小林 欣夫

Anaphylactic shock is the most critical iodine contrast media-mediated adverse reaction. Although nonionic iodine contrast media is widely used and is less likely to induce adverse reactions compared with ionic contrast media, patients with a history of contrast-induced allergic reactions provide a dilemma to interventional cardiologists because of the greater risk of nonionic or ionic contrast media-induced allergic reactions [1]. Most episodes of anaphylaxis develop early and resolve completely with appropriate treatment; however, approximately 10%-20% of these cases present with delayed onset of symptoms, follow a biphasic or protracted course, and create a very critical situation that requires immediate intervention [2,3]. We herein report a critical case of iodine contrast media-induced biphasic anaphylactic shock that required extracorporeal membrane oxygenation (ECMO) for hemodynamic stabilization with hemodialysis to retrieve contrast media.

Purpose: To detect stable ischemic left ventricular (LV)-segments confirmed via invasive fractional flow reserve (FFR) by quantitative longitudinal-strain (LS) determined using resting multilayer TTE. Methods: A retrospective analysis of 39 stable patients (32 males; 65.8 +/- 11.9 years) with 46 coronary arteries with >= 50% stenosis confirmed by invasive coronary angiography who underwent invasive FFR measurement and TTE (Vivid E9, GE). On TTE, regional LS (absolute values) were calculated in whole, endocardial, and epicardial layers perfused by stenotic coronary arteries. Results: Of the 46 vessels, FFR values of <0.75, >= 0.75, <= 0.80 and >0.80 were observed in 17, 29, 27 and 19 vessels, respectively. In a vessel-by-vessel analysis, the whole-layer and endocardial LS were significantly smaller in LV-segments perfused by vessels with an FFR < 0.75 than in those with an FFR >= 0.75, but epicardial LS was not. In ROC curves, the best cutoff values of whole-layer, endocardial and epicardial LS were, respectively, 14.0% (sensitivity, 94%; specificity 38%; area under the curve, 0.685), 10.0% (47%; 86%; 0.664) and 14.0% (100%; 24%; 0.640) to detect LV-segments with an FFR < 0.75; and 14.0% (82%; 37%; 0.561), 10.0% (33%; 84%; 0.573), and 14.0% (89%; 21%; 0.538) to detect LV-segments with an FFR <= 0.80. Conclusion: For stable subjects with coronary arteries with >= 50% stenosis, the regional whole-layer and endocardial LS were significantly smaller in LV-segments perfused by vessels with an FFR < 0.75 than in those with an FFR = 0.75, but epicardial LS was not; and that the whole-layer and endocardial LS had a modest diagnostic efficiency in identifying LV-segments perfused by vessels with an FFR < 0.75. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

Background/objectives: Several studies have already shown the correlation between the right ventricle (RV) hemodynamic values and either glucose uptake or fatty acid uptake in the RV, respectively. However, there are few studies to compare the RV metabolic alteration before and after treatment for pulmonary hypertension. The aims of this study are to assess right ventricular glucose and fatty acid in chronic thromboembolic pulmonary hypertension (CTEPH) patients before and after pulmonary thromboendarterectomy and to examine whether there is a correlation between right ventricular glucose and fatty acid uptake. Methods: To assess glucose and fatty acid accumulation in the RV, [F-18] fluoro-2-deoxyglucose (FDG)-positron emission tomography (PET) and I-123-beta-methyl iodophenyl pentadecanoic acid (BMIPP) imaging were performed in CTEPH patients before (FDG: n = 20, BMIPP: n = 13) and after (FDG: n = 12, BMIPP: n = 8) thromboendarterectomy. Results: Both [F-18] FDG uptake and I-123-BMIPP uptake in RV of post-PEA patients obviously decreased after this operation procedure (p < 0.01). The right ventricle [F-18] FDG uptake was also significantly correlated with I-123-BMIPP uptake (r = 0.45, p = 0.04). Conclusions: In this study, we observed that both glucose and fatty acid accumulated in the RV of patients with CTEPH. Although the exact details of the altered energy metabolism in the stressed RV remain unknown, this is the first study to evaluate both glucose and fatty acid uptake before and after thromboendarterectomy in patients with CTEPH, even though the number of the patient is limited. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

Background: Inflammatory responses, especially by CD4(+) T cells activated by dendritic cells, are known to be important in the pathophysiology of cardiac repair after myocardial infarction (MI). Although co-stimulatory signals through B7 (CD80/86) and CD28 are necessary for CD4(+) T cell activation and survival, the roles of these signals in cardiac repair after MI are still unclear. Methods and Results: C57BL/6 (Control) mice and CD28 knockout (CD28KO) mice were subjected to left coronary artery permanent ligation. The ratio of death by cardiac rupture within 5 days after MI was significantly higher in CD28KO mice compared with Control mice. Although there were no significant differences in the infarct size between the 2 groups, left ventricular end-diastolic and end-systolic diameters were significantly increased, and fractional shortening was significantly decreased in CD28KO mice compared with Control mice. Electron microscopic observation revealed that the extent of extracellular collagen fiber was significantly decreased in CD28KO mice compared with Control mice. The number of a-smooth muscle actin-positive myofibroblasts was significantly decreased, and matrix metalloproteinase-9 activity and the mRNA expression of interleukin-1 beta were significantly increased in CD28KO mice compared with Control mice. Conclusions: Deletion of CD28 co-stimulatory signals exacerbates left ventricular remodeling and increases cardiac rupture after MI through prolongation of the inflammatory period and reduction of collagen fiber in the infarct scars.

Purpose: This study evaluated the post-systolic strain index (PSI), and the time interval between aortic valve closure (AVC) and regional peak longitudinal strain (PLS), measured by transthoracic echocardiography (TTE), for detection of left ventricular (LV) myocardial ischemic segments confirmed by invasive fractional flow reserve (FFR). Materials and methods: 39 stable patients (32 males; 65.8 +/- 11.9 years) with 46 coronary arteries at >= 50% stenosis on invasive coronary angiography underwent 2D speckle tracking TTE (Vivid E9, GE Healthcare) and invasive FFR measurements. PSI, AVC and regional PLS in each LV segment were calculated. Results: FFR <= 0.80 was detected in 27 LV segments. There were no significant differences between segments supplied by FFR <= 0.80 and FFR >0.80 vessels in either PSI or the time interval between AVC and regional PLS. To identify LV segments +/- FFR <= 0.80, the receiver operator characteristic (ROC) curves for PSI, and the time interval between AVC and regional PLS had areas under the curve (AUC) values of 0.58 and 0.57, respectively, with best cut-off points of 12% (sensitivity 70.4%, specificity 57.9%) and 88 ms (sensitivity 70.4%, specificity 52.6%), respectively, but the AUCs were not statistically significant. Conclusion: In stable coronary artery disease patients with >= 50% coronary artery stenosis, measurement of PSI, and the time interval between AVC and regional PLS, on resting TTE, enabled the identification of LV segments with FFR <= 0.80 using each appropriate threshold for PSI, and the time interval between AVC and regional PLS, with reasonable diagnostic accuracy. However, the AUC values were not statistically significant. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

Background: Because it is difficult to distinguish between focal takotsubo cardiomyopathy and aborted myocardial infarction, there is little information about the prevalence and clinical features of focal takotsubo cardiomyopathy. Methods and Results: Our cardiac catheterization databases were queried to identify patients with focal takotsubo cardiomyopathy and other types of takotsubo cardiomyopathy. We defined focal takotsubo cardiomyopathy as hypo-, a-or dyskinesis in both anterolateral and septal segments without obstructive coronary artery disease explaining the wall motion abnormality. A total of 10 patients were diagnosed with focal takotsubo cardiomyopathy. The control group comprised patients with takotsubo cardiomyopathy with apical, mid-ventricular, or basal ballooning. Clinical features and in-hospital outcomes were compared between patients with focal takotsubo cardiomyopathy and those with other types of takotsubo cardiomyopathy. Among the 144 patients with takotsubo cardiomyopathy, the apical, mid-ventricular, basal, and focal types occurred in 85 (59.0%), 49 (34.0%), 0 (0%), and 10 patients (6.9%), respectively. The left ventricular ejection fraction was significantly higher in the focal group compared with the apical and mid-ventricular group (56 +/- 13 vs. 45 +/- 13 vs. 46 +/- 12%, P=0.03). In-hospital outcome was not significantly different among the 3 groups. Conclusions: Focal takotsubo cardiomyopathy is not rare. Biplane left ventriculography is useful for its diagnosis.

There has been a significant increase in the number of patients receiving cardiovascular implantable electronic devices (CIED) over the last two decades. CIED infection represents a serious complication after CIED implantation and is associated with significant morbidity and mortality. Recently, newly advanced technologies have offered attractive and suitable therapeutic alternatives. Notably, the leadless pacemaker and anti-bacterial envelope decrease the potential risk of CIED infection and the resulting mortality, when it does occur. A completely subcutaneous implantable cardioverter defibrillator is also an alternative to the transvenous implantable cardioverter defibrillator (ICD), as it does not require implantation of any transvenous or epicardial leads. Among the patients who require ICD removal and subsequent antibiotics secondary to infection, the wearable cardioverter defibrillator represents an alternative approach to inpatient monitoring for the prevention of sudden cardiac death. In this review paper, we aimed to introduce the advanced technologies and devices for prevention of CIED infection.

Although apical ballooning is the most common morphological type of takotsubo cardiomyopathy, variants have been reported. Several case reports have demonstrated focal takotsubo cardiomyopathy. Most cases had left ventricular wall motion abnormality in the anterolateral segment. We present a case of focal ventricular ballooning localized especially in the inferior mid-ventricular segment. &lt Learning objective: Focal takotsubo cardiomyopathy localized especially in the inferior mid-ventricular segment is rare. However, it is important to distinguish focal takotsubo cardiomyopathy from acute coronary syndrome because patient follow-up and medical management are different. Cardiac magnetic resonance imaging is useful to make a definitive diagnosis for focal takotsubo cardiomyopathy.&gt

Purpose: Systemic autoimmune disease (SAD) frequently affects the pericardium, and pathology is characterized by both immunological and inflammatory processes. We hypothesized that these processes simultaneously influence mitral-valve (MV) deterioration and left-ventricular (LV) wall thickening in SAD subjects. Methods: 101 SAD subjects were selected (76 female; 53 +/- 17 years; systemic-lupus-erythematosus, 26%; vasculitis, 20%; scleroderma, 14%; polymyositis/dermatomyositis complex, 10%; mixed connective tissue disease, 11% and rheumatoid-arthritis, 2%). MV anterior-mitral-leaflet (AML) length, AML thickness index, AML doming height and LV mass index (LVMI) were measured using transthoracic-echocardiography (TTE) and the presence of MV calcification, MV sub-valvular thickening and pericardial effusion (PE) were estimated. AML thickness index was calculated as the ratio of AML thickness to aortic posterior wall thickness. The correlation between LVMI and ECG V1S + V5R voltage was used to assess the etiology of LV wall thickening. Results: 19 subjects (19%) had significant PE. PE subjects had a significantly greater AML thickness index (1.55 +/- 0.48 vs. 1.14 +/- 0.32, P < 0.001), AML doming height (1.26 +/- 1.54 mm vs. 0.03 +/- 0.91 mm, P < 0.001), more frequent MV sub-valvular thickening (26% vs. 5%, P - 0.003) and greater LVMI (104.7 +/- 34.6 g/m2 vs. 80.6 +/- 21.0 g/m2, P = 0.002). Significant correlation was observed between LVMI and ECG V1S + V5R voltage in 79 subjects without PE (R = 0.39, P < 0.001). However, in 18 subjects with PE, no such correlation was observed (R = 0.30, P = 0.23). Conclusions: MV, MV sub-valvular deterioration and increased LVMI, unrelated to high voltage ECG criteria, were frequently detected in SAD subjects with PE. Immunological and inflammatory processes in SAD may not only cause pericardium inflammation, but may also cause MV deterioration and LV wall thickening. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

Clopidogrel resistance is associated with stent thrombosis. Prasugrel achieves greater platelet inhibition with less variability among patients than does clopidogrel. Thus, a patient who had stent thrombosis due to clopidogrel resistance may receive prasugrel to prevent repeated episodes of stent thrombosis. This case report describes a case of repetitive stent thrombosis in which resistance not only to clopidogrel, but also to prasugrel, was observed. Learning objective: In the face of clopidogrel resistance, prescribing prasugrel may be an acceptable treatment option. However, cross-unresponsiveness may be observed between clopidogrel and prasugrel. Thus, platelet function assay should be performed in patients with stent thrombosis, even when clopidogrel is replaced with prasugrel.

Cardiac stem cells or precursor cells regenerate cardiomyocytes; however, the mechanism underlying this effect remains unclear. We generated CreLacZ mice in which more than 99.9% of the cardiomyocytes in the left ventricular field were positive for 5-bromo-4-chloro-3-indolyl-beta-D-galactoside (X-gal) staining immediately after tamoxifen injection. Three months after myocardial infarction (MI), the MI mice had more X-gal-negative (newly generated) cells than the control mice (3.04 +/- 0.38/mm(2), MI; 0.47 +/- 0.16/mm(2), sham; p < 0.05). The cardiac side population (CSP) cell fraction contained label-retaining cells, which differentiated into X-gal-negative cardiomyocytes after MI. We injected a leukemia inhibitory factor (LIF)-expression construct at the time of MI and identified a significant functional improvement in the LIF-treated group. At 1 month after MI, in the MI border and scar area, the LIF-injected mice had 31.41 +/- 5.83 X-gal-negative cardiomyocytes/mm(2), whereas the control mice had 12.34 +/- 2.56 X-gal-negative cardiomyocytes/mm(2) (p < 0.05). Using 5-ethy-nyl-2'-deoxyurinide (EdU) administration after MI, the percentages of EdU-positive CSP cells in the LIF-treated and control mice were 29.4 +/- 2.7% and 10.6 +/- 3.7%, respectively, which suggests that LIF influenced CSP proliferation. Moreover, LIF activated the Janus kinase (JAK) signal transducer and activator of transcription (STAT), mitogen-activated protein kinase/extracellular signal-regulated (MEK) extracellular signal-regulated kinase (ERK), and phosphatidylinositol 3-kinase (PI3K)-AKT pathways in CSPs in vivo and in vitro. The enhanced green fluorescent protein (EGFP)-bone marrow-chimeric CreLacZ mouse results indicated that LIF did not stimulate cardiogenesis via circulating bone marrow-derived cells during the 4 weeks following MI. Thus, LIF stimulates, in part, stem cell-derived cardiomyocyte regeneration by activating cardiac stem or precursor cells. This approach may represent a novel therapeutic strategy for cardiogenesis.

The radial artery is increasingly used as a second arterial conduit for myocardial revascularization. However, the radial artery is susceptible to vasospasm, which is thought to be the principal cause of graft failure. The radial artery is harvested as a skeletonized or a non-skeletonized graft, but the effect of different harvesting technique remains unknown. In this study, we compared the early- and mid-term angiographic findings to elucidate its influence on the graft luminal diameter. We harvested 39 radial arteries either as a skeletonized (n = 18) or a non-skeletonized graft (n = 21) using an ultrasonic scalpel. We constructed a composite straight graft by combining a right internal thoracic artery and a radial artery. All the radial artery grafts were sequentially anastomosed to coronary arteries. We measured the diameters of the radial arteries before the operation, within 1 month and 1 year after the operation. At early postoperative period, graft diameter was significantly larger in skeletonized grafts. Graft diameter at the point before the first and the second anastomosis was similar in skeletonized grafts, although that was significantly smaller before the second anastomosis in non-skeletonized grafts. However, 1 year after the operation, the graft diameter was comparable and equally reduced after the first anastomosis in both groups. Skeletonization with an ultrasonic scalpel increases the luminal diameter of the radial artery graft at early postoperative period, which, however, reduces possibly as adaptation to graft flow 1 year after the operation.

Sodium-ion batteries are attractive energy storage media owing to the abundance of sodium, but the low capacities of available cathode materials make them impractical. Sodium-excess metal oxides Na2MO3 (M: transition metal) are appealing cathode materials that may realize large capacities through additional oxygen redox reaction. However, the general strategies for enhancing the capacity of Na2MO3 are poorly established. Here using two polymorphs of Na2RuO3, we demonstrate the critical role of honeycomb-type cation ordering in Na2MO3. Ordered Na2RuO3 with honeycomb-ordered [Na1/3Ru2/3]O-2 slabs delivers a capacity of 180 mAhg(-1) (1.3-electron reaction), whereas disordered Na2RuO3 only delivers 135 mAhg(-1) (1.0-electron reaction). We clarify that the large extra capacity of ordered Na2RuO3 is enabled by a spontaneously ordered intermediate Na1RuO3 phase with ilmenite O1 structure, which induces frontier orbital reorganization to trigger the oxygen redox reaction, unveiling a general requisite for the stable oxygen redox reaction in high-capacity Na2MO3 cathodes.

Background: Endothelial dysfunction after drug-eluting stent implantation has been demonstrated. It may be associated with adverse cardiovascular events during follow-up. Olmesartan, an angiotensin II receptor antagonist, ameliorates endothelial dysfunction. The present study evaluated the protective effect of olmesartan on endothelial function after everolimus-eluting stent (EES) implantation. Methods: A total of 40 patients who underwent EES implantation were randomly assigned to the olmesartan group (20 patients with 30 lesions) or the non-olmesartan group (20 patients with 32 lesions). Endothelial function was estimated by measuring the coronary vasoreactivity in the segments 15 mm proximal and distal to EES in response to intracoronary infusion of acetylcholine (Ach; 10(-8) and 10(-7) mol/L) at 9-month follow-up. Endothelium-independent vasomotion was assessed after an intracoronary bolus of isosorbide dinitrate. Results: In both groups, Ach infusion did not induce significant vasoconstriction in the segment either proximal or distal to the EES. The changes in coronary diameter in response to 10(-8) mol/L (-2.0 +/- 4.4% vs. -0.6 4.1%, p = 0.33) and 10(-7) mol/L. (-1.8 +/- 7.9% vs. -0.3 +/- 7.6%, p = 0.57) Ach infusion in the segment proximal to EES were not significantly different between the olmesartan group and the non-olmesartan group. There were no significant differences in vasoconstriction in response to 10(-8) mol/L (-0.8 +/- 5.8% vs. -0.9 +/- 7.0%, p = 0.96) and 10(-7) mol/L (1.8 +/- 9.7% vs. -1.8 +/- 9.7%, p = 0.16) Ach infusion in the segment distal to EES between the 2 groups. Endothelium-independent vasodilation after nitrate infusion did not differ between the 2 groups. Conclusions: Endothelial dysfunction is not observed after EES implantation. Olmesartan does not improve endothelial function after EES implantation. (C) 2015 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.

Aims: Dipeptidyl peptidase-4 (DPP-4) inhibitors are reported to have protective effects on various cells but it is unclear how DPP-4 inhibitors have cardioprotective effects. Our aim was to study the mechanisms of cardioprotective effects by DPP-4 inhibition. Methods and results: C57BL/6 mice and DPP-4 knockout (DPP-4K0) mice were subjected to left coronary artery ligation to produce acute myocardial infarction (MI). C57BL/6 mice were then treated with vehicle or DPP-4 inhibitor. Left ventricular function, infarct size, the number of vessels, and myocardial ischemia were assessed at 5 days after MI. The treatment with DPP-4 inhibitor significantly improved cardiac function and decreased the infarct size. DPP-4 inhibitor increased the ratio of endothelial cell numbers to a cardiomyocyte. The extent of myocardial ischemia and the number of TUNEL-positive cells in the border area were significantly decreased by DPP-4 inhibitor. Stromal cell-derived factor-1 alpha (SDF-1 alpha) level in myocardium was significantly increased by DPP-4 inhibitor. Those cardioprotective effects after MI were also recognized in DPP-4K0 mice. DPP-4 protein was expressed on rat neonatal cardiomyocytes and DPP-4 inhibitor significantly reduced hypoxia-induced apoptosis in the cardiomyocytes. However, this effect was abolished by the pretreatment with a CXCR4 antagonist or a signal transducer and activator of transcription 3 (STAT3) inhibitor. The beneficial effects of DPP-4 inhibitor on heart failure after MI were abolished by cardiomyocyte-specific deletion of STAT3. Conclusions: DPP-4 inhibition may have direct protective effects on the post-MI heart by inducing an antiapoptotic effect and inhibiting a decrease in vessel number through the SDF-1 alpha/CXCR4-mediated STAT3 signaling pathway. (C) 2015 Elsevier Ltd. All rights reserved.

Background: Coronary artery drug eluting stents coated with polymer which contained immunosuppressant or anticancer drug. Such drugs eluted within several months to prevent stent restenosis. Damage of polymer of first and second generation drug eluting stents during percutaneous coronary intervention (PCI) were reported previously[1,2]. However, damage of polymer of third generation drug eluting stents during PCI were unknown. … Methods and results: A man with severely calcified 90% stenosis in the left anterior descending coronary artery (LAD) underwent PCI. After predilatation with balloon catheters, a third generation platinum chromium everolimus-eluting stent which coated abluminal bioabsorbable polymer (SYNERGY, Boston Scientific) was tried to advance in the LAD. However, it failed to deliver to the target lesion due to severe cartification. The delivery failure stent was scanned by electron microscopy. Damage to the bioabsorbable polymer of the platinum chromium everolimus-eluting stent was delamination of abluminal polymer (Fig. 1) Compared to the first and second generation drug eluting stents, damege to polymer of third generation drug eluting stent may occur easily and severely when it is delivered through a calcified coronary artery.

Introduction: Nicorandil has vasodilatory effects on both the epicardial coronary arteries and the coronary microvasculature, thereby increasing coronary blood flow. Intravenous administration of nicorandil can be applicable for fractional flow reserve (FFR) measurement as a hyperaemic agent and a possible alternative to adenosine. However, the effectiveness of intravenous nicorandil infusion for FFR measurement is largely unclear. Methods and analysis: This crossover randomised study is being performed to investigate the efficacy of intravenous administration of nicorandil for FFR measurement. Patients with an intermediate coronary artery stenosis who satisfy the eligibility criteria undergo FFR measurement with a consecutive randomised order of patient-blind infusions of continuous intravenous administration of adenosine and a single bolus intravenous administration of nicorandil. The primary end point of the study is the agreement between the FFR values obtained by the intravenous nicorandil and those obtained by the intravenous adenosine. Recruitment of this trial started in November 2015 and will end in March 2017, or until a total of 50 participants have been recruited. Ethics and dissemination: The protocol was approved by the Institutional Review Board at Chiba University Hospital. Study findings will be published in peer-reviewed journals.

BACKGROUND: Pulmonary vein isolation (PVI) has become an important option for treating patients with atrial fibrillation (AF). Periesophageal nerve (PEN) injury after PVI causes pyloric spasms and gastric hypomotility. This study aimed to clarify the impact of PVI on gastric motility and assess the prevalence of gastric hypomotility after PVI. METHODS: Thirty consecutive patients with AF underwent PVI under luminal esophageal temperature (LET) monitoring. The (13)C-acetate breath test was conducted before and after the procedure for all patients (PVI group). Gastric emptying was evaluated using the time to peak concentration of (13)CO2 (T max). This test was also conducted in another 20 patients who underwent catheter ablation procedures other than PVI (control group). RESULTS: The number of patients with abnormal T max (≥75 min) increased from seven (23%) to 13 (43%) and from three (15%) to five (25%) after the procedure in the PVI group and control group, respectively. The mean T max was longer after PVI than before PVI (64±14 min vs. 57±15 min, p=0.006), whereas there was no significant difference before and after the procedure in the control group. However, no significant difference in ΔT max was observed between the two groups (p=0.27). No patients suffered from symptomatic gastric hypomotility. CONCLUSIONS: Asymptomatic gastric hypomotility occurred more often after PVI. However, the average impact of PVI on gastric motility was minimal.