBF between both sites. DREs in animals treated with bunazosin and propranolol alone, or in combination, were similar to those in animals treated with vehicle. These results suggest that differences in ERPs between endocardium and epicardium with blockade of α1- and/or β-adrenoceptor are not due to concomitant alterations in RMBF, but to differences in electrophysiological properties of the endocardial and epicardial cells during the acute phase of myocardial ischemia.

Our objective was to investigate the effects of alpha1- or beta-adrenoceptor blockers on endocardial and epicardial refractory-period changes during myocardial ischemia in alpha-chloralose-anesthetized dogs. The first and second diagonal branches of the left anterior descending coronary artery were ligated. The refractory period was determined by an S1-S2 extrastimulus method. Dogs were treated with the alpha1-blocker bunazosin (0.1-0.2 mg/kg, i.v.; n = 16), the beta-blocker propranolol (0.2 mg/kg, i.v.; n = 15), or saline (n = 11). Dogs that developed ventricular tachycardia/fibrillation (VT/VF) during the experiment were excluded from the statistical assessment in refractory periods. In all groups, coronary ligation produced a significant shortening of the refractory period of ischemic epicardial tissue (p < 0.05) but only minimal shortening of ischemic endocardial refractory periods, resulting in an increased difference in repolarization time between the endo- and epicardial sites. Treatment with bunazosin ameliorated this ischemia-related shortening of refractory periods at both the endo- and epicardial sites, with a greater effect seen epicardially (p < 0.05), resulting in values similar to those in the nonischemic tissue. Treatment with propranolol prolonged refractory periods more in the epicardial (p < 0.01) than in endocardial sites, exacerbating the disparity in the refractory period between the endo- and epicardial sites (p < 0.05). Propranolol also prolonged the refractory period of nonischemic tissue (p < 0.05 and p < 0.01 in endo- and epicardial sites, respectively), resulting in a significant difference between the ischemic and normal myocardium at the endocardial site (p < 0.05). Results suggest that the alpha1-blocker bunazosin reduces the refractory-period disparity between the ischemic and normal myocardium without increasing the disparity between the endo- and epicardial surfaces, whereas propranolol produces a greater disparity.

イヌ急性虚血心で, I群薬disopyramide (DP) (n=14) , II群薬aropranolol (PR) (n=12) , III群薬M5-551 (MS) (n=14) , 対照 (生理的食塩水投与) (n=10) の電気生理学的性質, 血流量への影響を心内膜側と心外膜側心筋で検討した.麻酔後, 冠結紮前, 冠結紮15分後, 薬剤投与後に不応期, 局所電位幅, 血流量を測定した.冠結紮後, 自然ないし不応期測定中に心室頻拍/細動の発生した17頭は統計解析から除外した.DP群 (n=9) ; DP後, 不応期は虚血域 (I) , 正常域 (N) で延長したがI心外膜側の延長が大きかったため心内膜側 (ENDO) ―心外膜側 (EPI) 間差は拡大した (p

心室頻拍 (VT) 発生に及ぼす自律神経活動の影響を検討するために, VT発生前のホルター心電図記録の心拍変動解析により自律神経活動の変化を評価し, 病態, 時間帯による差異も検討した.全体でみると, VT発生に近づくにつれて高周波成分 (HF) の低下と低周波成分/高周波成分比 (LF/HF) の上昇の傾向が認められた.疾患別にみると, 心筋梗塞群, 肥大型心筋症群でとくにその傾向が顕著であったが, 拡張型心筋症群, 正常群では有意な変化はみられなかった.時間帯別にみると, 日中発生群は夜間発生群に較べLF/HFの上昇が顕著ではなかった.以上より, VT発生には副交感神経緊張の低下と交感神経緊張の亢進が関与していると考えられるが, これらは疾患, 時間帯などにより必ずしも一律でないことが示唆された.

To evaluate the switching from an angiotensin receptor blocker (ARB) to a drug combination containing an ARB and a diuretic drug in terms of effects on hypertension, cardiac load, and cardiac function.In a study conducted on 82 patients with a history of heart failure and hypertension who had been treated with an ARB but failed to reach the target blood pressure, ongoing oral ARB treatment was switched to a drug combination of losartan and hydrochlorothiazide (HCTZ). Using ambulatory blood pressure monitoring (ABPM), the variations in blood pressure and the effects on cardiac load and cardiac function were evaluated before and after treatment.Comparison of the ABPM findings before and after switching treatment showed significant improvements in mean systolic and diastolic blood pressure, improvements in systolic and diastolic blood pressure 1 hour before getting out of bed, and improvements in the plasma levels of human brain natriuretic peptide as an indicator of cardiac load.The drug combination of losartan and hydrochlorothiazide showed a stronger antihypertensive effect than that of the conventional ARB and improved heart function.

Risk stratification is important in the management of Brugada syndrome (BrS). Late potentials (LPs) and T-wave amplitude variability (TAV) in high-resolution ambulatory electrocardiography (ECG) were retrospectively investigated.One hundred and twenty-seven patients diagnosed with BrS on 12-lead ECG were classified into 3 groups: documented ventricular fibrillation (VF)/asystole (n=19), episodes of syncope alone (n=30), and asymptomatic (n=78). Healthy volunteers were enrolled as controls (n=25). In the BrS patients, LPs showed appreciable circadian periodicity; filtered QRS duration (fQRS) and duration of the terminal low-amplitude signal40 μV (LAS40) increased, whereas root mean square voltage of the terminal 40 ms of the fQRS (RMS40) decreased at night compared with the day. TAV did not have such a circadian periodicity. LP-positive incidence (night-time) and peak TAV were as follows: VF/asystolesyncope/asymptomaticcontrol (P0.001). VF/asystole was discriminated from control at a ratio of 81-84% by night-time LPs (fQRS116 ms, LAS4035 ms, RMS4025 μV) or peak TAV (54 μV); VF/asystole was discriminated from syncope/asymptomatic at a ratio of 60-69%, by night-time LPs (fQRS122 ms, LAS4042 ms, RMS4018μV) or peak TAV (58 μV). Combined analysis of LPs and peak TAV increased the discriminant ratio up to 93% and 77%, respectively.Analysis of both LPs and TAV (taking circadian periodicity into account) is useful in identification of high-risk BrS patients.

Multivessel disease and decreased left ventricular ejection fraction (LVEF) are believed to be significant predictors of the outcome in patients with acute inferior myocardial infarction (AIMI). We attempted to determine new electrocardiographic (ECG) markers for detecting concomitant left anterior descending (LAD) disease and/or decreased left ventricular function in patients with AIMI. Eighty patients with AIMI were evaluated within 6 h of the onset of symptoms and grouped according to the presence (Group 1) or absence (Group 2) of concomitant LAD disease. All of the patients underwent coronary angiography and left ventriculography 4-6 weeks from the onset of their infarction. We studied the validity of two new ECG markers: S-T depression deeper in lead V5 than in V4 (S-T decreases V5 > V4) and negative U waves (NUs) > 0.5 mm (50 muV) in leads V4-6. The sensitivity and specificity of S-T decreases V5 > V4, NUs in V4-6, or both, in detecting concomitant LAD disease were 56% and 83%, 59% and 87%, and 35% and 98%, respectively. LAD lesions in patients who showed either of these new markers (74% of those with S-T decreases V5 > V4 and 80% of those with NUs in V4-6) were mostly in the proximal segments (AHA segments #6 or #7). Patients with either S-T decreases V5 > V4 or NUs in V4-6 tended to have asynergy in the anterolateral segment, while there was a strong correlation between the asynergy of the anterolateral and septal segments in patients who showed both ECG markers.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetic microangiopathy causes acetylcholine-induced paradoxical vasoconstriction in arterioles (20-200 μm). Because conventional angiographic systems lack sufficient spatial resolution (100-200 μm), they are not useful for prediction of diabetic microangiopathy and for the prevention of lethal cardiovascular diseases.

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)

Upper-limb arterial anomalies are sometimes encountered during transradial coronary procedures. These anomalies may contribute to procedural failure or to vascular complications, and are a major reason why many operators tend to avoid transradial procedures. We investigated the frequency of right upperlimb arterial anomalies using antegrade arteriography in patients undergoing transbrachial coronary angiography or intervention, and discuss the potential impact of these anomalies on the transradial procedure.We prospectively studied 163 consecutive patients who underwent right transbrachial coronary angiography or intervention for the first time during the period from May 2007 to December 2007. Following the transbrachial procedure, we performed antegrade transbrachial arteriography of right upper-limb arteries in these patients and investigated the frequency and anatomy of arterial anomalies.A total of 40 upper-limb arterial anomalies were observed in 38 patients (23.3%). These included 8 abnormal origins (4.9%), 2 radio-ulnar loops (1.2%), 25 tortuosities (15.3%), 4 stenoses (2.5%) and 1 loop (0.6%). In patients with congenital lesions (8 patients; 4.9%), abnormal origin of the radial artery was the most common anomaly encountered, and in the acquired group (25 patients; 15.3%), tortuosity was the most common abnormality.Even with a 23.3% incidence of right upper-limb arterial abnormalities, 98.8% of patients were acceptable for transradial coronary intervention except for 1.2% of radio-ulnar loops.

To determine the optimal radial puncture point, we analyzed the anatomy and luminal diameter of the right radial artery (RA) by quantitative angiography.Difficulty of radial puncture has impeded the establishment of the transradial approach as the standard procedure for cardiac catheterization.Antegrade angiography was performed from the right brachial artery in 135 patients who underwent coronary angiography. Presence and location of a bifurcation in the area of the RA puncture were analyzed. Furthermore, inner luminal diameter of the RA was quantitatively measured. We used the line between the styloid process and the ulnar styloid process (R-U line) as an anatomical reference point.Radial arterial bifurcation with a superficial palmar branch was angiographically observed in 66 patients (48.9%). The inner luminal diameter was significantly larger at the proximal point to the point of bifurcation. The bifurcation level was located at a median of -3.33 mm (interquartile range: -5.60 to 4.69 mm) below the R-U line. Radial puncture at 10 mm proximal to the R-U line could avoid bifurcation in 91.9% of all cases. Mean radial, ulnar and brachial arterial inner diameters were 2.94 +/- 0.52 mm, 2.51 +/- 0.49 mm and 4.53 +/- 0.62 mm. The RA size within 10-60 mm above the R-U line was nearly invariable throughout the range. CONCLUSION The radial puncture level should be proximal to the radial bifurcation because of its lumen size. The ideal puncture point was found to be at least 10 mm proximal to the R-U line.

The aim of this study was to analyze the characteristics of peripheral arterial bends that interfere with coronary catheterization.Complex aortic and peripheral arterial bends are important factors in unsuccessful coronary catheterization. Methods.We classified peripheral arterial bends based on the difficulty of coronary catheterization: no bend, type A: easy; type B1: difficult but possible; type B2: difficult but possible with assistance of a device such as a long sheath; type C: impossible. We analyzed 1,626 consecutive cardiac catheterizations.Reproducibility (+/- 1 grade) was 98.9% in 256 patients undergoing multiple procedures from the same approach site. Peripheral arterial bend class distribution was as follows: no bend: 76.4%, type A: 12.5%, type B1: 5.0%, type B2: 5.5%, and type C: 0.6%. Fluoroscopy time and contrast volume were significantly greater in type B2/C (9.6 +/- 6.26 min versus 13.8 +/- 8.9 min, p0.0001 and 142.0 +/- 38.8 ml versus 168.4 +/- 53.6 ml, p0.0001, respectively). There were no differences in the distribution of types B and C by approach site; femoral approach, 6.4%% right upper limb approach, 6.1%; and left upper limb approach, 5.0%. Furthermore, in the patients who underwent multiple catheterizations from different approach sites, the arterial bend classes were similar. Predictors of a type B2/C arterial bend were mainly atherosclerotic risk factors, suggesting that longitudinal arterial elongation is the major cause of arterial bends.Peripheral arterial bends are a feature of the individual patient, not of the approach site.

SummaryA 72-year-old woman with a history of treatment with a single sirolimus-eluting stent (SES) for right coronary artery stenosis 21 months previously, was hospitalized to undertake invasive coronary evaluation due to recurrence of symptoms of effort angina. At the time of 9 months of angiographic follow-up, no in-stent restenosis was detected, however, several contrast filled “dimples” were noticed outside the stent border. At this time, further increments in the numbers of dimple formation were documented, in addition to progression of stenosis at the distal non-stented portion. Intravascular ultrasound demonstrated multiple cavity formations between the stent struts, due to positive remodeling occurring at the previously relatively disease-free side of the vessel wall. Surprisingly, optical coherence tomography demonstrated all the stent struts, including those located adjacent to cavities, were exclusively covered with neointima or other tissue components, completely attaching to the vessel wall throughout the stented segment. No evident thrombus formation was detected in these cavities. Despite no exposed stent struts, a hypothetical concern remains because such cul-de-sac formations may produce local blood flow turbulence within stents, which may be potentially associated with activation of local platelet aggregation. Careful long-term follow-up may be necessary for these patients.

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 ≥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.

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

雑種成犬30頭を利用し, 冠動脈結紮 (冠結紮) 2時間後の虚血心に対する心臓交感神経刺激と遮断の心室不応期, その不均一性への影響を検討した.神経刺激は心臓交感神経腹外側枝 (VLCN) を, 遮断はbunazosin, propranolol投与で行った.第一と第二鈍縁枝を結紮した.不応期はS1～S2法により, 虚血域8点, 境界域2点, 正常域2点で測定した.冠結紮前, VLCN刺激で不応期は虚血相当域のみ短縮した (p