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Objective Dedicated intensive-care unit (ICU) physician staffing is associated with a reduction in ICU mortality rates in general medical and surgical ICUs. However, limited data are available on the role of intensivists in ICU for cardiac disease, especially in Japan. This study investigated the association of collaborative intensivists and cardiologist care with clinical outcomes in patients with acute myocardial infarction (AMI) admitted to the ICU. Methods This study analyzed 106 patients admitted to the ICU at Nara Prefecture General Medical Center in Nara, Japan, from April 2017 to April 2019. Eligible patients were divided into either the high-intensity ICU management group (n=51) or the low-intensity ICU management group (n=55). The primary outcome of in-hospital mortality was compared in the two groups. Results The high-intensity ICU group was found to be associated with a lower mortality rate in a multivariate analysis than the low-intensity group (7.8% vs. 16.4%; odds ratio [OR]: 0.07; 95% confidence interval [CI]: 0.01-0.54; P=0.01). There were no significant differences in the length of either the ICU stay or hospital stay or the hospital costs between the two groups. A subgroup analysis revealed that the in-hospital mortality rate was lower in the high-intensity ICU group than in the low-intensity ICU group among patients with Killip class IV (16.7% vs. 34.6%; OR, 0.08; 95% CI, 0.01-0.67; P=0.02). Conclusion The presence of dedicated intensivists in high-intensity ICU collaborating with cardiologists might reduce in-hospital mortality in patients with Killip class IV AMI who require critical care.

Background: Fulminant myocarditis presentation (FMP) is a rare and severe presentation of myocarditis. The natural history of FMP and its clinical features associated with poor outcomes are incompletely understood because there is a lack of generalizable evidence. Methods: This multicenter retrospective cohort study included patients hospitalized with histologically proven myocarditis who underwent catecholamine or mechanical support from 235 cardiovascular training hospitals across Japan between April 2012 and March 2017. Clinical features and the prognostic predictors of death or heart transplantation within 90 days on the basis of clinical and pathologic findings were determined using the Kaplan-Meier method, log-rank test, and Cox regression analysis. Results: This study included 344 patients with histologically proven FMP (median age, 54 years; 40% female). The median follow-up was 600 days (interquartile range, 36 to 1599 days) and the cumulative risk of death or heart transplantation at 90 days was 29% (n=98). Results from multivariable Cox regression analysis showed that older age, nonsinus rhythm, low left ventricular wall motion ( Conclusions: The results from analyses of data from this multicenter registry demonstrated that patients with FMP are at a higher risk of death or heart transplantation in real-world settings. These observations inform which clinical and pathologic findings may be useful for prognostication in FMP. Registration: URL: https://www.umin.ac.jp/ctr ; Unique identifier: UMIN000039763.

It is important for the improvement of mechanical properties of quenching and partitioning (QP) steels to control the martensite transformation behavior and the stability of untransformed austenite. In this study, we evaluated the martensite transformation restart temperature (Mr) via a dilatometer during the reheat austempering pattern. This heat pattern corresponding to the typical heat treatment for QP steel involves quenching to TQ, a temperature between the martensite transformation start temperature (Ms) and the finish temperature, and austempering above Ms. In Fe-8Ni-0.2C alloy, Mr equals TQ, regardless of the progress of bainite transformation during austempering at 673 K (400 °C). In Fe-8Ni-1Si-0.2C alloy, Mr decreases parabolically from TQ with the progress of bainite transformation, and this behavior corresponds to the assumed carbon concentration by bainite transformation. These results indicate that the self-stabilization of the entire untransformed austenite during the first quench from Ms to TQ was preserved, regardless the bainite transformation. Moreover, the stabilization by the carbon concentration in untransformed austenite was added to this self-stabilization.

The carbon distribution behavior and crystal structure of as-quenched martensite in Fe-1Mn-C (C: 0.07 to 0.8 mass pct) steels were quantitatively investigated by atom probe tomography (APT) and X-ray diffraction with Rietveld analysis. APT revealed that the martensite steels contained quantities of carbon in solid solution far beyond its solubility in body-centered cubic (bcc)-Fe in all the alloys investigated; the carbon atoms were non-homogeneously distributed as carbides or aggregates on dislocations due to autotempering. Tetragonality was observed in the steels with interstitial solute carbon concentrations in the range of 0.1 to 0.7 mass pct, but was not evident below 0.1 mass pct. The appearance and disappearance of tetragonality in the low-carbon steels may be explained by the disordered bcc ↔ ordered body-centered tetragonal (bct) mechanism, considering the partial tetragonality due to the heterogeneity of the interstitial solute carbon distribution. The existence of tetragonality in the autotempered low-carbon steels can alternatively be understood by a mechanism based on the kinetic decrease of tetragonality during cooling, where the microscopic strain release is the rate-controlling process. The excess carbon solubility in the autotempered low- and medium-carbon martensite is due to the existence of tetragonal distortions, owing to the slow kinetics of the tetragonality decrease during cooling.

A novel coronavirus, named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), suddenly emerged in China in 2019, spread globally and caused the present COVID-19 pandemic. Therefore, to mitigate SARS-CoV-2 infection effective measures are essential. Chlorous acid (HClO2) has been shown to be an effective antimicrobial agent. However, at present there is no experimental evidence showing that HClO2 can inactivate SARS-CoV-2. Therefore, in this study, we examined the potential of HClO2 to inactivate SARS-CoV-2 in presence or absence of organic matter and the results were compared with that of sodium hypochlorite (NaClO), another potent antimicrobial agent. When concentrated SARS-CoV-2 was incubated with 10 ppm HClO2 for 10 s, viral titre was decreased by 5 log of 50% tissue culture infective dose per mL (TCID50 ml−1). However, the same concentration of NaClO could not inactivate SARS-CoV-2 as effectively as HClO2 did even after incubation for 3 min. Furthermore, 10 ppm HClO2 also inactivated more than 4.0 log of TCID50 within 10 s in the presence of 5 % fetal bovine serum used as mixed organic matters. Our results obtained with HClO2 are more effective against SARS-CoV-2 as compared to NaClO that can be used for disinfectant against SARS-CoV-2 .

Adenosine-sensitive atrial tachycardias (ATs) originating from the para-Hisian region have been reported, and their responsible mechanism is considered to be reentry. As an alternative strategy to ablation at the earliest activaton site (EAS) close to the atrioventricular node, previous reports safely eliminated these ATs at the entrance of the SCZ, indicated by a manifest entrainment-guided strategy, but no report has successfully ablated those ATs using the same strategy in the left atrium. We described a case of adenosine-sensitive AT originating from the para-Hisian region that could be eliminated at a remote site from the EAS indicated by the demonstration of manifest entrainment from the anteroseptal LA.

The steels consisting of multi-phase structure show an advantage for their high strength and good formability. The ductile to brittle transition with decreasing temperature has been investigated by Charpy impact test with sub-size specimen for the ferrite + pearlite structure steel sheet. The transition curve of the absorbed energy showed a two-step transition behavior, and the “middle shelf” appeared clearly in the curve. The cleavage-like fracture with few dimples appeared on the fracture surface of the specimens at the middle shelf, and the plastic strain was detected just below the fracture surface. This result suggested that the fracture at the middle shelf propagates with the quasi-cleavage fracture accompanied with plastic deformation. Although the traces of fracture surface corresponded to (001), (011), and (112) bcc-iron planes, the (001) cleavage plane was not dominant for the fracture propagation path at the middle shelf.

Background The appropriate number of board-certified cardiologists (BCC) for the treatment of acute myocardial infarction (AMI) has not been thoroughly examined in Japan. This study investigated whether the number of BCC/50 cardiovascular beds affects acute outcome in AMI treatment. Methods and Results: Data on 751 board-certified teaching hospitals and 63,603 patients with AMI were obtained from the Japanese Registry Of All cardiac and vascular Diseases (JROAD) and JROAD Diagnosis Procedure Combination (JROAD-DPC) databases between 1 April 2012 and 31 March 2014. The hospitals were categorized into 3 groups based on the median number of BCC/50 cardiovascular beds: first tertile, 5.0 (IQR, 4.0-5.7); second, 8.3 (IQR, 7.4-9.8); third, 15.3 (IQR, 12.5-22.7), and the patients with AMI admitted to the categorized hospitals were compared (first tertile, 12,002 patients; second, 23,930; third, 27,671). On hierarchical logistic modeling, the adjusted OR for 30-day mortality were 0.86 (95% CI: 0.74-1.00) for the second tertile and 0.75 (95% CI: 0.65-0.88) for the third tertile. Conclusions Patients with AMI admitted to hospitals with a large number of BCC/50 cardiovascular beds had a lower 30-day mortality rate. This tendency was independent of patient and hospital characteristics. This is the first study to provide new information on the association between the number of BCC and in-hospital AMI-related mortality in Japan.

The middle shelf (MS) exhibits medium absorbed energy during a two-step ductile to brittle transition and appears clearly in a ferrite + pearlite steel sheet. The analysis involved using the electron backscattered diffraction technique and indicated that the traces of fracture surface and secondary cracks at MS and lower shelf (LS) correspond to low index crystallographic planes in bcc iron. Although the {001} cleavage plane in the ferrite grain is dominant for the fracture propagation path at LS, the traces at MS correspond to {001}, {112}, and {011} planes. The potential of fracture in the {001} plane at MS (i.e., the number of traces normalized by the number of equivalent planes) exceeds that in the {112} plane. However, the difference between the same is significantly lower than that at LS. Furthermore, the{112} and {011} planes are typical slip planes in bcc iron. This suggests that the fracture at MS propagates on the {001} plane with cleavage fracture as well as on the {112} and {011} planes with a slipping-off mechanism.

The lath martensite in steel is the basic structure which brings the high strength on many types of advanced high-strength steels (AHSSs). The properties of AHSSs depend on the strengthening mechanism of martensite. However, the mechanism is not clear because of the complex substructure of lath martensite. In this study, we evaluated the effects of solute carbon content and prior austenite grain size on the yield strength of fully lath martensite structure in low and ultra-low carbon Fe-Ni alloys. Although the grain refinement increased the strength in low-carbon alloys, it did not affect in the interstitial-free alloy. The Hall–Petch coefficient increased with the carbon content increasing, and saturated gradually. This behavior was similar to that in the ferritic steel, and more carbon content was required for the saturation in the lath martensite.

Aims Excess sodium causes the development of cardiovascular diseases in conjunction with enhancing renin-angiotensin-aldosterone system (RAAS). Natriuretic peptides are sodium regulators and prevent pathological cardiac alterations by counteracting RAAS. However, it is unknown whether natriuretic peptides inhibit the sodium effect in adverse cardiac alterations. Here, we investigated whether excess salt intake could exacerbate cardiac remodeling in mice with impaired natriuretic peptide signaling. Materials and methods Mice lacking the gene encoding the natriuretic peptide receptor, guanylyl cyclase-A (GC-A), and wild-type mice were administered with either a vehicle substance or a subpressor dose of aldosterone (100 ng/kg/min), alongside low salt (0.001% NaCl), normal salt (0.6% NaCl), or high salt diets (6.0% NaCl) for four weeks. Mice were then sacrificed and the hearts were evaluated by histology and RT-PCR. Key findings Salt load did not induce cardiac changes in vehicle and aldosterone groups in wild-type mice. On the other hand, cardiac hypertrophy and interstitial fibrosis were significantly exacerbated in a salt dependent manner in GC-A knockout (KO) mice administered aldosterone, and were associated with enhanced gene expression relevant to hypertrophy, fibrosis, and oxidative stress conditions. Of note, excess salt intake increased the expression of Sgk1, serum and glucocorticoid responsive kinase-1, in aldosterone-administered GC-A KO mice. These molecular changes were not observed in wild-type mice. Significance The results of the present study demonstrate that excess salt intake induced cardiac remodeling in conjunction with aldosterone administration in GC-A KO mice, indicating that GC-A signaling attenuated the deleterious salt effect in aldosterone-induced cardiac remodeling.

Soluble fms-like tyrosine kinase-1 (sFlt-1), an endogenous inhibitor of vascular endothelial growth factor and placental growth factor, is involved in the pathogenesis of cardiovascular disease. However, the significance of sFlt-1 in heart failure has not been fully elucidated. We found that sFlt-1 is decreased in renal failure and serves as a key molecule in atherosclerosis. In this study, we aimed to investigate the role of the decreased sFlt-1 production in heart failure, using sFlt-1 knockout mice. sFlt-1 knockout mice and wild-type mice were subjected to transverse aortic constriction and evaluated after 7 days. The sFlt-1 knockout mice had significantly higher mortality (52% versus 15%; P =0.0002) attributable to heart failure and showed greater cardiac hypertrophy (heart weight to body weight ratio, 8.95±0.45 mg/g in sFlt-1 knockout mice versus 6.60±0.32 mg/g in wild-type mice; P

Objective A high proportion of uncovered stent struts is associated with late stent thrombosis after drug-eluting stent (DES) implantation, which frequently results in myocardial infarction or death. However, the predictors of uncovered stent struts remain unknown. Here, using optical coherence tomography (OCT), we studied the baseline tissue characteristics of the target coronary segment and evaluated their influence on the neointimal coverage of the strut in the chronic phase. Methods We analyzed 118 coronary lesions treated with OCT-guided DES implantation. OCT examinations of target lesions were performed before and after DES implantation, and tissue characteristics were evaluated within 5 mm outer segment of both stent edges. At follow-up, stent strut coverage was assessed within 5 mm inner segment from each stent edge. On the basis of the proportion of uncovered stent struts in the chronic phase, target segments were divided into poorly covered (the highest quartile with % uncovered struts, n=29) and well-covered (the remaining lower quartiles with % uncovered struts, n=89) groups. Results Clinical parameters were similar between the two groups. On baseline OCT images, thin-cap fibroatheroma (TCFA) and large calcification were more frequently observed in the poorly covered group than the well-covered group (10.3 vs. 0.0%, P=0.0032, and 27.6 vs. 9.0%, P=0.017, respectively). Furthermore, multivariable analysis showed TCFA and large calcification at the proximal edge, but not at the distal edge, were predictors of uncover stent struts. Conclusion TCFA and large calcification at the proximal stent edge are strong predictors of uncovered stent struts. OCT is useful for selecting stent landing sites in terms of future occurrence of uncovered stent struts.

Foodborne disease caused by campylobacters is one of the major global problems for food safety. Infection source of Campylobacter to human is mainly through contaminated meat particularly chicken. Contamination of meat with Campylobacter usually occurs during processing at slaughterhouse and to prevent such contaminations, sodium hypochlorite is commonly used. However, it is well known that bactericidal activity of sodium hypochlorite becomes weak under organic matter rich conditions. In this study, we compared the strength of bactericidal activity of chlorous acid and sodium hypochlorite against Campylobacter jejuni and Campylobacter coli strains under organic matter rich conditions. Bactericidal activity against 5 representative C. jejuni and C. coli strains in chicken juice (an organic matter rich condition) showed that minimum concentration of chlorous acid required for complete killing of C. jejuni and C. coli cells is 200–400 ppm while that of sodium hypochlorite is 2,000 to 4,000 ppm. Similar results were obtained by using Bolton broth. Furthermore, it was observed that 400 ppm of chlorous acid but not 400 ppm of sodium hypochlorite is highly effective in killing of 25 different Campylobacter strains (12 C. jejuni and 13 C. coli strains) under the same conditions. To determine whether 400 ppm of chlorous acid treatment had killed bacterial cells or induced them into viable but non-culturable (VBNC) state, live and dead cell assay using DAPI and propidium iodide fluorescent dyes was done. Such assay clearly indicated that Campylobacter cells were indeed killed and not induced to VBNC state. Moreover, SDS-PAGE analysis of whole-cell lysates of campylobacters indicated distinct effects in protein profiles of chlorous acid but not sodium hypochlorite treated cells. The results strongly suggest that chlorous acid could efficiently kill C. jejuni and C. coli cells with much lower concentration than sodium hypochlorite and the bactericidal mechanisms of chlorous acid may be due to damages of bacterial proteins. Thus, chlorous acid could be a better disinfectant in chicken slaughtering and processing to kill campylobacters and prevent contamination.

In order to contribute to weight reduction of car body, advanced high-strength sheet steels have been intensively investigated. A cold-rolled sheet steel of 1180 MPa grade with superior press formability and sheet steel for hot stamping with 1800 MPa of tensile strength have been developed typically. The microstructure control for those materials and some other practical properties, such as crashworthiness, antihydrogen embrittlement, and so on, will be discussed.

Upper bainite in steels has many common features with lath martensite in steels. But there are some studies that indicate that bainite transformation start temperature (Bs) is greater than T0 on steels containing high carbon content. We measured Bs on Fe–9 mass% Ni alloys containing 0.003–0.89 mass% C. In low carbon alloys, Bs is below T0, and the increasing of carbon content decreases Bs standing in a line that is parallel to T0. On the other hand, in high carbon alloys, carbon content does not affect Bs which stands around 753 K. The border between these two tendencies and Bs in high carbon alloys seem to correspond to the intersection point between the line of Bs on low carbon alloys and the calculated γ/(γ + θ) phase boundary.

Placental growth factor (PlGF) contributes to atherogenesis through vascular inflammation and plaque destabilization. High levels of PlGF may be associated with mortality and cardiovascular disease, but the relationship between PlGF level and adverse outcomes in patients with CKD is unclear. We conducted a prospective cohort study of 1351 consecutive participants with CKD enrolled in the Novel Assessment of Risk management for Atherosclerotic diseases in CKD (NARA-CKD) study between April 1, 2004, and December 31, 2011. During a median follow-up of 3 years, 199 participants died and 383 had cardiovascular events, defined as atherosclerotic disease or heart failure requiring hospitalization. In adjusted analyses, mortality and cardiovascular risk increased in each successive quartile of serum PlGF level; hazard ratios (HRs) (95% confidence intervals [95% CIs]) for mortality and cardiovascular risk, respectively, were 1.59 (0.83 to 3.16) and 1.55 (0.92 to 2.66) for the second quartile, 2.97 (1.67 to 5.59) and 3.39 (2.20 to 5.41) for the third quartile, and 3.87 (2.24 to 7.08) and 8.42 (5.54 to 13.3) for the fourth quartile. The composite end point of mortality and cardiovascular events occurred during the study period in 76.4% of patients in both the highest PlGF quartile (≥19.6 pg/ml) and the lowest eGFR tertile (

The antimicrobial activity of weakly acidified chlorous acid water (WACAW) against Staphylococcus aureus, non-pathogenic Escherichia coli, enterohemorrhagic E. coli (EHEC O157:H7), Candida albicans, and spore-forming Bacillus and Paenibacillus species was evaluated in vitro. The antiviral activity was also examined using feline calicivirus (FCV). Diluted WACAW (>100 ppm) effectively reduced the number of non-spore-forming bacteria (>4 log10 CFU reductions) within 5 min. Treatment with this sanitizer at 400 ppm for 30 min achieved>5 log10 CFU reductions in spore-forming Bacillus and Paenibacillus species while an equivalent concentration of sodium hypochlorite (NaClO) resulted in only a 0.98 and 2.72 log10 CFU reduction, respectively. The effect of this sanitizer against FCV was equivalent to that of NaClO. Immersion in WACAW (400 ppm) achieved >4 and 2.26 log10 CFU reductions in Campylobacter jejuni and EHEC, respectively, on artificially contaminated broiler carcass pieces. Finally, theantimicrobial activity of this sanitizer was shown to be maintained for at least 28 d when in contact with nonwoven fabric (100% cotton). This study showed that pH control of chlorous acid is expected to modify its antimicrobial activity and stability. WACAW is expected to have applications in various settings such as the food processing and healthcare industries.

BACKGROUND The renin-angiotensin system (RAS) is activated in heart failure (HF) as a compensatory mechanism, being related to cardiac remodeling and poor prognosis. Although RAS inhibitors are used as first-line drugs for HF, plasma renin activity (PRA) is upregulated by RAS inhibitors via a negative feedback mechanism. The clinical significance of PRA during RAS inhibitor therapy is poorly understood in acute decompensated HF (ADHF). Therefore we examined the impact of PRA in HF patients already receiving RAS inhibitors. METHODS AND RESULTS Of 611 consecutive patients with ADHF and emergency admission to hospital, we studied the impact of PRA on the prognosis of ADHF in 293 patients already receiving RAS inhibitors before admission. The patients were divided into 2 groups according to median PRA (≥ vs.

BACKGROUND Heart failure (HF) with preserved (HFpEF) left ventricular ejection fraction (LVEF) is a syndrome with complex pathophysiology. Little is known about changes in LVEF that occur over time in HFpEF patients. A fundamental clinical question about HFpEF is whether HFpEF is an early manifestation of HF with reduced LVEF (HFrEF). If so, which patients with HFpEF are likely to show a decline in LVEF to less than 50%? The aim of the present study was to examine longitudinal changes in LVEF in patients with HFpEF. METHODS AND RESULTS Among 279 consecutive HFpEF patients admitted as emergencies, we examined 100 who underwent echocardiography at least 1 year after discharge. EF >50% was used as the definition of HFpEF. During a mean duration from hospitalization to follow-up echocardiography of 31.5 months, 11% of patients had LVEF ≤50% (mildly reduced LVEF), known as mildly reduced (HFmrEF). The utility of LVEF during hospitalization to predict HFmrEF was assessed with receiver-operating characteristic curve analysis. A cutoff value of 55% had sensitivity of 90.9% and specificity of 97.7%. Logistic regression analysis indicated that LVEF ≤55% and ischemic etiology were strong predictors of progression from HFpEF to HFmrEF (odds ratio [OR] 435, 95% confidence interval [CI] 52.65-10,614, P

Background Urinary neutrophil gelatinase‐associated lipocalin (U‐ NGAL ) is an early predictor of acute kidney injury and adverse events in various diseases; however, in acute decompensated heart failure patients, its significance remains poorly understood. This study aimed to investigate the prognostic value of U‐ NGAL on the first day of admission for the occurrence of acute kidney injury and long‐term outcomes in acute decompensated heart failure patients. Methods and Results We studied 260 acute decompensated heart failure patients admitted to our department between 2011 and 2014 by measuring U‐ NGAL in 24‐hour urine samples collected on the first day of admission. Primary end points were all‐cause death, cardiovascular death, and heart failure admission. Patients were divided into 2 groups according to their median U‐ NGAL levels (32.5 μg/gCr). The high‐U‐ NGAL group had a significantly higher occurrence of acute kidney injury during hospitalization than the low‐U‐ NGAL group ( P =0.0012). Kaplan‐Meier analysis revealed that the high‐U‐ NGAL group exhibited a worse prognosis than the low‐U‐ NGAL group in all‐cause death (hazard ratio 2.07; 95% CI 1.38‐3.12, P =0.0004), cardiovascular death (hazard ratio 2.29; 95% CI 1.28‐4.24, P =0.0052), and heart failure admission (hazard ratio 1.77; 95% CI 1.13‐2.77, P =0.0119). The addition of U‐ NGAL to the estimated glomerular filtration rate significantly improved the predictive accuracy of all‐cause mortality ( P =0.0083). Conclusions In acute decompensated heart failure patients, an elevated U‐ NGAL level on the first day of admission was related to the development of clinical acute kidney injury and independently associated with poor prognosis.

Percutaneous coronary intervention (PCI)-related cardiac enzyme elevation is an independent risk factor for adverse clinical outcomes, but preprocedural predictors of this complication have not been established. This study evaluated the morphological characteristics of culprit lesions by frequency-domain optical coherence tomography (FD-OCT), and examined their predictive value for procedure-related myocardial injury in patients undergoing elective PCI.Sixty-eight patients treated by FD-OCT-guided elective PCI were studied. On the basis of the presence or absence of postprocedural plasma cardiac troponin T (cTnT) elevation, patients were divided into elevation (cTnT-E, n=25) and nonelevation (cTnT-nonE, n=43) groups. FD-OCT examinations of culprit lesions were performed before and after stent implantation, and tissue characteristics were evaluated within a 10-mm-long segment of each lesion.Clinical parameters were similar between the two groups. Stent length was significantly longer in the cTnT-E group than in the cTnT-nonE group. On baseline OCT images, thin-cap fibroatheroma and calcium deposition were more frequently observed within culprit segments of the cTnT-E group compared with the cTnT-nonE group (32.0 vs. 11.6%, P=0.043, and 72.0 vs. 46.5%, P=0.039, respectively). In addition, colocalization of these two findings was a powerful predictor of PCI-related cTnT elevation (odds ratio 8.40, 95% confidence interval 1.65-52.78, P0.01). Further, the predictive value of this colocalization was enhanced when the analysis included only spotty calcification (odds ratio 21.00, 95% confidence interval 2.65-454.22, P=0.003).FD-OCT examination showed that colocalization of thin-cap fibroatheroma and spotty calcification was a powerful predictor of PCI-related cTnT elevation. FD-OCT is useful for stratifying risk during PCI to avoid procedure-related complications.

In this study, three different microstructures of dual-phase (DP) steel obtained by varying the intercritical annealing temperature were observed three dimensionally by a serial-sectioning method and their metrics and topological properties were quantified. The results demonstrated that martensite in DP steels has various morphologies such as layers, particles, holes, and voids. The fraction of these characteristic morphologies was examined as a function of the intercritical annealing temperature.

Aims Ablation of right-sided accessory pathways (APs) is sometimes challenging because several anatomical features of the tricuspid annulus (TA) and surrounding structures differ from those of the mitral annulus. This study investigated the electrophysiological characteristics and efficacy of a non-contact mapping (NCM) system for catheter ablation of right-sided APs. Methods and results We examined nine APs in six consecutive patients who underwent catheter ablation of right-sided APs with NCM. In Case 6, we compared NCM with contact activation mapping. Three of six patients had two APs, and one of these had previously failed ablation. We observed atrial activation during sinus rhythm or atrial pacing using a multiple-electrode array (MEA) deployed in the right atrium near the TA. Non-contact mapping identified the AP location as a peri-TA breakout point that appeared prior to or simultaneously with the delta wave onset in all APs. In Case 6 we confirmed that the peri-TA breakout identified by NCM corresponded to the earliest ventricular activation identified by contact mapping. We successfully ablated nine APs by radiofrequency (RF) energy application to the breakout sites, while one AP located just above the pole of the MEA required additional conventionally guided mapping and ablation. The mean RF duration was 189.8 ± 119.0 s. After 33.2 ± 9.4 months of follow-up, one para-hisian AP and one right lateral AP recurred, but these were successfully ablated in a second procedure using NCM. Conclusion Non-contact mapping was able to identify the location of right-sided APs accurately and quickly.

Dual-energy computed tomography (DE-CT) uses polyenergetic X-rays at 100- and 140-kVp tube energy, and generates 120-kVp composite images that are referred to as polyenergetic images (PEIs). Moreover, DE-CT can produce monoenergetic images (MEIs) at any effective energy level. We evaluated whether the image quality of coronary angiography is improved by optimizing the energy levels of DE-CT. We retrospectively evaluated data sets obtained from 24 consecutive patients using cardiac DE-CT at 100- and 140-kVp tube energy with a dual-source scanner. Signal-to-noise ratios (SNRs) were evaluated in the left ascending coronary artery in PEIs, and in MEIs reconstructed at 40, 50, 60, 70, 80, 90, 100, 130, 160 and 190 keV. Energy levels of 100, 120 and 140 kVp generated the highest SNRs in PEIs from 10, 12 and 2 patients, respectively, at 60, 70 and 80 keV in MEIs from 2, 10 and 10 patients, respectively, and at 90 and 100 keV in those from one patient each. Optimization of the energy level for each patient increased the SNR by 16.6% in PEIs (P < 0.0001) and by 18.2% in MEIs (P < 0.05), compared with 120-kVp composite images. The image quality of coronary angiography using DE-CT can be improved by optimizing the energy level for individual patients.

Background: Clinical studies using invasive modalities have reported that statin therapy stabilizes coronary plaque vulnerability. The serial changes of lipid-rich coronary plaques (LRCPs) during rosuvastatin treatment were evaluated non-invasively in patients with acute coronary syndrome (ACS) using dual-source computed tomography (DSCT). Methods and Results: A total of 11 consecutive ACS patients, and 13 LRCPs were serially evaluated on DSCT before and 24 weeks after rosuvastatin treatment. Compared with the baseline, there was no change in post-treatment minimal lumen diameter, lumen volume, or longitudinal length of LRCPs. By contrast, the ratio of lipid core volume to plaque volume significantly decreased from 48.0±9.9% to 43.7±10.6% (P=0.04), and plaque volume decreased from 144.5±85.5mm3 to 119.8±78.0mm3 (P=0.07). The remodeling index of target LRCPs significantly decreased from 1.16±0.10 to 1.06±0.12 (P=0.02). Percent reduction of plaque volume was significantly greater in patients with a lower ratio of low-density lipoprotein to high-density lipoprotein (L/H ratio ≤1.5) at follow-up than patients with higher L/H ratio (>1.5; median -31.7% vs. -6.8%, P=0.03). Conclusions: Rosuvastatin therapy reduced the volume of lipid cores and LRCPs and increased the CT attenuation value of LRCPs. DSCT is an effective modality for the non-invasive evaluation of LRCPs in patients with ACS. (Circ J 2011; 75: 2621-2627)

Echocardiography and magnetic resonance imaging revealed biventricular non-compaction cardiomyopathy with ventricular (VSD) and atrial (ASD) septal defects in an unconscious, 23-year-old hypoxemic man. Doppler echocardiography showed a left-to-right shunt across the VSD and a right-to-left shunt across the ASD. Cardiac catheterization revealed elevated right atrial pressure, although pulmonary pressure was normal. We considered that the atrial right-to-left shunt had induced the hypoxemia, which was related mainly to right ventricular dysfunction in this biventricular non-compaction cardiomyopathy, but it was not related to pulmonary hypertension.

Lath-shaped upper bainite structures play a very important role in many high-strength steels (HSSs) and ultra high-strength steels (UHSSs). Although bainite transformation is strongly affected by the initial structure, the effect of the second phase in a multi-phase structure is yet to be clearly understood. It is significant for the advancement of UHSS to study this effect. The aim of this study is to clarify the effect of martensite, which forms before bainite, in Fe-0.2C-8Ni alloy. The bainite transformation from an austenite and martensite dual-phase structure is faster than that from single-phase austenite and the nucleation of bainitic ferrite laths are accelerated around martensite. This effect of martensite on bainite kinetics is equivalent to that of polygonal ferrite when their volume fractions are almost the same. This suggests that the boundary between martensite and austenite is a prior nucleation site of bainitic ferrite. Martensite also affects the crystallographic features of bainite. The orientations of bainitic ferrite laths tend to belong to the same block with martensite adjacent. This tendency intensifies with an increase of the transformation temperature of bainite, resulting in the formation of huge blocks consisting of bainitic ferrite and martensite laths at high temperatures (693K and 723K). In contrast, at a low temperature (643K), bainitic ferrite laths belong to same packet as martensite and have several orientations. This change of crystallographic features with transformation temperature can explain with the driving force of the nucleation of bainitic ferrite.

Background— In-stent thrombosis is mainly triggered by adenosine diphosphate (ADP)-dependent platelet aggregation after percutanous coronary stent implantation. Ectonucleoside triphosphate diphosphohydrolase (E-NTPDase) rapidly hydrolyzes ADP to adenosine monophosphate, inhibiting platelet aggregation. We tested the hypothesis that local delivery of human placental E-NTPDase (pE-NTPDase) gene into injured arteries via gene-eluting stent could prevent subacute in-stent thrombosis. Methods and Results— We generated gene-eluting stents by coating bare metal stents with cationic gelatin hydrogel containing pE-NTPDase cDNA (pE-NTPDase stent), and implanted the stents into rabbit femoral arteries (FA) prone to production of platelet-rich thrombi due to repeated balloon injury at 4-week intervals. After the second injury, E-NTPDase gene expression was severely decreased; however, the implantation of pE-NTPDase stent increased E-NTPDase mRNA levels and NTPDase activity to higher level than normal FA. The FAs with pE-NTPDase stents maintained patency in all rabbits ( P Conclusions— Human pE-NTPDase gene transfer via cationic gelatin-coated stents inhibited subacute in-stent thrombosis and suppressed neointimal hyperplasia and inflammation without antiplatelet drugs.

Background: Late stent thrombosis related to delayed neointimal growth is a major concern after drug-eluting stent (DES) implantation. The time course of neointimal growth and risk factors of uncovered stent struts after sirolimus-eluting stent (SES) was studied using optical coherence tomography (OCT). Methods and Results: The 60 patients were enrolled and classified into G1 (follow-up period 25 months, n=15). The time elapsed since SES implantation was associated with a significant increase in mean neointimal area and neointimal thickness, and also with a significant decrease in the number of uncovered stent struts (G1: 14.8%, G2: 11.7%, and G3: 4.1%, P

Background Placental growth factor (PlGF), a homolog of vascular endothelial growth factor, is reported to stimulate angiogenesis and arteriogenesis in pathological conditions. It was recently demonstrated that PlGF is rapidly produced in myocardial tissue during acute myocardial infarction (MI). However, the effects of exogenous PlGF administration on the healing process after MI are not fully understood. The purpose of the present study was to examine whether PlGF treatment has therapeutic potential in MI. Methods and results Recombinant human PlGF (rhPlGF: 10 microg) was administered continuously for 3 days in a mouse model of acute MI. rhPlGF treatment significantly improved survival rate after MI and preserved cardiac function relative to control mice. The numbers of CD31-positive cells and alpha-smooth muscle actin-positive vessels in the infarct area were significantly increased in the rhPlGF group. Endothelial progenitor cells (Flk-1(+)Sca-1(+) cells) were mobilized by rhPlGF into the peripheral circulation. Furthermore, rhPlGF promoted the recruitment of GFP-labeled bone marrow cells to the infarct area, but only a few of those migrating cells differentiated into endothelial cells. Conclusions Exogenous PlGF plays an important role in healing processes by improving cardiac function and stimulating angiogenesis following MI. It can be considered as a new therapeutic molecule.

The aim of the present study is to clarify the roles of circulating ADAMTS13 and von Willebrand factor (VWF) in the formation of coronary artery thrombi in acute myocardial infarction (AMI). Twenty-six AMI patients, 37 age-matched healthy controls, and 20 young controls were studied. Plasma ADAMTS13 activity and levels of VWF antigen (VWF: Ag) and unusually large VWF multimer (UL-VWFM) were measured in the femoral vein (FV), aortic root (Ao), and coronary sinus (Cs) immediately before percutaneous coronary intervention (PCI) during the acute phase of AMI, as well as 6 months later. During the acute phase of AMI, plasma levels of VWF: Ag were similar in FV, Ao, and Cs, and were higher than those of age-matched control. In contrast, ADAMTS13 activity in three sampling points in AMI patients was similar to that of age-matched controls. Thus, the ratio of VWF: Ag to ADAMTS13 activity in the acute phase of AMI was significantly higher in all three sampled sites than that of age-matched controls. In the chronic phase, plasma levels of VWF: Ag, ADAMTS13 activity, and the ratio of VWF: Ag to ADAMTS13 activity were similar to those of age-matched controls. UL-VWFM was detected in the acute phase of AMI but not in the chronic phase. The present study showed that the plasma VWF: Ag levels are increased and ADAMTS13 activity is relatively decreased in both systemic and coronary circulation during the acute phase of AMI, suggesting that an imbalance between the enzyme and its substrate may play a role in the formation of occlusive thrombi in a coronary artery.

Mineralocorticoid receptor (MR) blockers attenuate cardiac remodeling in experimental models of heart failure, myocardial infarction and pressure-overload, in which the renin-angiotensin-aldosterone system is activated. Mice lacking the gene encoding guanylyl cyclase-A (GC-A), a common receptor for atrial and brain natriuretic peptide (ANP and BNP, respectively), show marked cardiac hypertrophy and fibrosis, which are almost completely inhibited by both genetic and pharmacological blockade of type 1 angiotensin II receptors. However, the effect of eplerenone, a specific MR blocker, on cardiac remodeling in GC-A knockout (GC-A KO) mice remains unknown. Male 12-week-old GC-A KO mice were assigned to control, eplerenone and hydralazine groups (n=6-7/group). Treatment with eplerenone at a dose of 100 mg/kg body weight/d reduced heart weight/body weight ratios, interstitial fibrosis and blood pressure to levels similar to those seen in wild type mice, in association with reduced transcription of atrial natriuretic peptide, brain natriuretic peptide, transforming growth factor-beta1, collagen I and collagen III. Although hydralazine (5 mg/kg body weight/d) exerted a similar effect on blood pressure, it did not inhibit the cardiac remodeling in GC-A KO mice. In conclusion, eplerenone attenuates cardiac remodeling in GC-A KO mice, most likely in a blood pressure-independent manner, which suggests that signaling downstream of MR is involved in the ventricular remodeling of GC-A KO mice.

Objective To obtain a better understanding of the pharmacokinetics of atrial and brain natriuretic peptides (ANP and BNP, respectively), two peptide mediators used in the treatment of congestive heart failure (CHF). Although both peptides exert their effects by binding to a common receptor (natriuretic peptide receptor A) with about the same affinity, their respective loading and maintenance doses differ. Methods Sixteen CHF patients were randomized to be infused for 2 h with α-human ANP (0.05 μg/kg per minute) or BNP (0.01 μg/kg per minute). Plasma concentrations of both peptides were measured 0, 2, 5, 15, 30, 60 and 120 min post-infusion. The pharmacokinetic parameters were then calculated using a 1-compartment model. Results The plasma BNP concentrations in the ANP and BNP groups before infusion were 464.7 ± 339.8 and 506.8 ± 332.5 pg/ml, respectively. Following infusion, ANP disappeared from the circulation more rapidly than BNP: their plasma half-lives were 2.4 ± 0.7 and 12.1 ± 3.0 min, and their total body clearance volumes were 48.2 ± 24.1 and 10.1 ± 2.7 ml/min per kilogram, respectively. Conclusion ANP has a shorter half-life in the plasma of CHF patients than BNP, which suggests that it controls hemodynamics more readily than BNP.

Background Although sonothrombolysis has been studied for development of recanalization that is safer and more efficacious than the methods currently used, there have been no studies of the efficacy of sonothrombolysis for the platelet-rich thrombi that typically cause acute myocardial infarction (AMI). The effects of adding ultrasound (US) to pharmacological lysis of platelet-rich thrombi was examined in a rabbit model of femoral artery occlusion. Methods and Results In 35 rabbits, the right femoral artery was balloon-injured repeatedly at 4-week intervals to induce platelet-rich thrombi. Two hours after the induction of occlusive thrombi, 27,500 IU/kg tissue plasminogen activator (tPA) were injected via an ear vein, with or without transcutaneous US (continuous wave, 1 MHz, 0.75 W/cm2), or 13,750 IU/kg tPA was administered with US (n=10). Significantly higher rates of successful thrombolysis (Thrombolysis In Myocardial Infarction grade 3) were observed with US (90.0%) than without it (10.0%), irrespective of the dose of tPA used (p

To study the time dependence of the resist profiles in nanoimprint lithography, numerical simulation has been done by using conventional finite element method, where the resist is assumed as a viscous fluid body over the glass transition temperature. On the other hand, the resist shape is quenched by rapid cooling just after pressing the resist. Time dependent resist profiles are experimentally observed for various pressing times. The resist filling rate into the mold cavity is evaluated and they relatively agree with each other qualitatively. Also, the dependence of the time evolutions on the aspect ratio of the mold groove is simulated and there exist minimum aspect ratio to shorten the process time.

Introduction: Takotsubo Cardiomyopathy (TTC) is characterized by transient hypokinesis of the left ventricular (LV) apex and mid-ventricular regions, and hyperkinesis of the LV base, without significant coronary artery stenosis. The precise pathogenic mechanism of TTC remains unknown. Earlier reports assumed that catecholamine excess is involved in the pathogenesis of TTC, from the elevation of plasma catecholamine concentration or by 123I-metaiodobenzylguanidine myocardial scintigraphy. However, there have been no pathological findings that directly support this scenario in human, so far. In this study, we investigated clinical and pathological features in TTC heart including expression of G-protein receptor kinase 2 (GRK2), which is a marker for acute desensitization of β-adrenergic receptors (β-ARs), and compared with those in non-TTC heart. Methods and Results: The clinical and pathological features from 20 TTC patients (TTC group) and non-TTC patients (non-TTC group) were analyzed. In TTC patients, LV biopsy was performed at the acute phase. Non-TTC group of patients consisted of 14 patients with ventricular tachycardia or conduction disorder, who underwent LV biopsy to rule out primary myocardial diseases. Pathological data showed that the contraction band was more frequently observed in TTC than in non-TTC group (p=0.017) (Figure A), and the percentage of interstitial fibrosis area of TTC was higher than that of non-TTC group (12.1±7.7% vs 7.4±3.0%, p=0.036) (Figure B). Moreover, the percentage of GRK2 positive stained area in TTC was greater than in non-TTC group (49.0±17.8% vs 15.7±11.9%, p Conclusions: The present study demonstrates up-regulation of GRK2 for the first time in human TTC, and supports the involvement of catecholamine toxicity in the pathogenesis of TTC.

Background: Placental growth factor (PlGF), a member of the vascular endothelial growth factor (VEGF) family, has recently emerged as a predictor of survival and cardiovascular risk. Along with others, we have shown an independent association between PlGF and cardiovascular events in CKD patients, but not much is known about patients receiving dialysis. Methods: We studied 205 dialysis patients undergoing cardiac catheterization at the Nara Medical University between April 1, 2004, and December 31, 2012. Serum levels of PlGF and VEGF were measured with ELISA in all the patients. Results: During a median follow-up of 20 months, 121 participants died from any cause or experienced a cardiovascular event. In the fully adjusted analysis, having an above-median PlGF or VEGF level was associated with a hazards ratio for adverse outcomes of 2.55 (1.72-3.83) and 1.39 (0.95-2.04), respectively. Using a multimarker strategy in a model with age, serum albumin, history of coronary artery disease, brain natriuretic peptide and PlGF, patients with 2, 3 and 4 positive markers had a 3.82-, 5.77- and 6.59-fold higher risk of mortality or a cardiovascular event, respectively, compared to those with no positive markers. The model with PlGF had a significantly higher c-statistic, integrated discrimination improvement index and category-free net reclassification improvement index than the model without PlGF. Conclusion: PlGF is independently associated with mortality and cardiovascular events, but the association between VEGF and adverse events was attenuated with covariate adjustment. The addition of PlGF to models with established clinical predictors provides additional useful prognostic information in patients receiving dialysis.

Objective— Percutaneous coronary intervention (PCI) is currently the most widely accepted treatment for acute myocardial infarction (AMI). It remains unclear, however, whether post-AMI conditions might exacerbate neointimal hyperplasia and restenosis following PCI. Given that both a medial smooth muscle cell lineage and a bone marrow (BM)-derived hematopoietic stem cell lineage are now thought to contribute to neointima formation, the primary aims of the present study were to determine whether AMI augments neointimal hyperplasia at sites of arterial injury, and whether BM-derived cells contribute to that process. Methods and Results— We simultaneously generated models of AMI and arterial injury in the same mice, some of which had received BM transplantation. We found that AMI augments neointimal hyperplasia at sites of femoral artery injury by &35% ( P Conclusions— Conditions after AMI could exacerbate postangioplasty restenosis, not by increasing mobilization of BM-derived cells, but by stimulating signaling via TNF-α, TNFR1 and IL-6.

Objectives Our aim was to investigate cardiac expression of placental growth factor (PlGF) and its clinical significance in patients with acute myocardial infarction (AMI). Background Placental growth factor is known to stimulate wound healing by activating mononuclear cells and inducing angiogenesis. The clinical significance of PlGF in AMI is not yet known. Methods Fifty-five AMI patients and 43 control subjects participated in the study. Peripheral blood sampling was performed on days 1, 3, and 7 after AMI. Blood was also sampled from the coronary artery (CAos) and the coronary sinus (CS), before and after acute coronary recanalization. Cardiac expression of PlGF was analyzed in a mouse AMI model. Results In AMI patients, peripheral plasma PlGF levels on day 3 were significantly higher than in control subjects. Plasma PlGF levels just after recanalization were significantly higher in the CS than the CAos, which indicates cardiac production and release of PlGF. Peripheral plasma levels of PlGF on day 3 were negatively correlated with the acute phase left ventricular ejection fraction (LVEF), positively correlated with both acute phase peak peripheral monocyte counts and chronic phase changes in LVEF. Placental growth factor messenger ribonucleic acid expression was 26.6-fold greater in a mouse AMI model than in sham-operated mice, and PlGF was expressed mainly in endothelial cells within the infarct region. Conclusions Placental growth factor is rapidly produced in infarct myocardium, especially by endothelial cells during the acute phase of myocardial infarction. Placental growth factor might be over-expressed to compensate the acute ischemic damage, and appears to then act to improve LVEF during the chronic phase.