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Implantable cardioverter-defibrillator (ICD) implantation to prevent sudden cardiac death (SCD) in post-myocardial infarction (MI) patients varies by geography but remains low in many regions despite guideline recommendations.This study aimed to characterize the care pathway of post-MI patients and understand barriers to referral for further SCD risk stratification and management in patients meeting referral criteria.This prospective, nonrandomized, multi-nation study included patients ≥18 years of age, with an acute MI ≤30 days and left ventricular ejection fraction 50% ≤14 days post-MI. The primary endpoint was defined as the physician's decision to refer a patient for SCD stratification and management.In total, 1,491 post-MI patients were enrolled (60.2 ± 12.0 years of age, 82.4% male). During the study, 26.7% (n = 398) of patients met criteria for further SCD risk stratification; however, only 59.3% of those meeting criteria (n = 236; 95% CI: 54.4%-64.0%) were referred for a visit. Of patients referred for SCD risk stratification and management, 94.9% (n = 224) attended the visit of which 56.7% (n =127; 95% CI: 50.1%-63.0%) met ICD indication criteria. Of patients who met ICD indication criteria, 14.2% (n = 18) were implanted.We found that ∼40% of patients meeting criteria were not referred for further SCD risk stratification and management and ∼85% of patients who met ICD indications did not receive a guideline-directed ICD. Physician and patient reasons for refusing referral to SCD risk stratification and management or ICD implant varied by geography suggesting that improvement will require both physician- and patient-focused approaches. (Improve Sudden Cardiac Arrest [SCA] Bridge Study; NCT03715790).

In critically ill patients, risk scores are used; however, they do not provide information for nutritional intervention. This study combined the levels of phenylalanine and leucine amino acids (PLA) to improve 30-day mortality prediction in intensive care unit (ICU) patients and to see whether PLA could help interpret the nutritional phases of critical illness. We recruited 676 patients with APACHE II scores ≥ 15 or intubated due to respiratory failure in ICUs, including 537 and 139 patients in the initiation and validation (multicenter) cohorts, respectively. In the initiation cohort, phenylalanine ≥ 88.5 μM (indicating metabolic disturbance) and leucine < 68.9 μM (indicating malnutrition) were associated with higher mortality rate. Based on different levels of phenylalanine and leucine, we developed PLA scores. In different models of multivariable analyses, PLA scores predicted 30-day mortality independent of traditional risk scores (p < 0.001). PLA scores were then classified into low, intermediate, high, and very-high risk categories with observed mortality rates of 9.0%, 23.8%, 45.6%, and 81.8%, respectively. These findings were validated in the multicenter cohort. PLA scores predicted 30-day mortality better than APACHE II and NUTRIC scores and provide a basis for future studies to determine whether PLA-guided nutritional intervention improves the outcomes of patients in ICUs.

The timely selection of severe heart failure (HF) patients for cardiac transplantation and advanced HF therapy is challenging. Peak oxygen consumption (VOWe retrospectively selected 377 acute HF patients discharged from the hospital. The primary outcome was a composite of all-cause mortality, or urgent cardiac transplantation. We divided these patients into the more GDMT (two or more types of GDMT) and less GDMT groups (fewer than two types of GDMT) and compared the performance of their peak VOOptimizing the cutoff value of peak VO

Background: With respect to total mortality and cardiovascular mortality, the feature and impact of guideline-directed medication (GDM) prescriptions for heart failure with reduced ejection fraction (HFrEF) with chronic kidney disease (CKD) are unknown. Therefore, we aimed to determine these aspects. Methods: GDM prescriptions and their impact on discharged patients with and without CKD were analyzed. To analyze differences in one-year clinical outcomes, propensity score matching was conducted on a cohort of patients with concomitant HFrEF and CKD who received more and fewer GDM prescriptions. Results: A total of 1509 patients were enrolled in Taiwan's HFrEF registry from May 2013 to October 2014, and 1275 discharged patients with complete one-year follow-up were further analyzed. Of these patients, 468 (36.7%) had moderate CKD, whereas 249 (19.5%) had advanced CKD. Patients with advanced CKD received fewer prescribed GDMs than other patients. Multivariate analysis revealed that peripheral arterial occlusive disease, thyroid disorder, advanced HF at discharge, diastolic blood pressure, digoxin use, and fewer prescribed GDMs were independent predictors of one-year total mortality. After propensity score matching, patients with fewer prescribed GDMs had higher one-year total mortality rate than those with more prescribed GDMs (P=0.036). Conclusions: CKD at discharge from HF hospitalization was associated with fewer GDM prescriptions, particularly in patients with more advanced CKD. The propensity-matched analysis indicated that more GDM prescriptions led to better clinical outcomes in HFrEF patients with CKD. Careful interpretation of changes in renal function during HF hospitalization may improve GDM prescriptions.

BACKGROUND: In patients with end-stage renal disease (ESRD), acute myocardial infarction (AMI) increases the risks of cardiovascular events, death, and bleeding. Several scores have been developed for predicting ischemic and bleeding outcomes in AMI patients, but none have been validated specifically for ESRD patients. OBJECTIVES: To compare and validate different risk scores as predictors of ischemic and bleeding outcomes in AMI patients with ESRD. METHODS: This retrospective study enrolled 340 patients who had received percutaneous coronary intervention for AMI while undergoing maintenance hemodialysis for ESRD. Ischemic risk scores (TIMI-STEMI, TIMI-NSTEMI, GRACE, DAPT) and bleeding risk scores (PRECISE-DAPT, CRUSADE, ACUITY, ACTION, SWEDEHEART) were calculated. The ischemic outcome mainly focused on major adverse cardiovascular events (MACEs) within 14 days after hospitalization, and the bleeding outcome was 14-day major bleeding according to the CRUSADE criteria. RESULTS: The GRACE score was superior in discriminating ischemic outcomes, especially in 14-day MACEs [area under curve (AUC) 0.791, p < 0.001]. None of the scores could ideally discriminate 14-day CRUSADE major bleeding, while the PRECISE- DAPT score had the best discriminative power (AUC 0.636, p < 0.001). Either GRACE score > 222 or PRECISE-DAPT score > 48 was associated with higher net adverse cardiovascular events (a composite of 14-day MACEs and 14-day CRUSADE major bleeding). CONCLUSIONS: In AMI patients with ESRD, the GRACE score can effectively discriminate the risk of short-term ischemic events. None of the scores could ideally discriminate the bleeding risk, but a high PRECISE-DAPT score still represented a higher rate of bleeding events.

Background. Several risk scores have been developed to predict and analyze in-hospital mortality and short- and long-term outcomes of ST-elevation myocardial infarction (STEMI) patients after primary percutaneous coronary intervention (PPCI); these can classify patients as having a high or low risk of death or complications. Objective. To compare the prognostic precision of four risk scores for predicting in-hospital mortality in patients with STEMI treated with PPCI. Methods. We performed a retrospective cohort analysis of patients with STEMI who underwent PPCI between 2012 and 2019 (N = 1346). GRACE (Global Registry of Acute Cardiac Events), CADILLAC (Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications), Zwolle, and TIMI (Thrombolysis in Myocardial Infarction) risk scores were calculated for each patient according to different variables. We evaluated the predictive accuracy of these scores for in-hospital mortality using the C statistic, which was obtained using logistic regression and receiver operating characteristic curves. Results. The GRACE, CADILLAC, Zwolle, and TIMI risk scores all had good predictive precision for in-hospital mortality, with C statistics ranging from 0.842 to 0.923. The GRACE and CADILLAC risk scores were found to be superior. Conclusions. All GRACE, CADILLAC, Zwolle, and TIMI risk scores showed a high predictive value for in-hospital mortality due to all causes in patients with STEMI treated with PPCI. The GRACE and CADILLAC risk scores revealed a better accuracy for predicting in-hospital mortality than the Zwolle and TIMI risk scores.

BackgroundUse of statistical models for assessing the clinical risk of readmission to medical and surgical intensive care units is well established. However, models for predicting risk of coronary care unit (CCU) readmission are rarely reported. Therefore, this study investigated the characteristics and outcomes of patients readmitted to CCU to identify risk factors for CCU readmission and to establish a scoring system for identifying patients at high risk for CCU readmission.MethodsMedical data were collected for 27,841 patients with a history of readmission to the CCU of a single multi-center healthcare provider in Taiwan during 2001-2019. Characteristics and outcomes were compared between a readmission group and a non-readmission group. Data were segmented at a 9:1 ratio for model building and validation.ResultsThe number of patients with a CCU readmission history after transfer to a standard care ward was 1,790 (6.4%). The eleven factors that had the strongest associations with CCU readmission were used to develop and validate a CCU readmission risk scoring and prediction model. When the model was used to predict CCU readmission, the receiver-operating curve characteristic was 0.7038 for risk score model group and 0.7181 for the validation group. A CCU readmission risk score was assigned to each patient. The patients were then stratified by risk score into low risk (0–12), moderate risk (13–31) and high risk (32–40) cohorts check scores, which showed that CCU readmission risk significantly differed among the three groups.ConclusionsThis study developed a model for estimating CCU readmission risk. By using the proposed model, clinicians can improve CCU patient outcomes and medical care quality.

Aims: The current study aims to verify the feasibility and safety of chronic total occlusion (CTO)-percutaneous coronary intervention (PCI) via the distal transradial access (dTRA).Methods: Between April 2017 and December 2019, 298 patients who underwent CTO PCI via dTRA were enrolled in this study. The baseline demographic and procedural characteristics were listed and compared between groups. The incidences of access-site vascular complications and procedural complications and mortality were recorded.Results: The mean J-CTO (Japanese chronic total occlusion) score was 2.6 ± 0.9 points. The mean access time was 4.6 ± 2.9 min, and the mean procedure time was 115.9 ± 55.6 min. Left radial snuffbox access was performed successfully in 286 patients (96.5%), and right radial snuffbox access was performed successfully in 133 patients (97.7%). Bilateral radial snuffbox access was performed in 107 patients (35.9%). 400 dTRA (95.5%) received glidesheath for CTO intervention. Two patients (0.7%) developed severe access-site vascular complications. None of the patients experienced severe radial artery spasm and only 2 patients (0.5%) developed radial artery occlusion during the follow-up period. The overall procedural success rate was 93.5%. The procedural success rate was 96.5% in patients with antegrade approach and 87.7% in patients with retrograde approach.Conclusions: It is both safe and feasible to use dTRA plus Glidesheath for complex CTO intervention. The incidences of procedure-related complications and severe access-site vascular complications, and distal radial artery occlusion were low.

Vascular smooth muscle cells (SMCs) are important vascular components that are essential for the regulation of vascular functions during vascular atherosclerogenesis and vascular injury. Oxidized low-density lipoprotein (oxLDL) is known to induce SMC activation and foam cell transformation. This study characterized the role of hepatoma-derived growth factor (HDGF) in oxLDL-induced foam cell formation in cultured primary rat aortic SMCs. OxLDL exposure significantly increased HDGF expression and extracellular release. It also upregulated atherogenic regulators in SMCs, including TLR4, MyD88, LOX-1, and CD36. Exogenous HDGF stimulation not only increased the expression of cognate receptor nucleolin, but also the innate immunity regulators TLR4/MyD88 and lipid metabolism regulators, including LOX-1 and CD36. Oil red O staining showed that HDGF did not initiate, but enhanced oxLDL-driven foam cell formation in SMCs. Further signaling characterization demonstrated that oxLDL evoked activation of PI3K/Akt and p38 MAPK signaling pathways, both of which were involved in the upregulation of HDGF, LOX-1, and CD36 induced by oxLDL. Gene knockdown experiments using LOX-1 targeted siRNA demonstrated that LOX-1 expression was critical for oxLDL-induced HDGF upregulation, while HDGF gene depletion completely abolished oxLDL-triggered TLR4, LOX-1, and CD36 overexpression and foam cell formation in SMCs. These findings strongly suggest that oxLDL-induced HDGF upregulation participates in subsequent LOX-1 and CD36 expression in aortic SMCs and mechanistically contributes to the formation of SMC-derived foam cells. The oxLDL/LOX-1/HDGF axis may serve as a target for anti-atherogenesis therapy.

The outbreak of the new coronavirus disease 2019 (COVID-19) has notably affected the medical system worldwide and influenced the health-seeking behavior of people while depleting medical resources, causing a delay in ST-elevation myocardial infarction (STEMI) management In this single-center, retrospective cohort study, we compared the clinical pictures of nontransfer patients who presented to the emergency department directly and received primary percutaneous cardiovascular intervention (PPCI) from February 1 to April 30, 2020 (group 2, N = 28), with patients who received PPCI from February 1 to April 30, 2016–2019 (group 1, N = 130) A total of 158 patients with STEMI who received PPCI were included in the study A decrease in the percentage of patients with door-to-balloon time

Microglia-related neuroinflammation is associated with a variety of neurodegenerative diseases. Flavonoids have demonstrated different pharmacological effects, such as antioxidation, neuroprotection and anti-inflammation However, the effect of flavonoid 6-methoxyflavone (6-MeOF) on microglia-mediated neuroinflammation remain unknown.The current study aim to study the antineuroinflammatory effects of 6-MeOF in lipopolysaccharide- (LPS-) induced microglia in vitro and in vivo.Pretreatment of BV2 microglia cells with 6-MeOF for 1 h then stimulated with LPS (100 ng/ml) for 24 h. The expression levels of pro-inflammatory factors, NO and reactive oxygen species (ROS) were performed by the enzyme-linked immunosorbent assay (ELISA), Griess assay and flow cytometry. Western blotting was used to assess MAPK, NF-κB signal transducer and antioxidant enzymes-related proteins. Analysis of ROS and microglial morphology was confirmed in the zebrafish and mice brain, respectively.Our results demonstrated that 6-MeOF dose-dependently prevent cell death and decreased the levels of pro-inflammatory mediators in LPS-stimulated BV2 microglia cells. Phosphorylated NF-κB/IκB and TLR4/MyD88/p38 MAPK/JNK proteins after exposure to 6-MeOF was suppressed in LPS-activated BV-2 microglial cells. 6-MeOF also presented antioxidant activity by reduction of NO, ROS, iNOS and COX-2 and the induction of the level of HO-1 and NQO1 expressions in LPS-activated BV2 microglial cells. Furthermore, we demonstrated that 6-MeOF inhibited LPS-induced NO generation in an experimental zebrafish model and prevent the LPS-induced microgliosis in the prefrontal cortex and substantia nigra of mice.These results explored that 6-MeOF possesses potential as anti-inflammatory and anti-oxidant agents against microglia-associated neuroinflammatory disorders.

Aims Vascular smooth muscle cells (VSMCs) are important regulators of vascular functions and their conversion to osteoblasts is a key to development of vascular calcification. This study aimed to characterize in vitro effect of hepatoma-derived growth factor (HDGF) on phenotypic conversion of cultured aortic VSMCs into osteoblast-like cells. Materials and methods Cell proliferation and migration assays were used to examine cell behaviors. Western blotting, alkaline phosphatase activity and calcium staining were used to evaluate osteoblastic marker expression and function, respectively. Key findings Recombinant HDGF treatment enhanced VSMC growth and motility. Treatment of osteogenic medium (OM) increased expression of not only HDGF but also osteoblastic markers, including Runx2 and osteopontin (OPN), while VSMC marker α-smooth muscle actin (α-SMA) declined. Coincidentally, HDGF and OM treatment alone stimulated signaling activities in both PI3K/Akt and MAPK pathways. Conversely, inhibition of Akt and p38 significantly blocked the OM-upregulated HDGF, Runx2, and OPN expression and NF-κB phosphorylation, but did not reversed the α-SMA downregulation, implicating the involvement of Akt and p38 activities in the osteoblastic transformation of VSMCs. Small interfering RNA-mediated HDGF gene silencing effectively prevented the Runx2 and OPN upregulation, alkaline phosphatase activation, and calcium deposition, but did not affect the α-SMA levels in the transformed cells, supporting the involvement of HDGF in regulation of Runx2 and OPN expression. Significance In conclusion, in synergism with other osteogenic factor, HDGF may promote the progression of osteobastic transformation of VSMCs via Akt and p38 signaling pathways and contribute to vascular calcification in arteriosclerosis. Chemical compounds studied in this study HDGF (PubChem CID:); LY294002 (PubChem CID: 3973); PD98059 (PubChem CID: 4713); SB203580 (PubChem CID: 176155); SB431542 (PubChem CID: 4521392); SP600125 (PubChem CID: 8515); Wortmannin (PubChem CID: 312145).

Atrial fibrillation (AF) is an important complication of acute myocardial infarction (AMI). The association between AF and serum lipid profile is unclear and statin use for lowering the incidence of new-onset AF remains controversial. The objective of this study was to investigate whether statins confer a beneficial effect on AF after AMI. Data available in the Taiwan National Health Insurance Research Database on 32886 AMI patients between 2008 and 2011 were retrospectively analyzed. Total 27553 (83.8%) had complete 1-yr follow-up data. Cardiovascular outcomes were analyzed based on the baseline characteristics and AF type (existing, new-onset, or non-AF). AF groups had significantly higher incidence of heart failure (HF), stroke, all-cause death, and major adverse cardiac and cerebrovascular event (MACCE) after index AMI (all P

Background. Circular RNA (circRNA) is a noncoding RNA that forms a closed-loop structure, and its abnormal expression may cause disease. We aimed to find potential network for circRNA-related competitive endogenous RNA (ceRNA) in atrial fibrillation (AF). Methods. The circRNA, miRNA, and mRNA expression profiles in the heart tissue from AF patients were retrieved from the Gene Expression Omnibus database and analyzed comprehensively. Differentially expressed circRNAs (DEcircRNAs), differentially expressed miRNAs (DEmiRNAs), and differentially expressed mRNAs (DEmRNAs) were identified, followed by the establishment of DEcircRNA-DEmiRNA-DEmRNA regulatory network. Functional annotation analysis of host gene of DEcircRNAs and DEmRNAs in ceRNA regulatory network was performed. In vitro experiment and electronic validation were used to validate the expression of DEcircRNAs, DEmiRNAs, and DEmRNAs. Results. A total of 1611 DEcircRNAs, 51 DEmiRNAs, and 1250 DEmRNAs were identified in AF. The DEcircRNA-DEmiRNA-DEmRNA network contained 62 circRNAs, 14 miRNAs, and 728 mRNAs. Among which, two ceRNA regulatory pairs of hsa-circRNA-100053-hsa-miR-455-5p-TRPV1 and hsa-circRNA-005843-hsa-miR-188-5p-SPON1 were identified. In addition, six miRNA-mRNA regulatory pairs including hsa-miR-34c-5p-INMT, hsa-miR-1253-DDIT4L, hsa-miR-508-5p-SMOC2, hsa-miR-943-ACTA1, hsa-miR-338-3p-WIPI1, and hsa-miR-199a-3p-RAP1GAP2 were also obtained. MTOR was a significantly enriched signaling pathway of host gene of DEcircRNAs. In addition, arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, and hypertrophic cardiomyopathy were remarkably enriched signaling pathways of DEmRNAs in DEcircRNA-DEmiRNA-DEmRNA regulatory network. The expression validation of hsa-circRNA-402565, hsa-miR-34c-5p, hsa-miR-188-5p, SPON1, DDIT4L, SMOC2, and WIPI1 was consistent with the integrated analysis. Conclusion. We speculated that hsa-circRNA-100053-hsa-miR-455-5p-TRPV1 and hsa-circRNA-005843-hsa-miR-188-5p-SPON1 interaction pairs may be involved in AF.

Background. The outcomes of patients with concomitant left main coronary artery (LMCA) and right coronary artery (RCA) diseases are reportedly worse than those with only LMCA disease. To date, only few studies have investigated the clinical impact of percutaneous coronary intervention (PCI) on RCA stenosis during the same hospitalization, in which LMCA disease was treated. This study was aimed at comparing the outcomes between patients with and without right coronary artery intervention during the same hospital course for LMCA intervention. Methods and Results. From a total of 776 patients who were undergoing PCI to treat LMCA disease, 235 patients with concomitant RCA significant stenosis (more than 70% stenosis) were enrolled. The patients were divided into two groups: 174 patients received concomitant PCI for RCA stenosis during the same hospitalization, in which LMCA disease was treated, and 61 patients did not receive PCI for RCA stenosis. Patients without intervention to the right coronary artery had higher 30-day cardiovascular mortality rates and 3-year RCA revascularization rates compared to those with right coronary artery intervention. Patients without RCA intervention at the same hospitalization did not increase the 30-day total death, 3-year myocardial infarction rate, 3-year cardiovascular death, and 3-year total death. Conclusions. In patients with LM disease and concomitant above or equal to 70% RCA stenosis, PCI for RCA lesion during the same hospitalization is recommended to reduce the 30-day cardiovascular death and 3-year RCA revascularization rate.

Chronic heart failure is a serious complication of myocardial infarction, one of the major causes of death worldwide that often leads to adverse cardiac hypertrophy and poor prognosis. Hypoxia-induced cardiac tissue remodeling is considered an important underlying etiology. This study aimed to delineate the signaling profiles of RhoA/ROCK, PI3K/Akt, and MAPK and their involvement in regulation of remodeling events in cultured H9c2 cardiomyoblast cells. In addition to its growth-suppressive effect, the hypoxia-mimetic chemical, cobalt chloride (CoCl2) significantly induced RhoA kinase activation as revealed by increased MBS phosphorylation and ROCK1/2 expression in H9c2 cells. CoCl2 treatment up-regulated type I collagen and MMP-9, but did not affect MMP-2, implicating its role in tissue remodeling. Kinetic signal profiling study showed that CoCl2 also elicited Smad2 hyperphosphorylation and its nuclear translocation in the absence of TGF-β1. In addition, CoCl2 activated Akt-, ERK1/2-, JNK-, and p38 MAPK-mediated signaling pathways. Kinase inhibition experiments demonstrated that hydroxyfasudil, a RhoA kinase inhibitor, significantly blocked the CoCl2- and lysophosphatidic acid-evoked Smad2 phosphorylation and overexpression of type I collagen and MMP-9, and that PI3K and ERK interplayed with RhoA and its downstream Smad2 signaling cascade. In conclusion, this study demonstrated that RhoA/ROCK, PI3K/Akt, and MAPK pathways are mechanistically involved in the CoCl2-stimulated tissue remodeling in H9c2 cardiomyoblast cells. Targeting signaling mediators might be used to mitigate hypoxia-related Smad2 phosphorylation and cardiac remodeling events in ischemic cardiomyopathy.

Elevation of free fatty acids (FFAs) is known to affect microvascular function and contribute to obesity-associated insulin resistance, hypertension, and microangiopathy. Proliferative and synthetic vascular smooth muscle cells (VSMCs) increase intimal thickness and destabilize atheromatous plaques. This study aimed to investigate whether saturated palmitic acid (PA) and monounsaturated oleic acid (OA) modulate autophagy activity, cell proliferation, and vascular tissue remodeling in an aortic VSMC cell line. Exposure to PA and OA suppressed growth of VSMCs without apoptotic induction, but enhanced autophagy flux with elevation of Beclin-1, Atg5, and LC3I/II. Cotreatment with autophagy inhibitors potentiated the FFA-suppressed VSMC growth and showed differential actions of PA and OA in autophagy flux retardation. Both FFAs upregulated lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) but only OA increased LDL uptake by VSMCs. Mechanistically, FFAs induced hyperphosphorylation of Akt, ERK1/2, JNK1/2, and p38 MAPK. All pathways, except OA-activated PI3K/Akt cascade, were involved in the LOX-1 upregulation, whereas blockade of PI3K/Akt and MEK/ERK cascades ameliorated the FFA-induced growth suppression on VSMCs. Moreover, both FFAs exhibited tissue remodeling effect through increasing MMP-2 and MMP-9 expression and their gelatinolytic activities, whereas high-dose OA significantly suppressed collagen type I expression. Conversely, siRNA-mediated LOX-1 knockdown significantly attenuated the OA-induced tissue remodeling effects in VSMCs. In conclusion, OA and PA enhance autophagy flux, suppress aortic VSMC proliferation, and exhibit vascular remodeling effect, thereby leading to the loss of VSMCs and interstitial ECM in vascular walls and eventually the instability of atheromatous plaques. J. Cell. Biochem. 118: 1249-1261, 2017. © 2016 Wiley Periodicals, Inc.

To investigate the postprocedural cardiovascular events and vascular outcomes, including hand ischemia and neurological compromise, after transulnar (TU) catheterization in ipsilateral radial artery occlusion.Previous randomized trials have shown that the transulnar (TU) approach for coronary angiogram and intervention has safety and outcomes similar to those of the transradial (TR) approach. However, the safety of the TU procedure when ipsilateral radial artery occlusion occurs is unknown.We retrospectively reviewed 87 TU cases with ipsilateral radial artery occlusion confirmed by a forearm angiogram. Eighty percent of these patients had a history of ipsilateral radial artery cannulation or surgery. We avoided the use of over-sized sheaths or applied a sheathless approach during surgery.No ulnar artery occlusion was observed by subsequent Doppler ultrasound or pulse oximetry. No patient developed hand ischemia or serious complications requiring surgery or blood transfusion during the follow-up period of 32.2 ± 24.0 months. Review of the preprocedural forearm angiograms showed that 95.7% of the patients possessed significant collaterals supplying flow from the interosseous artery to the occluded radial artery remnant. Thus, the blood circulation to the palmar arch and digital vessels was maintained even when the ulnar artery was temporarily occluded by an in-dwelling ulnar arterial sheath.TU catheterization was safe in patients with coexisting ipsilateral radial artery occlusions and feasible for use in complex intervention procedures. Cautious manipulation of ulnar artery cannulation and hemostasis helped decrease the risk of hand ischemia.

Microglia, resident innate immune cells in central nervous system, regulates neuroinflammation and is associated with a variety of neuropathologies. The present study investigated the antineuroinflammatory effects of hispidulin (HPD), a naturally flavone compound, in lipopolysaccharide- (LPS-) stimulated BV2 microglia cells. The expression levels of nitric oxide (NO), reactive oxygen species (ROS), and pro-inflammatory factors were determined by the Griess method, flow cytometry, and enzyme-linked immunosorbent assay (ELISA). Western blotting was used to measure various transcription factors such as Akt, nuclear factor-kappa B (NF-κB), and signal transducer and activator of transcription 3 (STAT3) activities. Our experimental results demonstrated that HPD increased cell viability and reduced apoptosis in LPS-treated BV2 microglia cells. Moreover, HPD significantly reduced the levels of NO, ROS, inducible nitric oxide synthase (iNOS), cyclooxygenase- (COX-) 2, tumor necrosis factor- (TNF-) α, interleukin- (IL-) 1β, IL-6, and prostaglandin E2 (PGE2) in a dose-dependent manner. Phosphorylation of NF-κB/IκB, Akt, and STAT3 proteins expression by HPD was suppressed in LPS-induced BV2 microglial cells. We concluded that HPD may inhibit neuroinflammatory responses by inhibiting NF-κB pathway activation and ROS formation. These results propose that HPD has potential as anti-inflammatory agents against microglia-mediated neuroinflammatory disorders.

BACKGROUND: Controlling modifiable risk factors (MRFs) in patients with cardiovascular diseases has been shown to be effective in reducing re-hospitalization rates. The aim of this study was to investigate the rates of controlled MRFs and clinical outcomes after pharmacist interventions in patients with myocardial infarction (MI) after hospital discharge. METHODS: This prospective randomized clinical study was conducted at one medical center in Taiwan, and enrolled patients with MI from January 1, 2012 to December 31, 2014. Patients received medication reconciliation and education from a pharmacist before hospital discharge. The intervention group (IG) received continuous consultations from the pharmacist after discharge, whereas the control group (CG) did not. Primary outcomes included achieving blood pressure < 140/70 mmHg, low-density lipoprotein-cholesterol (LDL-C) < 70 mg/dL, and hemoglobin A1c (HbA1c) < 7% targets. The secondary outcome was major adverse cardiac events (MACEs), defined as re-hospitalization due to MI, unstable angina and stroke. RESULTS: Two hundred and eight patients completed the study protocol (106 in the IG and 102 in the CG). The rate of achieving blood pressure goal was similar between the two groups. More patients in the IG achieved LDL-C and HbA1c goals than those in the CG at 1 year and 2 years post discharge. However, there was no significant difference in the cumulative incidence of MACEs between the two groups (5.7% vs. 9.8%) (p = 0.262). Diabetes was the only independent predictor of re-hospitalization due to a MACE. CONCLUSIONS: Pharmacist interventions led to a higher rate of optimal controlled MRFs but did not significantly reduce the MACE rate in the patients with MI.

Hyperglycaemia causes endothelial dysfunction, which is the initial process in the development of diabetic vascular complications. Upon injury, endothelial cells undergo an endothelial-to-mesenchymal transition (EndMT), lose their specific marker, and gain mesenchymal phenotypes. This study investigated the effect of liraglutide, a glucagon-like peptide 1 (GLP-1) receptor agonist, on EndMT inhibition and neointima formation in diabetic mice induced by streptozotocin. The diabetic mice with a wire-induced vascular injury in the right carotid artery were treated with or without liraglutide for four weeks. The degree of neointima formation and re-endothelialisation was evaluated by histological assessments. Endothelial fate tracing revealed that endothelium-derived cells contribute to neointima formation through EndMT in vivo. In the diabetic mouse model, liraglutide attenuated wire injury-induced neointima formation and accelerated re-endothelialisation. In vitro, a high glucose condition (30 mmol/L) triggered morphological changes and mesenchymal marker expression in human umbilical vein endothelial cells (HUVECs), which were attenuated by liraglutide or Activin receptor-like 5 (ALK5) inhibitor SB431542. The inhibition of AMP-activated protein kinase (AMPK) signaling by Compound C diminished the liraglutide-mediated inhibitory effect on EndMT. Collectively, liraglutide was found to attenuate neointima formation in diabetic mice partially through EndMT inhibition, extending the potential therapeutic role of liraglutide.

We investigated the accuracy of various bleeding risk scores to estimate the bleeding risk in patients with acute myocardial infarction (AMI) managed with percutaneous coronary intervention (PCI) access via the radial artery.We retrospectively enrolled 1,651 patients who were definitively diagnosed with ST-elevation myocardial infarction (STEMI) or non-STEMI (NSTEMI). We assessed the predictive validities of 30-day bleeding events in various scoring systems using receiver operating characteristic curves.Overall, ACUITY-HORIZONS exhibited the highest area under the curve to predict 30-day bleeding, followed by ACTION and CRUSADE; HAS-BLED displayed the lowest score. With a cut-off of 17, ACUITY-HORIZONS demonstrated the best discrimination for the Thrombolysis in Myocardial Infarction (TIMI) 30-day serious bleeding rate. We observed significant differences among all-cause death, cardiovascular death, and major adverse cardiac events between the ACUITY-HORIZONS groups with a score of ≤ 17 and > 17. ACUITY-HORIZONS score > 17, initial systolic blood pressure (SBP) < 90 mmHg, and Killip III and IV upon admission positively predicted the 30-day bleeding risk, whereas myocardial infarction (MI) and TIMI major bleeding within 30 days, heart failure at admission, and initial SBP < 90 mmHg positively predicted the 30-day mortality.Comparatively, ACUITY-HORIZON is the most reliable system in predicting 30-day bleeding for patients with AMI via transradial PCI. In the transradial scenario, bleeding and MI within 30 days are substantially related to 30-day mortality.

This study investigated the efficacy and safety of ticagrelor compared with clopidogrel in patients with end-stage renal disease (ESRD) and acute myocardial infarction (AMI). We retrospectively enrolled patients who had received regular dialysis and had undergone percutaneous coronary intervention (PCI) for AMI at our hospital between January 2013 and December 2016. Outcomes analyzed included cardiovascular death, death from any cause, MI, stroke, and bleeding events. Patients were allocated to the ticagrelor group (N = 74) or the clopidogrel group (N = 116) according to the treatment they had received. No statistically significant differences were found between the groups in terms of in-hospital primary endpoint (composite of cardiovascular death, MI, and stroke: 12.2% and 15.5% for ticagrelor and clopidogrel, respectively; p = 0.518), secondary endpoint, or any bleeding events (39.2 vs. 34.5%; p = 0.511). No statistically significant differences were found for the 1-year primary endpoint (p = 0.424), secondary endpoint, and any bleeding events (p = 0.663). Risk factors for in-hospital cardiovascular death were shock and cardiopulmonary resuscitation at initial AMI presentation, lack of beta-blocker use, and in-hospital gastrointestinal bleeding. Risk factors for 1-year cardiovascular death were shock at initial AMI presentation and lack of beta-blocker use. Only respiratory failure was a risk factor for in-hospital and 1-year gastrointestinal bleeding. In patients with ESRD and AMI, ticagrelor resulted in numerically fewer but statistically nonsignificant rates of in-hospital and 1-year cardiovascular events with no significant increase in bleeding events compared with clopidogrel.

Although established guidelines currently recommend the use of the CHA2DS2-VASc score for evaluating embolic risk in AF patients, few studies have evaluated the use of the CHA2DS2-VASc score for predicting cardiovascular outcomes in patients with acute myocardial infarction (AMI). The aim of this study was to determine whether CHA2DS2-VASc score is a predictor of a major adverse cardiocerebral vascular event (MACCE) in AMI patients. This study analyzed data in the Taiwan National Health Insurance Research Database from January 2008 to December 2012. Cardiovascular outcomes were analyzed according to the baseline characteristics, presence of AF, and CHA2DS2-VASc score. Twenty nine thousand four hundred fifty-two patients with non-fatal AMI, 1171 patients (8.3%) were with AF. The Cox regress model showed with the exception of women sex and peripheral artery disease, all the baseline characteristics considered risks in CHA2DS2-VASc scores were independently associated with the increased incidence of MACCE within 1 year after AMI. A CHA2DS2-VASc score of

Background Following acute ST elevation myocardial infarction (STEMI), restoration of large-vessel patency does not mean complete perfusion recovery. Little is known regarding the predictors of successful myocardial reperfusion for the STEMI patients undergoing pharmacologic and mechanical reperfusion strategies. Aim of the work The aim of this clinical study was to find out the predictors of myocardial functional recovery following reperfusion of acute STEMI, represented by 3-month global longitudinal strain (GLS) value assessed by speckle tracking echocardiography. Material/methods The study population included 400 patients presented with first acute STEMI with successful reperfusion by thrombolysis (group I) or primary percutaneous coronary intervention (PPCI) (group II). Electrocardiography (ECG) at baseline and 90 minutes after coronary reperfusion was performed with assessment of ST resolution. Basal and 3-month follow-up echocardiography was performed with assessment of ejection fraction (EF), myocardial performance index (MPI), systolic myocardial excursion (S'), and GLS. Results There was nonsignificant difference between patients of both groups regarding age (P = 0.422) and gender (P = 0.272). Also, there was a nonsignificant difference between both groups regarding the risk factors of coronary artery disease like hypertension (P = 0.511), diabetes mellitus (P = 0.332), and smoking (P = 0.381). But there was significant statistical difference between both groups regarding dyslipidemia (P = 0.012). Ninety-minute ST resolution was significantly higher in PPCI group (P = 0.042). Moreover, PPCI group had significant improvement of EF (P = 0.013) during follow-up, and highly significant improvement of MPI, S' and GLS (P ˂ 0.001) compared to the basal echocardiographic study. The percentage of change (∆) of each of the echocardiographic parameter was compared between both groups and revealed statistically significant improvement regarding EF, highly significant improvement of MPI, S' and GLS in favor of PPCI arm (group II). Multivariate regression analysis demonstrated that pain to reperfusion time, MI territory, ST resolution, and basal GLS value are the most important predictors for LV functional recovery. Conclusion The study found pain to reperfusion time, MI territory, ST resolution, basal GLS value are the most important predictors of myocardial functional recovery. Regular follow-up with echocardiography for STEMI patients with different reperfusion strategies has informative impact on long-term clinical outcome. Also the study confirmed that PPCI is better than thrombolysis not only in restoring epicardial coronary flow but also in restoring microvascular and tissue perfusion assuring better myocardial functional recovery and better long-term clinical outcomes.