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Aims: Extracellular vesicles (EVs) are membrane-derived vesicles that mediate intercellular communications. Neutrophils produce different subtypes of EVs during inflammatory responses. Neutrophil-derived trails (NDTRs) are generated by neutrophils migrating toward inflammatory foci, whereas neutrophil-derived microvesicles (NDMVs) are thought to be generated by neutrophils that have arrived at the inflammatory foci. However, the physical and functional characteristics of neutrophil-derived EVs are incompletely understood. In this study, we aimed to investigate the differences between NDTRs and NDMVs. Methods: The generation of neutrophil-derived EVs were visualized by live-cell fluorescence images and the physical characteristics were further analyzed using nanotracking analysis assay, scanning electron microscopic analysis, and marker expressions. Functional characteristics of neutrophil-derived EVs were analyzed using assays for bactericidal activity, monocyte chemotaxis, phenotype polarization of macrophages, and miRNA sequencing. Finally, the effects of neutrophil-derived EVs on the acute and chronic inflammation were examined in vivo. Results: Both EVs share similar characteristics including stimulators, surface marker expression, bactericidal activity, and chemoattractive effect on monocytes via MCP-1. However, the integrin-mediated physical interaction was required for generation of NDTRs whereas NDMV generation was dependent on PI3K pathway. Interestingly, NDTRs contained proinflammatory miRNAs such as miR-1260, miR-1285, miR-4454, and miR-7975, while NDMVs contained anti-inflammatory miRNAs such as miR-126, miR-150, and miR-451a. Although both EVs were easily uptaken by monocytes, NDTRs enhanced proinflammatory macrophage polarization whereas NDMVs induced anti-inflammatory macrophage polarization. Moreover, NDTRs showed protective effects against lethality in a murine sepsis model and pathological changes in a murine chronic colitis model. Conclusion: These results suggest that NDTR is a proinflammatory subtype of neutrophil-derived EVs distinguished from NDMV.

Aims To investigate sex differences in the association of metabolic syndrome (MetS) and/or low-density lipoprotein cholesterol (LDL-C) with the incidence of cardiovascular and cerebrovascular disease (CCVD). Methods and results A total of 4 702 458 individuals, aged between 40 and 70, without a previous diagnosis of CCVD, underwent at least two health screenings between 2009 and 2011. Of them, 4 193 878 individuals (48.6% women) fulfilled the study requirements. The main outcome measured was the incidence of CCVD. By the end of 2017, 68 921 CCVD events occurred. Men in high LDL-C only, MetS only, and both MetS and high LDL-C groups had higher risks of CCVD. Women in MetS only and both MetS and high LDL-C groups, but not those in high LDL-C only group, had higher risks of CCVD than those in the reference group. The effect of the interaction between the presence of MetS and high LDL-C levels on the primary outcome was found among women (P for interaction 0.016) but not among men (P for interaction 0.897). A combination of MetS and LDL-C > 3.4 mmol/L increased the risk of CCVD as compared to MetS or LDL-C > 3.4 mmol/L alone in both men and women. Conclusions Metabolic syndrome confers an increased risk of CCVD irrespective of sexes; LDL-C > 3.4 mmol/L alone has a greater influence on CCVD occurrence in men than in women. Metabolic syndrome and high LDL-C beget a synergistically detrimental impact on the incidence of CCVD in both men and women. Treatment of dyslipidaemia and metabolic syndrome should be tailored according to patient characteristics.

BACKGROUND Antihypertensive therapy using renin–angiotensin system blockers and calcium channel blockers to target blood pressure variability (BPV) has not yet been established. We aimed to compare the ability of losartan and amlodipine to lower BPV and systolic blood pressure (SBP) in essential hypertensive patients. METHODS Patients were randomly assigned either losartan 50 mg or amlodipine 5 mg. Medications were uptitrated and hydrochlorothiazide was added according to protocol for 6 months. The primary endpoint was the office visit-to-visit SD of SBP. The secondary endpoints included average real variability (ARV), office SBP, and home SBP. RESULTS The losartan group (n = 71) and amlodipine group (n = 73) finished the scheduled visits between April 2013 and May 2017. The office visit-to-visit SD of SBP was comparable between the losartan and amlodipine groups (11.0 ± 4.2 vs. 10.5 ± 3.8, P = 0.468). The office visit-to-visit ARV of SBP was significantly elevated in the losartan group (10.6 ± 4.3 vs. 9.1 ± 3.4, P = 0.02). The absolute SBP decrement from baseline to 6 months was similar between groups, although the office mean SBP at 6 months was higher in the losartan group (132.3 ± 12.9 vs. 127.5 ± 9.0 mm Hg, P = 0.011). In home blood pressure analysis, evening day-to-day BPV indexes (SD and ARV) were significantly higher in the losartan group at 6 months. CONCLUSIONS The lowering effect of the office visit-to-visit SD of SBP was similar between losartan and amlodipine. However, the losartan group showed a higher office visit-to-visit ARV of SBP and evening day-to-day home BPV indexes. Therefore, amlodipine may be better to lower BPV in essential hypertensive patients.

The differentiation and activity of bone-resorbing osteoclasts are tightly regulated to maintain the homeostasis of healthy bones. In this study, the role of protein tyrosine phosphatase 1B (PTP1B) during osteoclastogenesis was studied in myeloid-specific Ptpn1-deficient (cKO) mice. The mRNA and protein expression of PTP1B increased during the formation of mature osteoclasts from mouse bone macrophages on stimulation with macrophage-colony stimulating factor (M-CSF) and receptor activator of nuclear factor kB ligand (RANKL). The Ptpn1 cKO mice exhibited increased femoral trabecular bone volume with a decreased number and activity of osteoclasts compared with control mice. The in vitro culture of osteoclast precursors corroborated the inhibition of osteoclastogenesis in cKO cells compared with control, with concomitantly decreased RANKL-dependent proliferation, lower osteoclast marker gene expression, reduced nuclear expression of nuclear factor of activated T cells cytoplasmic 1 (NFATc1), diminished intracellular Ca2+ oscillations, and increased phosphorylation of Src on inhibitory tyrosine residue. In a ligature-induced periodontitis model, Ptpn1 cKO mice exhibited attenuated osteoclastogenesis and alveolar bone loss following the induction of inflammation. The Ptpn1-deficient mice were similarly protected from ovariectomy-induced bone loss compared with control mice. These results provide a novel regulatory role of PTP1B in osteoclastogenesis and suggest a potential as a therapeutic target for bone-lytic diseases. This article is protected by copyright. All rights reserved.

Iatrogenic vascular injuries may occur during venipuncture, arterial cannulation, or catheterization procedures. Brachial arteriovenous fistula (AVF) resulting from antecubital vascular access is rare and develops slowly. We report the case of an 18-year-old man who had developed iatrogenic brachial AVF. He had a history of several venipunctures in the left arm at the age of 10 months. Doppler ultrasonography and computed tomographic angiography were used to establish a diagnosis of brachial AVF, and surgical correction of the AVF was performed. As our case indicates, delayed surgery can be considered as a treatment option and may be associated with a decreased risk of vascular complications in the management of iatrogenic brachial AVF in infants.

We aimed to evaluate the relationship between post-stent fractional flow reserve (FFR) and intravascular ultrasound (IVUS) parameters for stent optimization. IVUS and FFR measurements were performed in 101 coronary lesions after successful percutaneous coronary intervention (PCI). Quantitative IVUS parameters for stent optimization such as minimal intra-stent cross sectional area (CSA), proximal, and distal reference lumen CSA, and plaque burden (PB) at both edges of the stent related to the post-stent FFR. Mean post-stent FFR was 0.91 ± 0.06. Post-stent FFR ≤ 0.90 was observed in 46 (45.5%) lesions. The 55 lesions with post-stent FFR > 0.9 had larger proximal CSA (9.2 ± 2.9 mm2 vs. 7.4 ± 2.3 mm2, p = 0.001), distal reference lumen CSA (7.4 ± 2.7 mm2 vs. 6.3 ± 2.1 mm2, p = 0.017), minimum intra-stent lumen CSA (7.4 ± 2.5 mm2 vs. 6.1 ± 1.7 mm2, p = 0.004), and lower proximal reference PB (45 ± 8.2% vs. 50 ± 11%, p = 0.017) than did those with post-stent FFR ≤ 0.90. Post-stent FFR had an inverse correlation with age, left anterior descending artery (LAD) against non-LAD, and proximal reference PB and a positive correlation with pre-stent FFR, proximal and distal reference lumen CSA, and minimum intra-stent lumen CSA. Meanwhile, no correlation was found between post-stent FFR and stent length. Pre-stent FFR (β = 0.544), proximal reference lumen CSA (β = 0.530) and age (β = − 0.251) were found to be independently associated with the post-stent FFR. Post-procedural FFR might partly reflect the appropriateness of PCI results in terms of the adequate expansion of the stent and full lesion coverage on IVUS.

Background Elevated B-type natriuretic peptide (BNP) levels in patients hospitalized for acute myocardial infarction (AMI) are associated with heart failure and mortality. However, the role of BNP after hospital discharge is not clear. Therefore, we assessed the relationship between short-term follow-up BNP levels and clinical outcomes including all-cause mortality and major adverse cardiovascular events (MACE) in patients with AMI after hospital discharge. Methods From a prospective single-center percutaneous coronary intervention (PCI) registry, a total of 442 out of 2157 patients with AMI who had measurements for both initial and follow-up BNP levels within 2 months after discharge were retrospectively enrolled. Patients were divided into 4 groups (low-low, high-low, low-high, and high-high) according to their follow-up log-transformed BNP median values. Results The median follow-up period was 441 days (interquartile range [IQR], 362–861 days). Logistic regression analysis demonstrated that short-term follow-up BNP level was a significant predictor for all-cause mortality (odds ratio [OR], 2.265; 95% confidence interval [CI], 1.455–3.527) and MACE (OR, 1.43; 95% CI, 1.101–1.858) after adjustments for covariates. The initial BNP level did not predict both all-cause mortality and MACE. The group with high initial and high follow-up BNP levels was significantly associated with all-cause mortality (OR, 3.465; 95% CI, 1.122–10.700). Conclusions Short-term follow-up BNP level after hospital discharge was a powerful prognostic marker for all-cause mortality and MACE in patients with AMI. The combination of short-term follow-up BNP level with initial BNP level was a better predictor of all-cause mortality.

Cardiac remodeling characterized by cardiac fibrosis is a pathologic process occurring after acute myocardial infarction. Fibrosis can be ameliorated by interferon-gamma (IFN-γ), which is a soluble cytokine showing various effects such as anti-fibrosis, apoptosis, anti-proliferation, immunomodulation, and anti-viral activities. However, the role of IFN-γ in cardiac myofibroblasts is not well established. Therefore, we investigated the anti-fibrotic effects of IFN-γ in human cardiac myofibroblasts (hCMs) in vitro and whether indoleamine 2,3-dioxygenase (IDO), induced by IFN-γ and resulting in cell cycle arrest, plays an important role in regulating the biological activity of hCMs. After IFN-γ treatment, cell signaling pathways and DNA contents were analyzed to assess the biological activity of IFN-γ in hCMs. In addition, an IDO inhibitor (1-methyl tryptophan; 1-MT) was used to assess whether IDO plays a key role in regulating hCMs. IFN-γ significantly inhibited hCM proliferation, and IFN-γ-induced IDO expression caused cell cycle arrest in G0/G1 through tryptophan depletion. Moreover, IFN-γ treatment gradually suppressed the expression of α-smooth muscle actin. When IDO activity was inhibited by 1-MT, marked apoptosis was observed in hCMs through the induction of interferon regulatory factor, Fas, and Fas ligand. Our results suggest that IFN-γ plays key roles in anti-proliferative and anti-fibrotic activities in hCMs and further induces apoptosis via IDO inhibition. In conclusion, co-treatment with IFN-γ and 1-MT can ameliorate fibrosis in cardiac myofibroblasts through apoptosis.

Chronic venous insufficiency (CVI) of the lower extremities manifests itself in various clinical spectrums, ranging from asymptomatic but cosmetic problems to severe symptoms, such as venous ulcer. CVI is a relatively common medical problem but is often overlooked by healthcare providers because of an underappreciation of the magnitude and impact of the problem, as well as incomplete recognition of the various presenting manifestations of primary and secondary venous disorders. The prevalence of CVI in South Korea is expected to increase, given the possible underdiagnoses of CVI, the increase in obesity and an aging population. This article reviews the pathophysiology of CVI of the lower extremities and highlights the role of duplex ultrasound in its diagnosis and radiofrequency ablation, and iliac vein stenting in its management.

Background/Introduction Physiology-guided PCI in the ACS setting remains debatable. Purpose We aimed to determine the long-term prognostic utility of fractional flow reserve (FFR)- or resting distal coronary pressure to aortic pressure ratio (Pd/Pa)-directed percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) cases. Methods This study included 11,415 coronary stenoses in 7945 patients, including 1668 ACS cases who underwent FFR and resting Pd/Pa. The primary endpoint was the rate of a composite of cardiac death, spontaneous myocardial infarction (MI), and repeat revascularisation. Results During a median follow-up of 3.9 years (IQR: 2.0–4.9), 108 events (12 cardiac deaths, 9 MIs, and 100 revascularisations) of the primary endpoint occurred in 101 patients. In the deferred lesions with FFR >0.80 or Pd/Pa >0.91, the primary endpoint rate was higher in ACS patients than those with stable ischaemic heart disease (SIHD) (adjusted HR 1.87, 95% CI 1.37–2.55 for FFR; adjusted HR 1.78, 95% CI 1.34–2.38 for Pd/Pa). Among ACS patients with FFR ≤0.8 or Pd/Pa ≤0.91, performed revascularisation was associated with a lower rate of the primary endpoint compared to deferred PCI. (6.0% vs. 15.4%, adjusted HR 0.42, 95% CI 0.23–0.77 for FFR; 4.3% vs. 14%, adjusted HR 0.33–0.71, 95% CI 0.33–0.71 for Pd/Pa). However, performed and deferred groups had similar outcome rates in ACS patients with FFR >0.80 or Pd/Pa >0.91. Conclusion ACS patients who deferred revascularisation based on physiology had higher cardiovascular events than did those with SIHD. FFR- and resting Pd/Pa-directed decision-making for PCI is likely useful even in the ACS setting. Funding Acknowledgement Type of funding source: None

Patients with severe coronavirus disease 2019 (COVID-19) demonstrate dysregulated immune responses including exacerbated neutrophil functions. Massive neutrophil infiltrations accompanying neutrophil extracellular trap (NET) formations are also observed in patients with severe COVID-19. However, the mechanism underlying severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-induced NET formation has not yet been elucidated. Here we show that 2 viral proteins encoded by SARS-CoV-2, the nucleocapsid protein and the whole spike protein, induce NET formation from neutrophils. NET formation was ROS-independent and was completely inhibited by the spleen tyrosine kinase inhibition. The inhibition of p38 MAPK, protein kinase C, and JNK signaling pathways also inhibited viral protein-induced NET formation. Our findings demonstrate one method by which SARS-CoV-2 evades innate immunity and provide a potential target for therapeutics to treat patients with severe COVID-19.

Acute limb ischemia (ALI) as a complication of acute carbon monoxide (CO) poisoning is rare. Several reports have utilized hyperbaric oxygen therapy (HBO2) as an adjunctive therapy for peripheral arterial diseases. However, no study has yet described the use of HBO2 for ALI precipitated by CO poisoning. Herein we report successful limb salvage achieved with adjunctive HBO2 and conventional therapies in a patient with CO-induced ALI. A 69-year-old man was admitted with acute CO poisoning; ALI of both lower extremities occurred on hospitalization day 3. Pre-existing risk factors for ALI other than CO were not definite. After conventional treatments including catheter-directed thrombolysis and endovascular thrombectomy, the right-side lesion remained and a left-side lesion was newly developed. In addition to prior therapies, 47 sessions of serial HBO2 were administered as adjunctive therapy, resulting in limb salvage. Acute CO poisoning can cause ALI as a rare complication. HBO2 may be utilized as an adjunctive treatment in ALI.

Background: Cardiac fibroblasts (CFs) are principal extracellular matrix-producing cells. In response to injury, CFs transdifferentiate into myofibroblasts. Intracellular calcium (Ca 2+ ) signaling, involved in fibroblast proliferation and differentiation, is activated in fibroblasts through transient receptor potential (TRP) channels, but the function of these channels has not been investigated in human ventricular CFs. Under evaluation in this study, was the role of TRP channels in the differentiation of human ventricular CFs induced by transforming the growth factor beta (TGF- β ), a pro-fibrotic cytokine. Methods: Human ventricular CFs were used in this study. The differentiation of CFs into myofibroblast was induced with TGF- β and was identified by the expression of smooth muscle actin. Results: Results indicate that Ca 2+ signaling was an essential component of ventricular CF dif­ferentiation. CFs treated with TGF- β demonstrated increased expression of a TRP channel, TRPV4, both at the mRNA and protein levels, which corresponded with CF-myofibroblast trans-differentiation, as evidenced by the upregulation of α -smooth muscle actin, a myofibroblast marker, and plasminogen activator inhibitor-1, which are fibrogenesis markers. An agonist of TRPV4 induced the conversion of CFs into myofibroblasts, whereas it’s antagonist as well a Ca 2+ chelating agent reduced it, indicating that the Ca 2+ influx throughTRPV4 is required for CF trans-differentiation. Overall, these results dem­onstrate that TRPV4-mediated Ca 2+ influx participates in regulating the differentiation of human ventricular CFs into myofibroblasts through the MAPK/ERK pathway. Conclusions: Overall, these results demonstrate that TRPV4-mediated Ca 2+ influx participates in regulating the differentiation of human ventricular CFs into myofibroblasts through the MAPK/ERK pathway.

OBJECTIVES We aimed to investigate specific subgroups in which the benefit of transradial coronary interventions (TRIs) would be enhanced. BACKGROUND The advantage of TRIs over transfemoral coronary interventions (TFIs) might differ according to a given clinical condition, urgency of the procedure, and operator volume pattern. METHODS Using a cohort from the 2014 Korean Percutaneous Coronary Intervention Registry, in-hospital outcomes of the TRI group (n = 22,993) were matched to those of the TFI group (n = 15,581). After propensity score matching, the composite endpoints between the groups and subgroups for all-cause death, nonfatal myocardial infarctions (MIs), or transfusions were analyzed. RESULTS The composite endpoints occurred less frequently in the TRI group than the TFI group [2.1% vs. 5.5%, OR 0.63, 95% CI 0.55-0.72]. The TRI group had a lower rate of death (OR 0.44, 95% CI 0.33-0.60) and nonfatal MI (OR 0.66, 95% CI 0.54-0.81) than the TFI group. The TRI group required fewer transfusions than the TFI group (OR 0.72, 95% CI 0.59-0.88). TRI benefits were consistent across subgroups except patients with chronic kidney disease and those treated in low tertile PCI volume centers. The favorable outcome of TRI was greater in the elderly (≥75 years), patients with ST-elevation MI, those who underwent emergent PCI, and those treated in high tertile PCI volume hospitals (P for the interaction

Extracellular vesicles (EVs) are membrane-derived heterogeneous vesicles that mediate intercellular communications. They have recently been considered as ideal vehicles for drug-delivery systems, and immune cells are suggested as a potential source for drug-loaded EVs. In this study, we investigated the possibility of neutrophils as a source for drug-loaded EVs. Neutrophil-like differentiated human promyelocytic leukemia cells (dHL-60) produced massive amounts of EVs within 1 h. The dHL-60 cells are also easily loaded with various cargoes such as antibiotics (penicillin), anticancer drug (paclitaxel), chemoattractant (MCP-1), miRNA, and Cas9. The EVs derived from the dHL-60 cells showed efficient incorporation of these cargoes and significant effector functions, such as bactericidal activity, monocyte chemotaxis, and macrophage polarization. Our results suggest that neutrophils or neutrophil-like promyelocytic cells could be an attractive source for drug-delivery EVs.

Background: There is limited data comparing the Xience everolimus-eluting stent (EES) and the Resolute zotarolimus-eluting stent (ZES) with the BioMatrix biolimus-eluting stent (BES). Methods: This open-label, randomized, noninferiority trial enrolled all-comer patients to be randomly treated with either BES, EES, or ZES in a 1:1:1 ratio in 15 centers across South Korea. The primary end point was a device-oriented composite outcome consisting of cardiac death, target-vessel myocardial infarction, and clinically indicated target lesion revascularization at 24 months. The BES was compared with the EES and the ZES by intention-to-treat analyses with a noninferiority margin of 3.8%, respectively. Results: Because of slow recruitment and low event rates, this trial was prematurely terminated after enrollment of 1935 (75%) of the intended 2580 patients. Of the 1911 patients randomized to either EES (n=638), BES (n=634), or ZES (n =639), the rate of device-oriented composite outcome was 3.6%, 2.2%, and 3.9%, respectively, at 24 months (BES versus EES: absolute risk difference −1.4% [upper limit of 1-sided 95% CI: −3.2%]; P for noninferiority P for noninferiority Conclusions: The BES was noninferior to either the EES or the ZES in all-comer patients for device-oriented composite outcome at the 24-month follow-up. However, caution is advised regarding interpretation of these results due to the premature termination of this study. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01397175.

Background/aims Transradial intervention (TRI) is becoming the preferred method over transfemoral intervention (TFI) because TRI is associated with lower incidence of major bleeding and vascular complications. However, there has been limited published data regarding the clinical outcomes of TRI versus TFI in Korean patients with ST-elevation myocardial infarction (STEMI). Methods A total of 689 consecutive STEMI patients who underwent primary percutaneous coronary intervention (PCI) with drug-eluting stents (DESs) from January to December of 2009 at nine university hospitals were enrolled in this study. Mid-term angiographic and 12-month cumulative clinical outcomes of the TRI group (n = 220, 31.9%) were compared to those of the TFI group (n = 469, 28.1%). Results After propensity score matching, in-hospital complications and the 12-month major clinical outcomes during follow-up in the two groups were similar to each other. However, the incidence rates of repeat revascularization (6.4% vs. 0.5%, p = 0.003), target vessel revascularization (6.4% vs. 0.5%, p = 0.003), and major adverse cardiac events (MACE; 11.6% vs. 4.6%, p = 0.018) in the TFI group were higher than those in the TRI group during the 12-month of follow-up. Conclusions In our study, TRI in STEMI patients undergoing primary PCI with DESs was associated with lower incidence of access site hematoma, 12-month repeat revascularization, and MACE compared to TFI. Therefore, TRI might play an important role in reducing bleeding complications while improving major clinical outcomes in STEMI patients undergoing primary PCI with DESs.

Neutrophils are key effectors in the host's immune response to sepsis. Excessive stimulation or dysregulated neutrophil functions are believed to be responsible for sepsis pathogenesis. However, the mechanisms regulating functional plasticity of neutrophils during sepsis have not been fully determined.We investigated the role of autophagy in neutrophil functions during sepsis in patients with community-acquired pneumonia.Neutrophils were isolated from patients with sepsis and stimulated with phorbol 12-myristate 13-acetate (PMA). The levels of reactive oxygen species generation, neutrophil extracellular trap (NET) formation, and granule release, and the autophagic status were evaluated. The effect of neutrophil autophagy augmentation was further evaluated in a mouse model of sepsis.Neutrophils isolated from patients who survived sepsis showed an increase in autophagy induction, and were primed for NET formation in response to subsequent PMA stimulation. In contrast, neutrophils isolated from patients who did not survive sepsis showed dysregulated autophagy and a decreased response to PMA stimulation. The induction of autophagy primed healthy neutrophils for NET formation and vice versa. In a mouse model of sepsis, the augmentation of autophagy improved survival via a NET-dependent mechanism.These results indicate that neutrophil autophagy primes neutrophils for increased NET formation, which is important for proper neutrophil effector functions during sepsis. Our study provides important insights into the role of autophagy in neutrophils during sepsis.

Background and objectives This trial evaluated the safety and efficacy of the Genoss drug-eluting coronary stent. Methods This study was a prospective, multicenter, randomized trial with a 1:1 ratio of Genoss drug-eluting stent (DES)™ and Promus Element™. Inclusion criteria were the presence of stable angina, unstable angina, or silent ischemia. Angiographic inclusion criteria were de novo coronary stenotic lesion with diameter stenosis >50%, reference vessel diameter of 2.5-4.0 mm, and lesion length ≤40 mm. The primary endpoint was in-stent late lumen loss at 9-month quantitative coronary angiography follow-up. Secondary endpoints were in-segment late lumen loss, binary restenosis rate, death, myocardial infarction (MI), target lesion revascularization (TLR), target vessel revascularization (TVR), and stent thrombosis during 9 months of follow-up. Results We enrolled 38 patients for the Genoss DES™ group and 39 patients for the Promus Element™ group. In-stent late lumen loss at 9 months was not significantly different between the 2 groups (0.11±0.25 vs. 0.16±0.43 mm, p=0.567). There was no MI or stent thrombosis in either group. The rates of death (2.6% vs. 0%, p=0.494), TLR (2.6% vs. 2.6%, p=1.000), and TVR (7.9% vs. 2.6%, p=0.358) at 9 months were not significantly different. Conclusion This first-in-patient study of the Genoss DES™ stent showed excellent angiographic outcomes for in-stent late lumen loss and major adverse cardiac events over a 9-month follow-up.

Background B-type natriuretic peptide (BNP) has prognostic significance in heart failure (HF), and reductions in BNP may predict clinical improvement. However, there are limited data regarding the prognostic value of BNP during short-term follow-up. The aim of this study was to evaluate the relationship between short-term follow-up BNP and mortality after discharge in patients with HF. Methods We analyzed 427 patients hospitalized with HF from the Wonju Severance Christian Hospital Heart Failure Registry from April 2011 to December 2013, with a planned follow-up period through February 2016. Of the 427 patients, 240 (mean age, 75 years; 102 males, 42.5%) had BNP measured on admission and within the short-term follow-up period (3 months). We compared all-cause mortality during the clinical follow-up period (median length of follow-up, 709.5 days) according to the median value of BNP on admission (as a baseline value) and over a short-term follow-up period after discharge. Results Median BNP at admission was 816.5 pg/ml, and median follow-up BNP was 369.7 pg/ml. Multivariate analysis revealed a positive association between risk of death and high BNP. High BNP during follow-up was significantly associated with a greater risk of all-cause mortality compared to low BNP (P

BACKGROUND AND OBJECTIVES Chronic kidney disease (CKD) is known to be a major adverse predictor in diabetes mellitus (DM) patients undergoing percutaneous coronary intervention (PCI). It is expected that the use of newer-generation drug-eluting stents (DES) would improve clinical outcomes in these patients. We evaluated the impact of CKD on clinical outcomes in diabetic patients undergoing PCI using newer-generation DES in a real-world setting. SUBJECTS AND METHODS A total of 887 patients who underwent PCI with newer-generation DES and who had a history of DM or HbA1c >6.5% at the time of hospitalization were analyzed. These patients were divided into groups without CKD (n=549) and with CKD (n=338). Among survivors at discharge, a patient-oriented composite outcome (POCO) including all-cause mortality, myocardial infarction (MI), and revascularization was evaluated, together with a device-oriented composite outcome (DOCO) including cardiac death, target vessel-related MI, and target lesion revascularization at a follow-up period of one year. RESULTS The incidence of POCO (5.4% vs. 14.0%, log-rank p

Coronary artery perforation (CAP) during percutaneous coronary intervention is a rare but serious complication. Treatment options of CAP include prolonged balloon inflation, covered stent, and coil embolization. Although most cases of CAP can be treated with prolonged balloon inflation, some cases, especially Ellis grade III CAP require covered stents or coiling. Covered stents may require a large bore guide catheter and have a high rate of restenosis, which can be a limiting factor in patients with severe peripheral arterial disease. Coil embolization is generally used in distal CAP because coiling in the proximal vessels results in a large territory of infarction. We present a case of an Ellis grade III CAP during rotational atherectomy successfully treated with a novel coiling technique whereby the thrombogenic coil extends through the perforation outside of the vessel, and the intraarterial portion of the coil is excluded from the lumen by drug-eluting stent placement over the proximal portion of the coil.

ObjectivesThis study evaluated the relationship between guideline adherence for recommended therapy on discharge and relevant 60-day and 1-year clinical outcomes in patients with acute heart failure (HF) with reduced ejection fraction and atrial fibrillation (AF).MethodsOf 5625 acute patients with HF in the Korean Acute Heart Failure registry, 986 patients with HF and documented AF were analysed. Guideline adherence scores were calculated for the prescription of ACE inhibitors, angiotensin receptor blockers, β-blockers, mineralocorticoid receptor antagonists and anticoagulants.ResultsIn patients with HF with AF, there was a significant trend of reduced 60-day and 1-year mortality rates and the composite end point with guideline adherence. According to the Cox proportion hazard model, poor adherence was associated with a significantly higher risk of 60-day mortality (HR 4.75; 95% CI 1.77 to 12.74) and the composite end point (HR 2.36; 95% CI 1.33 to 4.18) compared with good adherence. Furthermore, poor adherence was associated with a significantly higher risk of 1-year mortality compared with moderate (HR 1.64; 95% CI 1.15 to 2.33) and good adherence (HR 2.34; 95% CI 1.39 to 3.97) and with a higher risk of the 1-year composite end point compared with good adherence (HR 1.58; 95% CI 1.07 to 2.33).ConclusionBetter adherence to guidelines was associated with better 60-day and 1-year prognoses in patients with HF with AF.

This study evaluated the 5-year clinical outcomes of the Genoss DES, the first Korean-made sirolimus-eluting coronary stent with abluminal biodegradable polymer. We previously conducted the first-in-patient prospective, multicenter, randomized trial with a 1:1 ratio of patients using the Genoss DES and Promus Element stents; the angiographic and clinical outcomes of the Genoss DES stent were comparable to those of the Promus Element stent. The primary endpoint was major adverse cardiac events (MACE), which was a composite of death, myocardial infarction (MI), and target lesion revascularization (TLR) at 5 years. We enrolled 38 patients in the Genoss DES group and 39 in the Promus Element group. Thirty-eight patients (100%) from the Genoss DES group and 38 (97.4%) from the Promus Element group were followed up at 5 years. The rates of MACE (5.3% vs 12.8%, P = .431), death (5.3% vs 10.3%, P = .675), TLR (2.6% vs 2.6%, P = 1.000), and target vessel revascularization (TVR) (7.9% vs 2.6%, P = .358) at 5 years did not differ significantly between the groups. No TLR or target vessel revascularization was reported from years 1 to 5 after the index procedure, and no MI or stent thrombosis occurred in either group during 5 years. The biodegradable polymer Genoss DES and durable polymer Promus Element stents showed comparable low rates of MACE at the 5-year clinical follow-up.

The transradial approach is increasingly used for percutaneous coronary intervention (PCI), and we therefore aimed to compare the clinical outcomes after transradial intervention (TRI) and transfemoral intervention (TFI) in all patients undergoing PCI. Among 6,973 patients enrolled in a nationwide, prospective, multicenter registry (February 2013 to September 2013), 1,860 underwent TRI (n = 1,445, 77.7%) and TFI (n = 415, 22.3%). Bleeding and major adverse cardiac events (MACE; death, myocardial infarction, revascularization, or stent thrombosis) were compared. Bleeding occurred in 42 patients (2.3%) and was significantly less likely in the TRI versus TFI group (overall cohort: 1.5% vs 4.8%, p = 0.001; propensity score-matched: n = 728, 2.7% vs 5.2%, p = 0.048). Multivariate regression revealed that TRI was negatively associated with bleeding (odds ratio 0.42, 95% CI 0.21 to 0.83, p = 0.013). MACE occurred in 152 patients (8.2%). Kaplan-Meier estimates showed higher MACE-free survival rates in the TRI versus TFI group (overall cohort: 93.3% vs 86.7%, log-rank p = 0.026; propensity score-matched: 91.8% vs 86.5%, log-rank p = 0.04). Cox proportional analysis demonstrated that TRI independently predicted improved MACE (hazard ratio 0.64, 95% CI 0.43 to 0.91, p = 0.024). In conclusion, TRI is associated with reduced bleeding rates and better clinical outcomes than TFI in all patients undergoing PCI.

Background Higher systolic blood pressure (SBP) has been reported to be associated with a better prognosis in heart failure (HF) patients. This study aimed to investigate the prognostic impact of hypertension in patients hospitalized with systolic HF. Methods Pooled analysis of data from three Korean observational studies was performed. Patients ≥18 years hospitalized with systolic HF (ejection fraction ≤45%) ( n = 3538) were compared for the incidence of 1-year all-cause mortality according to the presence of preexisting hypertension and SBP quartiles on admission. Results Patients with hypertension (prevalence, 51.6%) presented more often with diabetes (43.9% vs. 23.0%, p p p = 0.900). Conversely, patients with higher SBP on admission had a lower incidence of all-cause death (quartile 4 vs. 1: 6.7% vs. 11.3%, p for trend = 0.004). In the multivariate analysis, an increase in SBP of 10 mmHg was associated with an 8.5% risk reduction of all-cause death (hazard ratio: 0.915, 95% confidence interval: 0.853–0.981, p = 0.013). Conclusions Higher SBP on admission was independently associated with a lower risk of 1-year all-cause mortality in systolic HF.

Atypical chest pain and diabetic autonomic neuropathy attract less clinical attention, leading to underdiagnosis and delayed treatment. To evaluate the long-term clinical impact of atypical chest pain and diabetes mellitus (DM), we categorized 11,159 patients with acute myocardial infarction (AMI) from the Korea AMI-National Institutes of Health between November 2011 and December 2015 into four groups (atypical DM, atypical non-DM, typical DM, and typical non-DM). The primary endpoint was defined as patient-oriented composite endpoint (POCE) at 2 years including all-cause death, any myocardial infarction (MI), and any revascularization. Patients with atypical chest pain showed higher 2-year mortality than those with typical chest pain in both DM (29.5% vs. 11.4%, p &lt, 0.0001) and non-DM (20.4% vs. 6.3%, p &lt, 0.0001) groups. The atypical DM group had the highest risks of POCE (hazard ratio (HR) 1.76, 95% confidence interval (CI) 1.48&ndash, 2.10), all-cause death (HR 2.23, 95% CI 1.80&ndash, 2.76) and any MI (HR 2.34, 95% CI 1.51&ndash, 3.64) in the adjusted model. In conclusion, atypical chest pain was significantly associated with mortality in patients with AMI. Among four groups, the atypical DM group showed the worst clinical outcomes at 2 years. Application of rapid rule in/out AMI protocols would be beneficial to improve clinical outcomes.

Background There have been few studies to evaluate the prognostic implications of guideline-directed therapy according to the temporal course of heart failure. This study assessed the relationship between adherence to guideline-directed therapy at discharge and 60-day clinical outcomes in de novo acute heart failure (AHF) and acute decompensated chronic heart failure (ADCHF) separately. Methods Among 5,625 AHF patients who were recruited from a multicenter cohort registry of Korean Acute Heart Failure, 2,769 patients with reduced ejection fraction were analyzed. Guideline-directed therapies were defined as the use of angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor II blocker (ARB), β-blocker, and mineralocorticoid receptor antagonist. Results In de novo AHF, ACEI or ARB reduced re-hospitalization (hazard ratio [HR], 0.57; 95% confidence interval [CI], 0.34–0.95), mortality (HR, 0.41; 95% CI, 0.24–0.69) and composite endpoint (HR, 0.52; 95% CI, 0.36–0.77) rates. Beta-blockers reduced re-hospitalization (HR, 0.62; 95% CI, 0.41–0.95) and composite endpoint (HR, 0.65; 95% CI, 0.47–0.90) rates. In ADCHF, adherence to ACEI or ARB was associated with only mortality and β-blockers with composite endpoint. Conclusion The prognostic implications of adherence to guideline-directed therapy at discharge were more pronounced in de novo heart failure. We recommend that guideline-directed therapy be started as early as possible in the course of heart failure with reduced ejection fraction., Graphical Abstract

May-Thurner syndrome (MTS) refers to venous outflow obstruction caused by extrinsic compression of the left common iliac vein (LCIV) by the overlying pulsatile right common iliac artery against lumbar vertebrae. The classic clinical presentation is acute unilateral left leg painful swelling due to deep venous thrombosis in a young woman in the second or third decade of life. We present a case of a 66-year-old woman who presented with late-onset left leg swelling caused by nonthrombotic venous hypertension due to degenerative lumbar disc bulge leading to LCIV compression against the left common iliac artery which was confirmed by computed tomography and intravascular ultrasound. Our case highlights the importance of high index of suspicion for MTS in elderly patients with unilateral leg swelling and the importance of multimodality imaging for understanding the mechanism and appropriate treatment of MTS.

Vascular closing devices (VCDs) are widely used to replace manual compression at the femoral puncture site and to reduce the discomfort of patients undergoing percutaneous coronary procedure by shortening bed rest. Among the vascular complications related to these devices, the femoral artery stenosis or occlusion is rarely reported, and its standard management is not well established. We report a case of symptomatic femoral artery stenosis caused by suture-mediated VCD and managed using rotational atherectomy device and balloon angioplasty. In addition, we propose the possible mechanisms for this complication.

Purpose Liver cirrhosis has been implicated in poor outcome after heart transplant. However, no distinct correlation has been known between pre-existing ascites and outcomes after heart transplantation. Methods From 1994 to 2018, 170 patients with advanced heart failure underwent heart transplantation. Abdominal sonography or CT was performed to assess ascites in 163 patients preoperatively. Among them, 49 patients (30.0%) had visualized ascites and enrolled in this study. We divided them into two groups [group A; mild ascites (n=35), B; moderate to massive ascites (n=14)] and compared the clinical outcomes. Results In this cohort (19 men and 30 women, mean age 41, range 12-68 years), the causes of heart failure were dilated cardiomyopathy (DCMP) in 29 patients (59.2%), ischemic CMP in 7 patients (14.3%), valvular disease in 7 patients (14.3%) and congenital heart disease in 6 patients (12.4%). There was no difference in baseline characteristics between groups, except preoperative ascites points (group A: 1.20±0.19 vs. group B: 2.29 ± 0.46; p=0.001). Calculating scoring systems related to liver disease, MELD score was 11.73 vs. 12.4 (p=0.517), MELD-XI score was 12.9 vs. 13.7 (p=0.205) and Child-pugh score was 6.2 vs. 7.3 (p=0.843). The mean duration of follow up was 38.8 ± 42.5 months. After transplantation, ascites points were significant improved in group B (2.29 ± 0.46 to 1.74 ± 0.81, p=0.003). The 1, 2, 5 and 10-year survival rates were 82.8% vs 74.3%, 78.4% vs 74.3%, 74.6% vs 74.3% and 74.6% vs 74.3%, respectively, and the survival rates was significant lower until 2 years in group B than A (p=0.035). However, there was no difference after 2 years (p=0.793). Cox-regression analysis showed a moderate to massive ascites was associated with an increased risk of all-cause death after transplantation (p Conclusion Liver cirrhosis with moderate to severe ascites affected worse overall survival until 2 years after heart transplantation.

Background and objectives Chronic impairment of β-adrenergic receptor signaling increases cardiac apoptosis, hypertrophy and fibrosis. The aim of this study was to investigate whether isoproterenol (ISO), an agonist of the adrenergic receptor, can enhance tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in human embryonic kidney (HEK) 293 cells. Materials and methods HEK 293 cells were treated with ISO and/or TRAIL for 24 hours. Cell viability was evaluated by microscopy and an established viability assay, and apoptotic cell death was analyzed by staining with fluorescein isothiocynate-annexin-V/propidium iodide (PI) and caspase activation. To confirm the mechanism of cell death induced by co-treatment with ISO and TRAIL, expression of TRAIL receptor 2 (death receptor 5, DR5) was evaluated by immunoblotting. Results Although ISO or TRAIL treatment decreased HEK 293 cell viability by 13% and 17%, respectively, co-treatment with ISO and TRAIL resulted in a markedly higher death rate of 35% after 24 hours. Increases were evident in early apoptotic cells (i.e., annexin-V positive/PI negative; 19.4%), late apoptotic cells (i.e., annexin-V positive/PI positive; 6.3%) and dead cells (i.e., annexin-V negative/PI positive; 1.1%) when cells were co-treated with ISO and TRAIL, compared to cells treated with either ISO or TRAIL. In addition, marked increases of cleaved cas-3, cleaved poly (adenosine diphosphate-ribose) polymerase and DR5 were observed in HEK 293 cells co-treated with ISO and TRAIL. Conclusion Treatments combining ISO with TRAIL may be responsible for death of HEK 293 cells through DR5 up-regulation. Activation of adrenergic receptors is responsible for the synergistic cell death observed with TRAIL.

To evaluate the pharmacodynamic efficacy of de-escalating P2Y12 inhibition from prasugrel to clopidogrel based on cytochrome P450 (CYP) 2C19 genotyping, we genotyped 50 Korean patients with AMI who underwent percutaneous coronary intervention (PCI) for CYP2C19 *2,*3, or *17 using real-time PCR. They were discharged on prasugrel 10 mg daily. A control group of 48 AMI patients who underwent PCI and were discharged on clopidogrel but did not undergo genotyping was identified retrospectively. Based on genotyping results available at 3 weeks, 12 patients found to have 2 copies of either CYP2C19 *2 or *3 loss of function alleles continued prasugrel while the remaining 38 patients switched to clopidogrel 75 mg daily. The rate of patients within the therapeutic window (TW) of on-treatment platelet reactivity (OPR), 85

Background/Aims: Newer P2Y 12 inhibitors, such as prasugrel and ticagrelor, have greater antiplatelet efficacy but may increase the risk of bleeding. In this study, we compared the pharmacodynamic efficacy of prasugrel and ticagrelor in East Asian patients with acute coronary syndrome (ACS). Methods: We selected 83 ACS patients undergoing percutaneous coronary intervention who were discharged with 90 mg ticagrelor twice daily (n = 24), 10 mg prasugrel daily (n = 39) or 5 mg prasugrel daily (n = 20). After 2 to 4 weeks, on-treatment platelet reactivity (OPR) was assessed in terms of P2Y 12 reaction units (PRUs) using the VerifyNow P2Y 12 assay (Accumetrics). We compared East Asian (85 < PRU ≤ 275) and Caucasian (85 < PRU ≤ 208) criteria for assessing the therapeutic window of OPR. Results: OPR was lowest in the ticagrelor group, followed by the 10 mg prasugrel and 5 mg prasugrel groups (49.1 ± 29.9 vs. 83.7 ± 57.1 vs. 168.5 ± 60.8, respectively; p < 0.001). The 5 mg prasugrel group had the highest proportion of patients with OPR values within the therapeutic window, followed by the 10 mg prasugrel and ticagrelor groups (90.0% vs. 46.2% vs. 12.5%, respectively; p < 0.001 for East Asian criteria; 60.0% vs. 43.6% vs. 12.5%, respectively; p < 0.001 for Caucasian criteria). Conclusions: Short-term administration of 5 mg prasugrel facilitated maintenance within the therapeutic window of OPR compared with the 10 mg prasugrel and ticagrelor groups. Thus, 5 mg prasugrel daily may be the optimal antiplatelet regimen for stabilized East Asian ACS patients.

Background and objectives Recently, Genoss drug-eluting stent (DES)™ stent comprising cobalt-chromium platform with an ultrathin strut thickness, sirolimus, and an abluminal biodegradable polymer was developed. Owing to the lack of substantial evidence for the safety and efficacy of this stent, we report 12-month results of the Genoss DES™ stent. Methods We analyzed subjects who were eligible for a 12-month follow-up from the ongoing Genoss DES™ registry, which is a prospective, single-arm, observational, multicenter trial to investigate the clinical outcomes after the successful Genoss DES™ stent implantation among all-comers. The primary endpoint was a device-oriented composite outcome, defined as cardiac death, target vessel-related myocardial infarction, and target lesion revascularization at 12-month follow-up. Results Among 622 subjects, the mean age of subjects was 66.5±10.4 years, 70.6% were males, 67.5% had hypertension, and 38.3% had diabetes. The implanted stent number, diameter, and length per patient were 1.5±0.8, 3.1±0.4 mm, and 36.0±23.3 mm, respectively. At 12-month clinical follow-up, the primary endpoint occurred only in 4 (0.6%) subjects. Conclusions The novel Genoss DES™ stent exhibited excellent safety and efficacy in real-world practice.

Objectives We investigated and compared the clinical outcomes between biodegradable polymer biolimus-eluting stents (BES) and durable polymer everolimus-eluting stents (EES) in a single-center prospective registry. Background There is limited data regarding the safety and efficacy of the biodegradable BES compared to second-generation drug-eluting stents. Methods From January 2010 to April 2012, a total of 1,279 patients were treated with BES (n = 647) or EES (n = 632) in a single center. We included 1,231 patients (BES = 625, EES = 606) after excluding 48 patients (BES = 22, EES = 26) with acute myocardial infarction accompanied by cardiogenic shock. The 1-year incidences of target lesion failure (TLF), patient-oriented composite outcomes (POCO), and stent thrombosis (ST) after the index procedure were compared in propensity score-matched analyses. Results Propensity score matching yielded 406 well-balanced pairs (EES = 406, BES-B = 406). In the propensity-matched population, the 1-year incidence of TLF (BES = 3.0% vs. EES = 2.5%, P = 0.666) and POCO (BES = 5.4% vs. EES = 6.4%, P = 0.552) were similar between the 2 groups. In addition, the incidence of definite or probable ST was also similar (BES = 0.74% vs. EES = 0.74%, P = 1.000). In subgroup analysis, the number of patients who reached the primary end-point did not differ significantly between the 2 groups. Conclusion In a single-center registry with unrestricted use of EES and BES-B, these stents showed comparable efficacy and safety in terms of TLF, POCO, and ST at 1-year follow-up. (J Interven Cardiol 2014;27:399–407)

Patient initials or identifier number SSC ### Relevant clinical history and physical exam A 51-year-old male patient without cardiovascular risk factor except smoking was referred from dept. of vascular surgery due to intermittent claudication of Rt. leg after surgical embolectomy of Rt.

Background The second-generation drug-eluting stents (DES) have shown superiority in many studies relating to safety and efficacy when compared with the first-generation DES. However, it is unclear whether there are differences in efficacy and safety among the second-generation DES after long-term follow-up. Methods This multicenter, prospective, randomized, open-labeled trial will directly compare the efficacy and safety among the patients treated with either everolimus-eluting stent (EES), zotarolimus-eluting stent with biolinx polymer (ZES-R), or biolimus-eluting stent (BES) with minimal exclusion criteria. The primary end point is a patient-oriented composite consisted of cardiac death, myocardial infarction not clearly attributable to a nontarget vessel and clinically indicated target lesion revascularization at 24-month clinical follow-up post-index procedure. With the hypothesis that “BES is non-inferior to EES” or “BES is non-inferior to ZES-R” in primary end point, approximately 2,600 patients will be assigned to one of the types of stents using a web-based randomization system. Conclusions The CHOICE trial will directly compare the efficacy and safety of EES, ZES-R, and BES in everyday clinical practice for long-term follow-up.

Background and Objectives: Stented segment length is a predictive factor for restenosis and stent thrombosis still in the drug-eluting stent (DES) era, and the benefit of routine intravascular ultrasound (IVUS) is still unclear. The aim of the present study was to investigate whether IVUS-guided percutaneous coronary intervention (PCI) improved the vascular outcomes as compared with conventional PCI in the treatment of diffuse coronary artery disease. Subjects and Methods: From our registry database from January 2006 to May 2009, we identified 85 consecutive patients with de novo coronary lesions treated with at least 64 mm of multiple, overlapping DES. The 2-year rate of major adverse cardiovascular events (MACE), defined as the composite of cardiovascular death, non-fatal myocardial infarction, target lesion revascularization (TLR), or stent thrombo sis, was compared according to the use of IVUS. Results: The 2-year MACE rate was lower in the IVUS-guided group than that of the angiography-guided group (8% vs. 33.3%, p=0.005). The incidence of TLR was lower in patients with IVUS use than in those without IVUS use (0% vs. 27.8%, p

ObjectivesThis study compared the prognostic role of high on-treatment platelet reactivity (HTPR) in predicting thrombotic events in a Korean population undergoing percutaneous coronary intervention (PCI) in the acute myocardial infarction (AMI) and non-AMI setting.BackgroundThe prognostic significance and optimal cutoff of HTPR might differ according to a given clinical condition, such as AMI and ethnicity.MethodsOn-treatment platelet reactivity was measured with a VerifyNow P2Y12 assay (Accumetrics, San Diego, California) in 1,226 patients (824 men; age 65 ± 10 years), including 413 AMI cases, 12 to 24 h after PCI between March 2008 and March 2010. The prevalence of cardiovascular (CV) events defined as a composite of death from CV causes, nonfatal myocardial infarction, or stent thrombosis at 1-year follow-up were compared according to HTPR between patients with and without AMI.ResultsThe optimal cutoff for HTPR was 272 IU of the P2Y12 reaction unit (PRU) (area under the curve: 0.708; 95% confidence interval [CI]: 0.607 to 0.809, p = 0.03), which was the upper-tertile threshold. Among AMI patients, 1-year CV events occurred more frequently in patients with versus without HTPR (n = 14 [8.8%] vs. n = 1 [0.4%], p < 0.001), whereas there was no difference in the composite endpoint on the basis of HTPR in patients without AMI (n = 7 [2.8%] vs. n = 8 [1.4%], p = 0.193).ConclusionsIncreased residual platelet reactivity is related to post-discharge CV events in subjects with AMI, whereas the prognostic significance of HTPR seems to be attenuated in patients with stable coronary disease after PCI.

Background: There is a paucity of data on the effects of adherence to treatment on outcomes for patients with acute heart failure (HF) in Korea. We used HF performance measures to evaluate overall adherence and whether this affects clinical outcomes. Methods and Results: Among 3,466 patients in the Korean Heart Failure Registry, 1,527 patients with left ventricular systolic dysfunction (LVSD) who survived hospitalization were evaluated. Modified validated performance measures were defined as follows: use at discharge of angiotensin-converting enzyme inhibitor (ACEI), angiotensin-receptor II blocker (ARB), β-blocker or aldosterone receptor antagonist. Adherence to performance measures were as follows: ACEI or ARB at discharge, 68.0%; β-blocker at discharge, 40.9%; aldosterone receptor antagonist at discharge, 37.5%. On multivariate analysis, adherence to the measure of ACEI or ARB use at discharge was significantly associated with mortality (odds ratio (OR), 0.344; 95% confidence interval (CI), 0.123-0.964), readmission (OR, 0.180; 95%CI, 0.062-0.522) and mortality/readmission (OR, 0.297; 95%CI, 0.125-0.707) at 60 days and that for β-blocker with mortality (OR, 0.337; 95%CI, 0.147-0.774) at 1 year. Conclusions: For patients with LVSD in Korea, adherence to treatment performance measures, including prescription of an ACEI/ARB and β-blocker use at discharge, is associated with improved clinical outcomes. (Circ J 2012; 76: 1151-1158)

Background and Objectives: Radial artery spasm is one of the most common complications of transradial coronary angiography (TRA): the radial artery is prone to cathecholamine-induced contraction and radial pain during TRA could increase the sympathetic tone. The object of this study was to evaluate whether the eutectic mixture of local anesthesia (EMLA) cream, in addition to lidocaine infiltration, could reduce the sympathetic response by reducing radial pain during TRA. Subjects and Methods: Seventy-six patients were randomized 1 : 1 to either EMLA or control groups. Radial pain was measured by the visual analogue scale (VAS) and the verbal rating scale (VRS-4). Sympathetic response, including systolic (SBP) and diastolic blood pressure (DBP), pulse rate (PR), stroke volume (SV) and total peripheral resistance (TPR), was measured by photoplethysmography. Results: Radial pain measured during lidocaine infiltration was significantly lower in the EMLA group (VAS: 3.1 vs. 4.0, p=0.04; VRS-4: 2.0 vs. 2.2, p=0.03) and the sympathetic response was significantly blunted in the EMLA group from baseline to lidocaine infiltration (ΔSBP, mm Hg: 5 vs. 13, p