Background: There is conflicting evidence for the link between calcification and plaque instability. Intravascular ultrasound (IVUS) studies have shown that calcified plaques are associated with stable plaques. In contrast, recent histopathological studies have revealed that plaque calcification is present in 69% of ruptured plaques in sudden coronary death. Furthermore, studies using electron-beam computed tomography have reported that calcium score relates to acute coronary events. The purpose of this study is to investigate the relationship between patterns of calcification and arterial remodeling of culprit lesions, comparing patients with acute coronary syndromes (ACS) with those with stable angina (SAP). Methods and Results: Preinterventional intravascular ultrasound (IVUS) images of 178 patients were studied; 61 with acute myocardial infarction (AMI), 70 with unstable angina pectoris (UAP) and 47 with SAP. The presence of calcifications within an arc of less than 90° for all calcifications was significantly higher in patients with either AMI or UAP than in SAP (P<0.0001). Moreover, the average number of calcium deposits within an arc of less than 90° per patient was significantly higher in AMI than in SAP (P<0.0005) (AMI: 1.4±1.3, SAP: 0.5±0.8, mean±SD). Conversely, the length of the calcium deposits was significantly longer in SAP patients (P<0.0001) (AMI: 2.2±1.6, UAP: 1.9±1.8, SAP: 4.3±3.2, mean±SD). In AMI patients, the typical pattern was spotty calcification, associated with a fibrofatty plaque and positive remodeling. In ACS patients showing negative remodeling, no calcification was the most frequent. Conversely, in SAP patients, the frequency of extensive calcification was the highest. Conclusion: These findings show that IVUS allows the identification of vulnerable plaques in coronary arteries, not only by identifying a large lipid core and positive remodeling, but also by identifying a spotty pattern of calcification.

Introduction: The clinical benefits of remote monitoring (RM) of cardiac-implanted devices have not been fully evaluated in Japan. We investigated the clinical benefits of RM in a single center in Japan.Methods: Patients with pacemakers, implantable cardioverter-defibrillators (ICD), or cardiac resynchronization therapy with defibrillators (CRT-D) were assigned to RM and non-RM groups. The outpatient wait times and times to notification of EVENTS that we defined sustained ventricular tachyarrhythmias, worsening heart failure, and inappropriate therapy for supraventricular tachyarrhythmias in this study, were compared between the 2 groups.Results: A total of 416 patients (RM: 61; non-RM: 355) were evaluated. The outpatient wait time was 17.6+/-22.1 min for the RM group and 35.6+/-25.2 min for the non-RM group (P<0.001). Seventy-seven and 306 EVENTS were observed in 38 and 256 patients during mean follow-up periods of 360+/-22 days and 429+/-10 days in the RM and non-RM groups, respectively. The times to notification of EVENTS were 8.1+/-16.2 days for the RM group and 38.7+/-33.2 days for the non-RM group (P<0.001).Conclusions: RM significantly shortened outpatient wait times and times to notification of EVENTS. Therefore, RM was clinically beneficial in a single center in Japan. (C) 2012 Japanese Heart Rhythm Society. Published by Elsevier B.V. All rights reserved.

For ubiquitous health care systems which continuously monitor a person's vital signs such as electrocardiogram (ECG), body surface temperature and three-dimensional (3D) acceleration by wireless, it is important to accurately detect the occurrence of an abnormal event in the data and immediately inform a medical doctor of its detail. In this paper, we introduce a remote health care system, which is composed of a wireless vital sensor, multiple receivers and a triage engine installed in a desktop personal computer (PC). The middleware installed in the receiver, which was developed in C++, supports reliable data handling of vital data to the ethernet port. On the other hand, the human interface of the triage engine, which was developed in JAVA, shows graphics on his/her ECG data, 3D acceleration data, body surface temperature data and behavior status in the display of the desktop PC and sends an urgent e-mail containing the display data to a pre-registered medical doctor when it detects the occurrence of an abnormal event. In the triage engine, the lethal arrhythmia detection algorithm based on short time Fourier transform (STFT) analysis can achieve 100 % sensitivity and 99.99 % specificity, and the behavior recognition algorithm based on the combination of the nearest neighbor method and the Naive Bayes method can achieve more than 71 % classification accuracy.

We are developing a BAN (body area network) using a machine measuring human 3D acceleration and electrocardiogram communicating to a PC by wireless during 24-hours. The purpose of our study is human healthy watching to alert to himself (herself) or care staffs by network if his (her) condition is bad, and not to alert if good. Our system estimate a person's bodily movement (walking, running, standing in a house, sitting in a train or else) from his/her acceleration data, and triage the electrocardiogram according to the estimated bodily movement then classify a human health condition. We collect acceleration and bodily movement records of our staffs and voluntary people for correct estimations and correct triages.

Sensing and wireless technologies have made remarkable advance recently, so wireless vital sensors for medical use, which are light-weight but accurate, have been commercially available. However, because of the low reliability of the wireless data transmission, sensed vital data are often lost in the wireless channel and this is a fatal drawback of the devices for continuous monitoring of patients in hospitals. This paper investigates the effect of using multiple receivers (receiver diversity technique) on the improvement of data loss rate for wireless vital data gathering. Experiments with a wireless vital sensor in hospital rooms reveal that putting receivers to higher positions such as ceiling is advantageous and the use of three receivers can sufficiently improve the data loss rate as compared with the use of a single receiver.

This paper introduces the concept of an online medical diagnosis system for ubiquitous health care using a wireless ECG sensor. To confirm the feasibility ofthe system, we conducted clinical tests by 67 subjects with a wireless ECG sensor and a Holter ECG monitor simultaneously for comparison purpose. We made five types of evaluations such as analyses on data loss rate, burst data loss length, ECG waveforms comparison, normalized cross-correlation and heart rate variability (HRV) by RR50. The results show that, as long as the sensed data are successfully received at a receiver, the wireless ECG sensor has a comparable performance with the Holter ECG monitor.

Vital sensor and wireless information communication technologies play important roles in providing continuous health monitoring systems. The key elements required for the vital sensor device are its simplicity and accuracy, whereas those for the wireless communication tool are its connectivity and comfortability. For a commercially available wireless vital sensor with capability of measuring three-dimensional acceleration, electrocardiogram and body surface temperature, we conducted a clinical test for evaluating its accuracy and connectivity. The result of the clinical test revealed that the accuracy of the vital sensor was almost the same as that of the Holter monitor in term of electrocardiogram recording capability, but its wireless connectivity was much lower, that is, the average data loss rate was 0.22 for the data from all the subjects with variance of 0.025. In addition to the clinical test, we conducted an experiment on improving the wireless connectivity by receiver diversity in a patient room. The experimental result revealed that the average data loss rate, which was 0.041 for the use of a single receiver, was effectively reduced to 0.0023 only for the use of two antenna receivers.

Acute myocardial infarction (AMI) is a social burden. However, being able to predict AMI could lead to prevention. A previous study showed only the relation between the lunar phase and the occurrence of AMI, but the period it takes for the moon to orbit around the earth and the period of the lunar phase differ. This study investigated the effect of the gravitation of the moon on AMI. Data was comprised of 1369 consecutive patients with first AMI at 5 hospitals from October, 1984 to December, 1997. The universal gravitation of the moon was calculated and compared to the earth onset time of AMI. Universal gravitation of the moon was derived by G*m/d(2) (G: universal gravitation constant, m: the mass of the moon, d: the distance between the center of the moon and the center of the earth). The relationship between m/d(2) and the cases of AMI was determined. There was an increase in cases, when there is a distance of more than 399864 km from the center of the earth to the center of the moon. The gravitation of more than 399864 km was determined to be weaker gravitation. It is confirmed that the number of AMI patients significantly increases at weaker gravitation periods in this multicenter trial. In conclusion, these results suggest that the gravitation of the moon may have an influence on the occurrence of AMI.

The circulating endothelial progenitor cells (EPCs) have an important role in angiogenesis, and the smooth muscle progenitor cells (SMPCs) participate in atherosclerosis. However, little is known about the effects of treatment of diabetes mellitus (DM) on EPCs and SMPCs. Therefore, we investigated the relations between the number of circulating vasucular progenitor cells before and after the treatment for DM. Ten previously untreated DM patients were enrolled in this study. Blood samples were collected before and after treatment. The peripheral mononuclear cells were purified and cultured to differentiate them into EPCs and SMPCs. After two weeks, the number of EPCs was determined by Dil-labeled acetylated low density lipoprotein and lectin binding. The number of SMPCs was evaluated by immunocytochemical staining of α-smooth muscle actin. Before treatment, the number of EPCs and SMPCs was significantly related to hemoglobin A1c and blood sugar. Serial examination revealed that improvement of glycemic control significantly increased the number of both EPCs and SMPCs. DM reduces the number of circulating EPCs and SMPCs according to its severity, and treatment of DM significantly increases the number of EPCs and SMPCs, which may be involved in angiogenesis and atherosclerosis in diabetes.

Background According to recent intravascular ultrasound (IVUS) studies; expansive remodeling (ER) at the culprit lesion has been observed in almost 50% of patients with acute coronary syndrome and constrictive remodeling (CR) in 30%. The purpose of this study is to investigate the difference between ER and CR at the culprit lesion in patients with acute myocardial infarction (AMI).Methods and Results Preinterventional IVUS images of 73 patients with AMI were identified. The remodeling index (RI) was defined as the ratio of the external elastic membrane (EEM) areas at the culprit lesion to the EEM areas at the proximal reference site. Expansive remodeling was defined as an RI > 1.05; CR, as an RI < 0.95. In patients with AM], 40 patients (55%) showed ER on IVUS, whereas CR was observed in 18 patients (25%). Patients with ER were significantly older than those with CR (P < .005). The frequency of the presence of calcifications was higher in patients with ER than in those with CR (P < .0005). In patients with AMI with ER, soft plaque with small calcium was the most frequent (58%). Multivariate analysis revealed that age and the presence of calcifications remained as independent predictors of ER.Conclusions These findings suggest that ER relates to old age and calcification, and CR may contribute to early plaque progression than ER in patients with AMI.

Circulating bone marrow-derived vascular progenitor cells contribute to angiogenesis, atherosclerosis, and the response to vascular injury. These vascular progenitor cells consist of two cell groups, endothelial progenitor cells (EPCs) and smooth muscle progenitor cells (SMPCs). Although HMG-CoA reductase inhibitors (statins) have been reported to inhibit atherosclerosis partially by increased EPCs, the effects of statins on SMPCs are unclear. Therefore, we investigated the relationship between EPCs and SMPCs and whether pravastatin has atheroprotective effects on SMPCs. Peripheral mononuclear cells (MNCs) were isolated and cultured on fibronectin-coated dishes in SMPC medium. MNCs were stained with acetylated low density lipoprotein and lectin, or α-smooth muscle actin, and cell numbers were counted. mRNA expression and vascular endothelial growth factor (VEGF) protein synthesis of MNCs were evaluated. Pravastatin significantly increased the number of EPC and decreased the number of SMPC. mRNA expression of VEGF, endothelial nitric oxide synthase, VEGF receptor-2 (KDR), and Akt were up-regulated, and VEGF secretion was increased by pravastatin. The present study demonstrated that pravastatin has promotive effects on the differentiation from MNCs to EPC cells, while inhibitory effects to SMPC cells. Our findings suggest a previously unreported mechanism of the effect of statin therapy on vascular progenitor cells.

Background: A newly developed automated mitral annular tracking method (AMAT) has recently become available and enables us to perform automated analysis of mitral annular dynamics. Purpose: To evaluate mitral annular dynamics using AMAT. Methods: AMAT was performed using a Toshiba Aplio SSA-770 ultrasound system in 15 normal healthy volunteers (group N), 16 patients with anterior MI (group A), and 12 inferior MI (group B). The distance between an annular point at end-diastole and at end-systole (distance D) was automatically measured using AMAT at the basal portion of the anterior, lateral, posterior, inferior, and inferoseptal wall. The angle between the mitral annular plane at end-diastole and the direction of movement of each mitral annular point from end-diastole to end-systole (angle A) was also automatically measured at all five mitral annular points. The coefficients of variation (CV) of both distance D and of angle A were calculated as indices of asynchrony of mitral annular dynamics. Results: CV of distance D in group A (22 +/- 9% (P < 0.01 vs group N)) and group B (22 +/- 10% (P < 0.01 vs group N)) were both significantly larger than in group N (13 +/- 4%). CV of angle A in group A (15 +/- 10% (P < 0.05 vs group N)) and group B (15 +/- 10% (P < 0.05 vs group N)) were also significantly larger than that in group N (8 +/- 3%). Conclusion: Automated analysis using AMAT showed that mitral annular dynamics of patients with MI were less symmetrical than in normal healthy volunteers.

Erythropoietin (EPO) has been suggested to have a cardioprotective effect against ischemia. The purpose of this study was to examine the effects of EPO on cardiac remodeling after myocardial infarction (MI). MI was induced by ligation of the coronary artery in Wistar rats. The rats with MI were randomly divided into untreated MI and two EPO-treated MI groups. EPO was administered subcutaneously by injection once a day for 4 days after MI at 5000 U/kg or 3 times a week for 4 weeks at 1000 U/kg. Five days after MI, EPO prevented the increase in activated caspase 3, matrix metalloproteinase-2, and transcriptional activation of activator protein-1 in non-infarcted myocardium. Four weeks after MI, left ventricular weight, left ventricular end-diastolic pressure, and left ventricular dimension were increased, and ejection fraction and E wave deceleration time were decreased. EPO significantly attenuated this ventricular remodeling and systolic and diastolic dysfunction. In addition, EPO significantly attenuated the interstitial fibrosis and remodeling-related gene expression in non-infarcted myocardium. Furthermore, EPO significantly enhanced angiogenesis and reduced apoptotic cell death in peri-infarcted myocardium. In conclusion, when administered after MI, EPO prevents cardiac remodeling and improves ventricular function with enhanced angiogenesis and reduced apoptosis.

Long-acting Ca(2+)-channel blockers have been reported to be effective in treating ischemic heart disease. However, their effects on cardiac remodeling after myocardial infarction (MI) are still unclear. We performed this study to examine the effect of azelnidipine on left ventricular (LV) remodeling, including systolic and diastolic dysfunction, in rats with MI. MI was induced by ligation of the left anterior descending artery. The rats were then separated into 3 groups: a sham-operated group (n = 9), untreated MI group (n = 10), and azelnidipine-treated MI group (n = 10). Four weeks after MI, hemodynamic measurements and Doppler echocardiographic assessment were performed. LV weight and LV end-diastolic dimension were significantly higher in the untreated MI group than in the sham-operated group. Azelnidipine significantly prevented the increases in these parameters. Azelnidipine also improved the ejection fraction (42 +/- 3%, P<0.05) and the E wave to A wave ratio (3.2 +/- 0.5, P<0.05), compared with the untreated MI group (31 +/- 3% and 5.3 +/- 0.8, respectively). In conclusion, azelnidipine can prevent LV remodeling and improve systolic and diastolic function after MI. Administration of long-acting Ca(2+)-channel blockers after MI is an effective strategy for treating MI.

OBJECTIVES We evaluate the acute effects on hemodynamics of bi-atrial (BiA) pacing with the optimal atrioventricular (AV) delays, in comparison with high right atrial (HRA) pacing and coronary sinus (CS) pacing.BACKGROUND Bi-atrial pacing has been suggested as one of the alternative therapy for preventing the recurrence of atrial fibrillation (AF). There are, however, few reports on the hemodynamic effects of BA pacing, and the results that exist are controversial.METHODS Twenty patients were paced from HRA, left lateral site of CS, and both sites with the optimal AV delays at 80 and 100 beats/min, in random order. After 5-min pacing, maximal P-wave duration in a 12-lead electrocardiogram, cardiac output (CO), pulmonary capillary wedge pressure (PCWP), and the transmittal flow pattern by transthoracic echocardiography were measured.RESULTS Compared with HRA and CS pacing, BA pacing delivered the shortest P-wave duration (HRA: 130 +/- 14 ms, CS: 132 +/- 19 ins, and BiA: 94 +/- 8 ms, respectively, p < 0.001) and the most improvement in CO and PCWP (HRA: 3.63 +/- 0.67 l/min and 9.2 +/- 4.3 mm Hg, CS: 3.71 +/- 0.70 Umin and 8.8 +/- 3.4 mm Hg, and BA: 3.88 +/- 0.63 l/min and 8.0 +/- 3.1 mm Hg, respectively, p < 0.01). Bi-atrial pacing also significantly increased the mitral flow time velocity integral and peak A-wave velocity by transthoracic echocardiography, compared with HRA and CS pacing (HRA: 7.6 +/- 1.4 cm and 68.8 +/- 12.2 cm/s, CS: 7.8 +/- 1.4 cm and 70.5 +/- 14.5 cm/s, and BiA: 8.2 +/- 1.2 cm and 76.3 +/- 14.2 cm/s, respectively, p < 0.01). Bi-atrial pacing most significantly decreased the intervals between the atrial pacing spike and the peak of A-wave (HRA: 180 +/- 28 ms, CS: 165 +/- 21 ms, and BA: 157 +/- 19 ms, respectively, p < 0.01). These improvements in hemodynamics significantly correlated with interatrial conduction delay.CONCLUSIONS Bi-atrial pacing made the most significant improvements of hemodynamics. These benefits may be due to the improvements in interatrial conduction delay and atrial dyssynchrony. (c) 2005 by the American College of Cardiology Foundation.

Background Hypertension is one of the risk factors for coronary artery disease. However, because most coronary blood flow to the left ventricle occurs during diastole, high diastolic blood pressure during exercise may have a protective effect against exercise-induced myocardial ischemia. The aim of the present study was to test this hypothesis.Methods and Results We identified 469 patients with sinus rhythm and known or suspected coronary artery disease who underwent exercise thallium-201 myocardial single-photon emission computed tomography and coronary arteriography. High diastolic blood pressure during exercise was defined as diastolic blood pressure at peak exercise >= 90 mm Hg. There was no significant difference in medications, number of diseased vessels, or Gensini score between patients with high (n=228) and normal (n=241) diastolic blood pressure during exercise, whereas patients with high diastolic blood pressure during exercise exhibited a higher pressure-rate product during exercise than patients with normal diastolic blood pressure during exercise. The reversibility score on thallium-201 myocardial scan was significantly smaller inpatients with high diastolic blood pressure during exercise than in patients with normal diastolic blood pressure during exercise (P=.021).Conclusions High diastolic blood pressure during exercise has A potential protective effect against exercise-induced ischemia, although the mechanism of such effects remains to be determined.

Osteopontin has been reported to have an important role in cardiac fibrosis. However, little is known about the effects of angiotensin-converting enzyme inhibitor (ACEI) and angiotensin type 1 receptor blockers (ARB) on osteopontin expression in infarcted myocardium. The purpose of this study was to elucidate the effects of an ACEI (perindpril) and an ARB (candesartan cilexitil) on cardiac function as assessed by Doppler echocardiography and cardiac osteopontin expression associated with cardiac remodeling in myocardial infarcted rats. ACEI or ARB was administered after myocardial infarction (MI). At 4 weeks after MI, cardiac function, and mRNAs in non-infarcted myocardium were analyzed. ACEI and ARB equally prevented left ventricular dilatation, reduction of ejection fraction, and the increase in E/A wave velocity ratio and the rate of E wave deceleration by MI. ACEI and ARB significantly suppressed increased mRNA expression of atrial natriuretic peptide, brain natriuretic peptide, osteopontin, and collagen I and III in the non-infarcted ventricle at 4 weeks. Immunohistochemically stained osteopontin was increased in interstitial fibrosis of non-infarcted myocardium. Both ACEI and ARB significantly prevented cardiac fibrosis and osteopontin expression. In conclusion, angiotensin blockade inhibits osteopontin expression in non-infarcted myocardium and prevents cardiac remodeling after MI.