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East Asians are the most populous race in the world and their health status is an important global issue. Compared with Caucasian populations, East Asian patients have a different benefit/risk ratio when using antithrombotic treatment. Despite this observation, treatment strategies in East Asian patients are mostly based on the American and European guidelines. Despite a lower platelet inhibitory response to clopidogrel, East Asian patients show a similar or even a lower rate of ischemic event occurrence and higher bleeding risk compared with Caucasian patients. For potent P2Y12 inhibitors (ticagrelor and prasugrel), East Asian patients have shown less favorable net clinical benefits compared with Caucasian patients, which may be related to differences in pharmacokinetic/pharmacodynamic profiles and therapeutic zone of antiplatelet effect. This updated consensus mainly focuses on state-of-the-art and current controversies in the East Asian population. In addition, when East Asian patients are administered potent P2Y12 receptor inhibitors, the strategies and ongoing trials to overcome the related hurdles are discussed.

We propose a novel high-order HDG method for the Biot’s consolidation model in poroelasticity. We present optimal h -version error analysis for both the semi-discrete and full-discrete (combined with temporal backward differentiation formula) schemes. Numerical tests are provided to demonstrate the performance of the method.

The Gensini score (GS) is a convenient, powerful tool for assessing the severity and complexity of coronary artery diseases. Our research investigated the relationship between the GS and periprocedural myocardial infarction (PMI). We recruited 4949 patients (3366 men, 1583 women; mean age 66.45 ± 10.09 years) with a single coronary artery revascularization. Based on the tertile of the GS 20 and 36, the population was divided into 3 groups: Low Group (0GS ≤ 20, N = 1809); Intermediate Group (20GS ≤ 36, N = 1579); High Group (GS36, N = 1561). PMI3 represented the endpoint for cTnI3-fold upper reference limit, while PMI5 represented the endpoint for cTnI5-fold upper reference limit. The incidence of PMI of High Group was statistically higher than that of Intermediate Group (P.05), while that of Intermediate Group was statistically higher than Low Group (P.05). With the adjustment of some general variables, GS was an independent significantly predictor for PMI3 (β = 0.006, P.05) and PMI5 (β = 0.007, P.05). Following receiver operating characteristic curve analysis, the optimal cut-off value to predict PMI are 22.5 for PMI3 and 27 for PMI5. The GS was an independent predictor of PMI in the single-coronary revascularization population. Additionally, the 22.5 of GS was the optimal cut-off value for determining the presence of PMI3, while the 27 of GS for PMI5.

Objectives The aim of the present study was to evaluate the angiographic efficacy, clinical safety, and effectiveness of the Restore paclitaxel-coated balloon in a randomized trial designed to enable the approval of the new device in China. Background Drug-coated balloon (DCB) angioplasty offers an effective treatment for in-stent restenosis. Restore is a new DCB with a SAFEPAX shellac-ammonium salt excipient that can avoid drug washing off during catheter delivery to the target lesion site. Methods In the noninferiority RESTORE ISR China (Compare the Efficacy and Safety of RESTORE DEB and SeQuent Please in Chinese Patient With Coronary In-stent Restenosis) trial, eligible patients with first occurrence of drug-eluting stent ISR were randomized to the Restore DCB or SeQuent Please DCB in a 1:1 ratio stratified by diabetes. Angiographic and clinical follow-up was planned at 9 months and 1 year, respectively, in all patients. The study was powered for the primary endpoint of 9-month in-segment late loss. Results Between May 2016 and July 2017, a total of 240 subjects at 12 sites were randomized to either the Restore group (n = 120) or the SeQuent Please group (n = 120). Nine-month in-segment late loss was 0.38 ± 0.50 mm with Restore versus 0.35 ± 0.47 mm with SeQuent Please; the 1-sided 97.5% upper confidence limit of the difference was 0.17 mm, achieving noninferiority of Restore compared with SeQuent Please (p for noninferiority = 0.02). Both DCBs had similar 1-year rates of target lesion failure (13.3% vs. 12.6%; p = 0.87). Conclusions In this head-to-head randomized trial, the Restore DCB was noninferior to the SeQuent Please DCB for the primary endpoint of 9-month in-segment late loss. (Compare the Efficacy and Safety of RESTORE DEB and SeQuent Please in Chinese Patient With Coronary In-stent Restenosis; NCT02944890)

We present a novel class of high-order space-time finite element schemes for the Poisson-Nernst-Planck (PNP) equations. We prove that our schemes are mass conservative, positivity preserving, and unconditionally energy stable for any order of approximation. To the best of our knowledge, this is the first class of (arbitrarily) high-order accurate schemes for the PNP equations that simultaneously achieve all these three properties. This is accomplished via (1) using finite elements to directly approximate the so-called entropy variable instead of the density variable, and (2) using a discontinuous Galerkin (DG) discretization in time. The entropy variable formulation, which was originally developed by Metti et al. [17] under the name of a log-density formulation, guarantees both positivity of densities and a continuous-in-time energy stability result. The DG in time discretization further ensures an unconditional energy stability in the fully discrete level for any approximation order, where the lowest order case is exactly the backward Euler discretization and in this case we recover the method of Metti et al. [17]., 15 pages

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Lysophosphatidycholine (LPC) is the main active component in oxidized low-density lipoprotein (ox-LDL). The pathological function of ox-LDL has been broadly studied in atherosclerosis. However, the specific relationship between LPC-induced unfolded protein response (UPR) and inflammation in human umbilical vein endothelial cells (HUVECs) remains elusive. In this study, we found elevated serum levels of LPC in atherosclerotic patients. LPC stimulation resulted in elevated secretion of interleukin (IL)-6 and IL-8 in HUVECs, accompanied with the activation of ER stress and NF-κB pathway. Additionally, suppression of ER stress by 4-phenylbutric acid (4-PBA), an ER stress inhibitor, alleviated the activation of the NF-κB pathway and secretion of inflammatory factors. Moreover, activating transcription factor 4 (ATF4) silencing inhibited the transcription and secretion of IL-6 and IL-8, and suppressed the adhesion of THP-1 cells to HUVECs. Activation of the NF-κB pathway and expression of its upstream factors, including Toll like receptor 4 and cellular inhibitor of apoptosis, were also inhibited by ATF4 silencing. The present findings suggest that suppression of UPR alleviates LPC-induced HUVECs inflammation by inhibition of NF-κB pathway, and indicate ATF4 as a potential target for the treatment of atherosclerosis.

Robust discretization methods for (nearly-incompressible) linear elasticity are free of volume-locking and gradient-robust. While volume-locking is a well-known problem that can be dealt with in many different discretization approaches, the concept of gradient-robustness for linear elasticity is new: it assures that dominant gradient fields in the momentum balance do not lead to spurious displacements. We discuss both aspects and propose novel Hybrid Discontinuous Galerkin (HDG) methods for linear elasticity. The starting point for these methods is a divergence-conforming discretization. As a consequence of its well-behaved Stokes limit the method is gradient-robust and free of volume-locking. To improve computational efficiency, we additionally consider discretizations with relaxed divergence-conformity and a modification which re-enables gradient-robustness, yielding a robust and quasi-optimal discretization also in the sense of HDG superconvergence.

To investigate the protective effects of Shexiang Tongxin dropping pill (, STDP) in a rat model of coronary microcirculatory dysfunction (CMD).Sprague-Dawley rats were allocated randomly into four groups: sham, CMD model, STDP, and nicorandil. After 4 weeks of treatment, CMD was induced by injection of sodium laurate (0.2 mL, 2 g/L) into the left ventricle while obstructing the ascending aorta. Rats in the sham group underwent an identical surgical procedure but were administered physiological (0.9% ) saline (0.2 mL). Twenty-four hours after surgery, blood samples were collected for biochemical analyses and enzyme-linked immunosorbent assays. Heart tissues were removed for histopathology staining; apoptosis and inflammatory cytokines were examined by Western blotting.The STDP group had a lower level of creatine kinase-myocardial band, lactate dehydrogenase, and cardiac troponin-I than that in the CMD model group. Infiltration of inflammatory cells, myocardial ischaemia, and microthrombosis were relieved in the STDP group compared with CMD model group. Levels of endothelin-1, nuclear factor-kappa B, tumour necrosis factor-α, interleukin-6, interleukin-1β, malondialdehyde, B-cell lymphoma (Bcl)-2-associated X protein, and caspase-3 were lower, and levels of nitric oxide, Bcl-2, and superoxide dismutase were higher, in the STDP group in comparison with the CMD model group.STDP pretreatment improved the CMD induced by sodium laurate via anti-inflammatory, anti-apoptosis, and anti-oxidant mechanisms.

Farnesyl pyrophosphate synthase (FPPS)-catalyzed isoprenoid intermediates are involved in diabetic cardiomyopathy. This study investigated the specific role of FPPS in the development of diabetic cardiomyopathy. We demonstrated that FPPS expression was elevated in both in vivo and in vitro models of diabetic cardiomyopathy. FPPS inhibition decreased the expression of proteins related to cardiac fibrosis and cardiomyocytic hypertrophy, including collagen I, collagen III, connective tissue growth factor, natriuretic factor, brain natriuretic peptide, and β-myosin heavy chain. Furthermore, FPPS inhibition and knockdown prevented phosphorylated c-Jun N-terminal kinase 1/2 (JNK1/2) activation in vitro. In addition, a JNK1/2 inhibitor downregulated high-glucose-induced responses to diabetic cardiomyopathy. Finally, immunofluorescence revealed that cardiomyocytic size was elevated by high glucose and was decreased by zoledronate, small-interfering farnesyl pyrophosphate synthase (siFPPS), and a JNK1/2 inhibitor. Taken together, our findings indicate that FPPS and JNK1/2 may be part of a signaling pathway that plays an important role in diabetic cardiomyopathy.

Background: Despite growing evidence indicating that patients with inflammatory bowel disease (IBD) have an increased risk of atrial fibrillation (AF), owing to the potential biases of confounding effects and reverse causation, the specific relationship between IBD and AF remains controversial. The aim of this study is to determine whether there is a causal effect of IBD on AF. Methods: A two-sample Mendelian randomization (MR) study was performed to evaluate the causal effect of IBD on AF. Statistical summaries for the associations between single nucleotide polymorphisms (SNPs) and traits of interest were obtained from independent consortia with European populations. The dataset of IBD was acquired from genome-wide association studies (GWAS), including more than 75,000 cases and controls. A GWAS with 60,620 AF cases and 970,216 controls was used to identify genetic variation underlying AF. The causal effect was estimated using the multiplicative random effects inverse-variance weighted method (IVW), followed by sensitivity analysis. Results: Using 81 SNPs, there was no evidence to suggest an association between genetically predicted IBD and risk of AF with multiplicative random-effects IVW MR analysis (odds ratio = 1.0000, 95% confidence interval: 0.9994 1.0005, p = 0.88). Conclusion: As opposed to current assumptions, no substantial evidence was found to support a causal role of IBD in the development of AF.

The SECURE-PCI study supports a perioperative loading dose of statins, although whether an intensive lipid-lowering strategy prior to percutaneous coronary intervention further benefits acute coronary syndrome patients remains controversial. Evolocumab, a proprotein-converting enzyme subtilisin/kexin type 9 (PCSK9) inhibitor, acts more quickly and effectively than statins and reduces the risk of cardiovascular events in post-myocardial infarction (MI) patients. Nonetheless, whether it can be safely used in perioperative MI patients and whether perioperative application can benefit patients are still unknown. This study aims to evaluate the safety and efficacy of this treatment regimen. A multicentre, prospective, randomized, controlled superiority trial will be conducted in 530 statin-naive MI patients. All eligible patients will be randomized to the evolocumab group (140 mg subcutaneously injected once before revascularization + 14 days after the first dose) or the control group (no evolocumab injection). Evolocumab will then be administered depending on the patient's lipid profile. Both groups will be treated simultaneously with standardized secondary preventive medications. The primary end points are major adverse cardiovascular events (a composite of death, recurrent MI, unanticipated revascularization, stroke and any rehospitalization for ischaemic causes) within 12 months. The secondary end point is post-infarction angina after pain relief. The safety end points include myopathy, impaired liver or renal function, and other adverse events during the follow-up period. This is the first trial to evaluate the safety and efficacy of evolocumab pre-treatment on prognosis in MI patients. Perioperative evolocumab injection may be a new, safe way to improve prognosis. Chinese Clinical Trial Registry ( http://www.chictr.org.cn ; ChiCTR1900024526). Registered on 13 July 2019 and updated on 31 May 2020. The study is currently recruiting patients.

Introduction: Interventional cardiology procedures (ICPs) have become the mainstay treatments in cardiology diseases and increased rapidly. This study aims to assess the occupational health hazards (OHHs) related to the long-time wearing of lead personal protective equipment and reveal health protection needs in interventional cardiologists. Methods and Results: We invited interventional and non-interventional cardiologists in tertiary III hospitals in China to participate in an online cross-sectional survey on their health status, utilization of personal protective equipment (PPE), and personal health protection (PHP) needs. Propensity score methods were used for comparisons of OHHs between the matched interventional and non-interventional cardiologists. Totally, 642 interventional and 402 non-interventional cardiologists completed the survey. The interventional cardiologists had significantly higher incidence of body pain (56.6% vs. 24.2%, p

The basis generation in reduced order modeling usually requires multiple high-fidelity large-scale simulations that could take a huge computational cost. In order to accelerate these numerical simulations, we introduce a FOM/ROM hybrid approach in this paper. It is developed based on an a posteriori error estimation for the output approximation of the dynamical system. By controlling the estimated error, the method dynamically switches between the full-order model and the reduced-oder model generated on the fly. Therefore, it reduces the computational cost of a high-fidelity simulation while achieving a prescribed accuracy level. Numerical tests on the non-parametric and parametric PDEs illustrate the efficacy of the proposed approach., Comment: 17 pages, 10 figures

We present a hybrid-mixed finite element method for a novel hybrid-dimensional model of single-phase Darcy flow in a fractured porous media. In this model, the fracture is treated as an $(d-1)$-dimensional interface within the $d$-dimensional fractured porous domain, for $d=2, 3$. Two classes of fracture are distinguished based on the permeability magnitude ratio between the fracture and its surrounding medium: when the permeability in the fracture is (significantly) larger than in its surrounding medium, it is considered as a {\it conductive} fracture; when the permeability in the fracture is (significantly) smaller than in its surrounding medium, it is considered as a {\it blocking} fracture. The conductive fractures are treated using the classical hybrid-dimensional approach of the interface model where pressure is assumed to be continuous across the fracture interfaces, while the blocking fractures are treated using the recent Dirac-$\delta$ function approach where normal component of Darcy velocity is assumed to be continuous across the interface. Due to the use of Dirac-$\delta$ function approach for the blocking fractures, our numerical scheme allows for nonconforming meshes with respect to the blocking fractures. This is the major novelty of our model and numerical discretization. Moreover, our numerical scheme produces locally conservative velocity approximations and leads to a symmetric positive definite linear system involving pressure degrees of freedom on the mesh skeleton only. The performance of the proposed method is demonstrated by various benchmark test cases in both two- and three-dimensions. Numerical results indicate that the proposed scheme is highly competitive with existing methods in the literature.

Background: Myocardial ischemia reperfusion (I/R) is characterized by a complex inflammatory response that stimulates the formation of inflammasome and production of Interleukin-1β (IL-1β). As a decoy receptor for IL-1β, the role of Interleukin-1 receptor type 2 (IL-1R2) in myocardial I/R injury is still unclear. Here, for the first time, we report the underlying mechanisms of IL-1R2 in protecting cardiomyocyte against I/R injury. Methods: Initially, the expression of IL-1R2 in myocardial I/R injury was determined by RT-PCR and western blot assays. IL-1R2-deficiency mice and AAV-9 virus carrying IL-1R2 under cTnT promoter were administrated to identify the protective role of IL-1R2 and RNA-sequencing was performed to explore the underlying mechanisms of IL-1R2 in myocardial I/R injury. Besides, neonatal rat ventricular myocytes (NRVM) were isolated to investigate the relationships of IL-1R2, NLRP3 inflammasome and Interleukin 17 receptor A (IL-17RA). Findings: We demonstrated that the expression of IL-1R2 in cardiomyocyte was induced by I/R injury both in vivo and in vitro. IL-1R2-deficient mice decreased cardiac systolic function, increased infarct size and cardiomyocyte apoptosis. Whereas, Overexpression of IL-1R2 in cardiomyocyte protected cardiomyocyte against I/R-induced cell death through reducing the NLRP3 inflammasome activation and IL-17RA expression both in vivo and in vitro. Interpretation: Collectively, the upregulation of IL-1R2 in cardiomyocyte provides therapeutic effects in protecting cardiomyocyte against cell death during myocardial I/R injury. Funding: Natural Key Research and Development Project of Zhejiang Province, China (2018C03015), National Key Research and Development Program of China (2016YFC1102203), Zhejiang Provincial Natural Science Foundation of China under Grant (LQ17H020002). Declaration of Interests: The authors have declared that no conflict of interest exists. Ethics Approval Statement: The collection of blood plasma from AMI patients and healthy controls was conducted with approval from the Institutional Animal Care and Use Committee, and all animal studies were conducted with approval from the Medical Ethics Committee of Sir Run Run Shaw Hospital, Zhejiang University School of Medicine.

Anti-proliferative drugs released from drug-eluting stents delay cell coverage and vascular healing, which increases the risk of late stent thrombosis. We assessed the potential effects of systemic methotrexate (MTX) on cell coverage, vascular healing and inflammation activation in vivo and in vitro.We applied MTX in the right common carotid artery in a rabbit stenting model to determine the impact on cell coverage and inflammation activation using a serial optical coherence tomography (OCT) analysis and elucidated the molecular mechanism of MTX in human umbilical vein endothelial cells (HUVECs).Low-dose MTX promoted the development of cell coverage and vascular healing, which was associated with fewer uncovered struts (%) and cross-sections with any uncovered struts (%) at 4 weeks of stenting. The MTX group also exhibited lower rates of heterogeneity, microvessels and per-strut low-signal-intensity layers, indicating neointimal instability at 12 weeks of stenting. In vitro, low-dose MTX strongly inhibited HUVEC apoptosis, promoted proliferation and inhibited inflammatory activation by targeting the phosphoinositide 3-kinase (PI3K)/AKT signalling pathway.Low-dose MTX may be a key means of promoting early cell coverage via the inhibition of the inflammatory response and stability of neointima by targeting inflammatory pathways after stent implantation.

Introduction Heparin-induced thrombocytopenia (HIT) is immune-mediated thrombotic thrombocytopenia following the use of heparin, which contributes to a high limb-amputation rate and mortality if not appropriately handled. There is growing evidence suggesting that novel oral anticoagulants (NOACs) may be effective for treating HIT. Material and methods We described five rare cases of patients with HIT associated with deep vein thrombosis treated with dabigatran, a member of NOACs. We also reviewed representative cases and literature investigating the use of NOACs to treat patients with HIT to further discuss the efficacy and safety. Results and conclusions Following the treatment of dabigatran after argatroban, the platelet count of patients with HIT gradually elevated and reached the normal range eventually. There was no incidence of new symptomatic, objectively-confirmed arteriovenous thromboembolism observed within the 90-day-period follow up. The patient in case 3 presented with gastric bleeding after dabigatran treatment and died in the end. The results suggested that dabigatran use after argatroban may be effective in the treatment of patients with HIT. However, safety should be reconsidered since severe complications were observed in case 3.

We present a novel monolithic divergence-conforming HDG scheme for a linear fluid-structure interaction (FSI) problem with a thick structure. A pressure-robust optimal energy-norm estimate is obtained for the semidiscrete scheme. When combined with a Crank-Nicolson time discretization, our fully discrete scheme is energy stable and produces an exactly divergence-free fluid velocity approximation. The resulting linear system, which is symmetric and indefinite, is solved using a preconditioned MinRes method with a robust block algebraic multigrid (AMG) preconditioner., 26 pages

BACKGROUND β-blockers are indicated in several cardiovascular diseases. However, data are limited on their effect on the periprocedural myocardial injury (PMI) incidence. This study was designed to evaluate the impact of using β-blockers before elective percutaneous coronary intervention (PCI) on PMI incidence. METHODS This study included 4,027 patients who underwent elective PCI and had no elevated serum troponin I (TnI) or creatine kinase-MB (CK-MB) levels before PCI. Patients were divided into four groups based on gender and age (cut-off point 75 years). Serum TnI and CK-MB levels were measured before and every eight hours after the procedure. PMI was defined as postprocedural TnI or CK-MB ≥5 times the upper limits of normal (ULN) values. Logistic regression analysis including factors such as age, sex, prior β-blocker therapy, previous MI, length of implanted stents, characteristics of lesion and so on was performed to assess the effects of prior β-blocker therapy on the incidence of PMI. RESULTS In 2,332 male patients

BACKGROUND: Periprocedural myocardial infarction (PMI) after percutaneous coronary intervention (PCI) is associated with the bad prognosis in patients. Current approaches to predict PMI fail to identify many people who would benefit from preventive treatment, and machine learning (ML) offers opportunity to improve the performance of ML models for PMI based on the big routine data. METHODS: By using electronic medical records, we retrospectively extracted all records of patients from 2007 to 2019 in our cardiovascular center. The main enrollment criterion was that inpatients with one single coronary stenosis with stents implantation this time. The primary outcome was PMI [PMI3: cTnI >3-fold upper reference limit (URL); PMI5: cTnI >5-fold URL]. Four different ML algorithms [Support Vector Machine (SVM), Logistic Regression (LR), Random Forest (RF), Artificial Neural Networks (ANN)] were evaluated and their diagnostic accuracy measures were compared. RESULTS: A total of (10,886) patients who were admitted in our hospital. PMI3 and PMI5 results were analyzed respectively. The incidence of PMI3 and PMI5 was 20.9% and 13.7%. In PMI3 Drop group, ANN (accuracy: 0.72; AUC: 0.77) showed the best power to predict the presence of PMI; In PMI3 Mean Group, RF (accuracy: 0.72; AUC: 0.77) showed the best power; In PMI5 Drop group, RF (accuracy: 0.67; AUC: 0.67) showed the best power; In PMI5 Mean group, RF (accuracy: 0.61; AUC: 0.67) showed the best power. CONCLUSIONS: ML methods may provide accurate prediction of PMI in CAD patients, and could be used as a precise model in the preventive treatment of PMI.

Aims:Postoperative Atrial fibrillation (POAF) after esophagectomy may prolong stay in intensive care and increase risk of perioperative complications. A minimally invasive approach is becoming the preferred option for esophagectomy, yet its implications for POAF risk remains unclear. The association between POAF and minimally invasive esophagectomy (MIE) was examined in this study.Methods:We used a dataset of 575 patients who underwent esophagectomy. Multivariate logistic regression analysis was performed to examine the association between MIE and POAF. A cox proportional hazards model was applied to assess the long-term mortality (MIE vs open esophagectomy, OE).Results:Of the 575 patients with esophageal cancer, 62 developed POAF. MIE was negatively associated with the occurrence of POAF (Odds ratio: 0.163, 95%CI: 0.033-0.801). No significant difference was observed in long-term mortality (Odds ratio: 2.144, 95%CI: 0.963-4.775).Conclusions:MIE may reduced the incidence of POAF without compromising the survival of patients with esophageal cancer. Moreover, the specific mechanism of MIE providing this possible advantage needs to be determined by larger prospective cohort studies with specific biomarker information from laboratory tests.

BackgroundBoth hemoglobin A1c (HbA1c) levels and visit-to-visit variability of lipid profiles are risk factors for cardiovascular disease (CVD). We conducted a retrospective cohort study to explore the relationship between HbA1c and lipid variability.MethodsWe retrospectively collected baseline and follow-up data on patients who underwent elective percutaneous coronary intervention (PCI) from January 2009 to April 2019. Univariate and multivariate linear regression analyses were performed to assess the association between HbA1c and lipid variability. Subgroup analyses employed multivariate linear regression analyses.ResultsA total of 4,445 patients were enrolled in the study. The median age and value of HbA1c were 64yrs old and 5.9%, respectively, 64% had hypertension and 25.5% diabetes. The variability of low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), total cholesterol (TC), and triglyceride (TG) was each significantly higher in patients with HbA1c≥6.5% than those with HbA1c＜6.5% group. Multivariate linear regression indicated that HbA1c level was a potential risk factor for the variability of LDL-C, non-HDL-C, TC and TG, which was independent of the mean values of lipids. Subgroup analyses demonstrated that the relationship between HbA1c and the variability of LDL-C, non-HDL-C, TC, and TG did not importantly vary across several subgroups. These results remained consistent when lipid variability was represented by the standard deviation (SD), coefficient of variation (CV) and variability independent of the mean (VIM), respectively.ConclusionHbA1c is a potential risk factor for the variability of LDL-C, non-HDL-C, TC and TG in patients undergoing elective PCI.

Background To investigate the causal association between serum 25-hydroxyvitamin D (25OHD), calcium (Ca), and parathyroid hormone (PTH) levels and the risk of coronary artery disease (CAD) in patients with diabetes using a Mendelian randomization approach. Methods Genetic signatures associated with serum 25OHD, Ca, and PTH levels were extracted from recently published genome-wide association study (GWAS), including 79,366, 39,400, 29,155 individuals, respectively. Genetic association estimates for CAD in patients with diabetes were obtained from a GWAS of 15,666 individuals with diabetes (3,968 CAD cases, 11,696 controls). The inverse-variance-weighted method was employed for the primary analysis, and other robust methods were applied for sensitivity analyses. Results Six, seven and five single nucleotide polymorphisms were identified as instrumental variables for serum 25OHD, Ca and PTH levels, respectively. There was no significant association between genetically predicted serum 25OHD levels and the risk of CAD in patients with diabetes (odds ratio (OR) = 1.04, 95% confidence interval (CI): 0.58 - 1.87, P = 0.888). Similarly, genetically predicted serum Ca (OR = 1.83, 95% CI: 0.62 – 5.35, P = 0.273) and PTH levels (OR = 1.27, 95% CI: 0.67 – 2.44, P = 0.464) were not significantly associated with the risk of CAD in patients with diabetes. These findings were robust in sensitivity analyses. Conclusions/interpretation Serum 25OHD, Ca and PTH levels may not be causally associated with the risk of CAD in patients with diabetes.

Introduction: Septal mass reduction is beneficial for hypertrophic obstructive cardiomyopathy (HOCM) patients with severe left ventricular outflow (LVOT) gradient and symptoms, with surgical myectomy or alcohol septal ablation (ASA) currently recommended in selected patients. Radiofrequency (RF) ablation of hypertrophied septum has been published as a novel method to alleviate LVOT obstruction in small populations. This study aims to investigate factors influencing clinical outcomes of radiofrequency septum ablation. Methods and results: In this study, twenty patients with HOCM who underwent endocardial ablation were included. Echocardiography and cardiac MRI (CMR) data was collected and analyzed pre- and (or) post- procedure. Nineteen patients underwent ablation successfully, while ablation was aborted in one patient with prior RBBB due to transient complete atrioventricular block (AVB). After six months of follow-up, NYHA heart functional class improved from III (2 - 3) to II (1 - 2) (p < 0.001), and resting LVOT gradient was significantly reduced (87.6 ± 29.5 mmHg vs. 48.1 ± 29.7, p < 0.001). LVOT gradient reduction was significantly higher in patients with limited basal septal hypertrophy (60.9 ± 8.3 vs. 27.9 ± 7.1, p = 0.01), shorter anterior mitral leaflet (56.1 ± 6.4 vs. 20.4 ± 5.0, p

Background: Atrial remodeling is a common pathological change in atrial fibrillation (AF), while the mechanism of atrial remodeling remains unclear. In the present study, we investigated the autophagy and collagen secretion in atrial fibroblasts in response to renin-angiotensin system (RAS) activation and elucidated the relationship between atrial fibroblast autophagy and atrial remodeling. Methods: Right atrial tissues was obtained from patients that underwent cardiac valve replacement after signed the informed consent form. In vivo, subcutaneous perfusion of angiotensin II (Ang II) was used to mimic activation of the RAS and induce atrial remodeling. Electrical remodeling and AF induction were assessed by electrophysiology and programmed stimulation. In vitro, atrial fibroblasts were isolated and cultured. Autophagic flux changes were assessed by mCherry‑GFP‑LC3 adenovirus transfection. All samples were collected, collagen expression, autophagy changes and atrial remodeling were evaluated by western blot, masson’s trichrome staining, immunohistochemistry and immunofluorescence mainly.Results: Atrial tissue samples from patients with atrial fibrillation showed more collagen deposition and enhanced autophagy than those with sinus rhythm. Chronic subcutaneous Ang II perfusion in mice promoted atrial remodeling and susceptible to AF induction. In cultured atrial fibroblasts, the expression of collagen I (COL-I) and collagen III (COL-III) and autophagy both increased when cells were treated with Ang II, and the autophagic flux was enhanced by Ang II. However, blocking autophagy reduced the expression of COL-I and COL-III. Besides, Ang II induced the phosphorylation of ERK and suppressed the phosphorylation of mTOR. In contrast, inhibition of the angiotensin II type 1 receptor (AT1) or ERK signaling pathway not only suppressed the autophagy induced by Ang II but also reduced COL-I and COL-III expression. Conclusions: In summary, these results suggest that Ang II promotes autophagy in atrial fibroblasts, which aggravates atrial remodeling and increases the susceptibility to AF induction. Autophagy may be a potential target for relieving atrial remodeling and AF after RAS activation.

Transcatheter aortic valve replacement (TAVR) induced pathological damage in cardiac conduction system leads to symptomatic bradycardia and electric dyssynchrony such as left bundle branch block (LBBB) is associated with an increased risk for heart failure. Left bundle branch pacing (LBBP) has emerged as an alternative method for delivering physiological pacing to achieve electrical synchrony of the left ventricle. We report a case of heart failure patient with new onset left bundle branch block (NO-LBBB) induced by TAVR, LBBP corrected the NO-LBBB and reversed the heart function with stable capture and correction threshold. This article is protected by copyright. All rights reserved.

OBJECTIVE: To investigate the prognosis of patients with vulnerable plaque indicated by coronary CT angiography (CCTA). METHODS: Totally 1963 patients underwent CCTA from February 2nd 2015 to September 13th 2015, and 2728 coronary borderline lesions (stenosis of 50%-70%) were detected. Among them 804 patients had vulnerable plaques and 1159 patients had stable plaques. The primary endpoint was major cardiac adverse events (MACE), including cardiac death, acute myocardial infarction and target lesion revascularization. RESULTS: Patients were followed up for a mean follow-up of 27.4±2.3 months. The incidence of MACE in the vulnerable plaque group was significantly higher than that in the stable plaque group (10.8%vs 2.3%, P < 0.01). After adjusting for age, gender, smoking, hypertension, diabetes, hyperlipidemia, the MACE hazard ratio ( HR) in the vulnerable plaque group was 5.022 (95% CI:3.254-7.751, P < 0.01).Subgroup analysis showed that in the vulnerable plaque group, the incidence of MACE in patients taking antiplatelet and statin ≤3 months and those taking antiplatelet and statin > 3 months was 17.0%and 5.8%, respectively ( HR=3.149, 95% CI:1.987-4.992, P < 0.01); but the difference did not seen in stable plaque group ( HR=1.721, 95% CI:0.798-3.712, P>0.05). CONCLUSION: This study confirmed the risk of MACE in patients with vulnerable plaque detected by CCTA and the drug treatment may reduce the risk for patients with vulnerable plaque.

Background Although several observational studies have shown an association between birth weight (BW) and atrial fibrillation (AF), controversy remains. In this study, we aimed to explore the role of elevated BW on the etiology of AF. Methods A two-sample Mendelian randomization (MR) study was designed to infer the causality. The genetic data on the associations of single nucleotide polymorphisms (SNPs) with BW and AF were separately obtained from two large-scale genome-wide association study with up to 321,223 and 1,030,836 individuals respectively. SNPs were identified at a genome-wide significant level (p-value − 8). The inverse variance-weighted (IVW) with fixed effects method was performed to obtain causal estimates as our primary analysis. MR-Egger regression was conducted to assess the pleiotropy and sensitivity analyses with various statistical methods were applied to evaluate the robustness of the results. Results In total, 122 SNPs were identified as the genetic instrumental variables. MR analysis revealed a causal effect of elevated BW on AF (OR = 1.21, 95% CI = 1.13–1.29, p-value = 2.39 × 10− 8). The MR-Egger regression suggested no evidence of directional pleiotropy (intercept = 0.00, p-value = 0.62). All the results in sensitivity analyses were consistent with the primary result, which confirmed the causal association between BW and AF. Conclusions The findings from the two-sample MR study indicate a causal effect of elevated BW on AF. This suggests a convenient and effective method to ease the burden of AF by reducing the number of newborns with elevated BW.

Vascular stiffening occurs with advanced age and under pathological conditions such as vascular calcification, during which the osteogenesis of smooth muscle cells (SMCs) plays a key role. However, whether the stiffness of cellular microenvironment influences osteogenic responses in vascular SMCs is not well understood. Here, we cultured SMCs on the poly(dimethylsiloxane) (PDMS) substrates with varying stiffness from 0.363 to 2.327 MPa. The cell osteogenic transdifferentiation was induced by β-glycerophosphate. Our findings demonstrated that the extent of osteogenesis in SMCs varied with the substrate stiffness. On three substrate stiffness, cells on the intermediate one (0.909 MPa) showed the highest extent of the osteogenesis based on the expression of osteogenic markers and calcium deposition. Transforming growth factor-β1 and autophagy were involved in this stiffness-dependent process. This work highlights the importance of substrate stiffness to the osteogenesis of vascular SMCs, giving new scientific information for understanding of SMCs-mediated vascular calcification and designing of vascular implants.

Background Atherosclerosis is associated with chronic inflammation and lipid metabolism. The neutrophil to lymphocyte ratio (NLR) as an indicator of inflammation has been confirmed to be associated with cardiovascular disease prognosis. However, few studies have explored the effects of blood lipid variability on NLR. The aim of this study was to explore the relationship between variability in blood lipid levels and NLR. Methods The association between variability in blood lipids and NLR was assessed with both univariate and multivariate linear regression. Multivariate linear regression was also performed for a subgroup analysis. Results The variability of high-density lipoprotein cholesterol (HDL-C) (regression coefficients [β] 4.008, standard error (SE) 0.503, P-valueP-valueP-valueP-value Conclusion The variability of HDL-C and LDL-C are risk factors for the value and variability of NLR, while the relationship between variability of HDL-C and NLR is more stable than the variability of LDL-C in the subgroup analysis, which provides a new perspective for controlling inflammation in patients undergoing PCI.

Myocardial ischemia/reperfusion (MI/R) injury, a complicated pathophysiological process, is regulated by lots of signaling pathways. Here in our present study, we identified TANK-binding kinase 1 (TBK1), an IKK-related serine/threonine kinase, as a protective regulator in MI/R injury. Our results indicated that TBK1 was decreased in MI/R injury in mice. However, after overexpressing TBK1 through an intramyocardial injection of TBK1 adenovirus, TBK1 overexpression improved cardiac function detected by echocardiography, decreased infarct size detected by Evans Blue and TTC staining, reduced cardiomyocyte apoptosis measured by TUNEL staining and alleviated disruption of mitochondria and cardiac muscle fibers detected by TEM in response to MI/R injury. Consistently, TBK1 overexpression ameliorated mitochondrial oxygen consumption rate (OCR) in neonatal rat cardiomyocytes (NRCMs) in response to hypoxia/reoxygenation (H/R) injury. Mechanistically, TBK1 overexpression upregulated Bcl-2 (an anti-apoptotic protein) but downregulated Bax (a pro-apoptotic protein) in vivo and in vitro. Collectively, our findings uncovered a pivotal function of TBK1 in MI/R injury through regulating the levels of apoptotic proteins for the first time, which might represent a promising target in treating MI/R patients in the future.

Vascular remodeling is one of the most critical complications caused by hypertension. Previous studies have demonstrated that rosuvastatin has anti-inflammatory, antioxidant, and antiplatelet effects and therefore can be used to treat cardiovascular disease. In this study, we explored the beneficial effects of rosuvastatin in reversing aortic remodeling in spontaneously hypertensive rats. After treating with different doses of rosuvastatin, its antilipid, antiapoptosis, and anti-inflammatory effects were determined. We also examined whether rosuvastatin can improve the structure and function of the aorta. We found that rosuvastatin treatment of spontaneously hypertensive rats for 2 months at 2 different doses can effectively reduce the media thickness of the aorta compared with the control group. Similarly, rosuvastatin improved the vascular relaxation function of the aortic rings at a high level of acetylcholine in vitro. Mechanistically, it was found that rosuvastatin increased the expression of endothelial nitric oxide synthase and plasma nitrite/nitrate levels. Besides, rosuvastatin suppressed the apoptosis and inflammation and upregulated the expression of gap-junction complex connexin 43 both in media and endothelium. Finally, rosuvastatin inhibited the AT1R/PKCα/HSP70 signaling transduction pathway. In summary, these findings demonstrated that rosuvastatin could improve the vascular structure and function mainly by increasing endothelial nitric oxide synthase expression and preventing apoptosis and inflammation. This study provided evidence that rosuvastatin has beneficial effects in reversing the remodeling of the aorta due to hypertension.

Background and Objective Peripherally inserted central catheter (PICC) is a novel drug delivery mode which has been widely used in clinical practice. However, long-term retention and some improper actions of patients may cause some severe complications of PICC, such as the drift and prolapse of its catheter. Clinically, the postoperative care of PICC is mainly completed by nurses. However, they cannot recognize the correct position of PICC from X-ray chest images as soon as the complications happen, which may lead to improper treatment. Therefore, it is necessary to identify the position of the PICC catheter as soon as these complications occur. Here we proposed a novel multi-task deep learning framework to detect PICC automatically through X-ray images, which could help nurses to solve this problem. Methods We collected 348 X-ray chest images from 326 patients with visible PICC. Then we proposed a multi-task deep learning framework for line segmentation and tip detection of PICC catheters simultaneously. The proposed deep learning model is composed of an extraction structure and three routes, an up-sampling route for segmentation, an RPNs route, and an RoI Pooling route for detection. We further compared the effectiveness of our model with the models previously proposed. Results In the catheter segmentation task, 300 X-ray images were utilized for training the model, then 48 images were tested. In the tip detection task, 154 X-ray images were used for retraining and 20 images were used in the test. Our model achieved generally better results among several popular deep learning models previously proposed. Conclusions We proposed a multi-task deep learning model that could segment the catheter and detect the tip of PICC simultaneously from X-ray chest images. This model could help nurses to recognize the correct position of PICC, and therefore, to handle the potential complications properly.

Background During ablation for atrial fibrillation (AF), energy delivery toward the left atrial posterior wall may cause esophageal injury (EI). Ablation index (AI) was introduced to estimate ablation lesion size, however, the impact of AI technology on the risk of EI has not been explored. Method From March 2019 to December 2019, 60 patients with paroxysmal AF undergoing first-time ablation were prospectively enrolled. The first 30 consecutive patients were ablated with the AI target value of 400 (AI-400 group), and the later 30 consecutive patients were ablated with the AI target value of 350 at the posterior wall (AI-350 group). Endoscopic ultrasonography was used to evaluate EI postablation. EI was classified as a category 1 (erythema or erosion) or a category 2 (hematoma or ulceration). Results Compared with the AI-400 group (59.9 ± 8.4 years; male, 60%), the AI-350 group (59.1 ± 9.9 years; male, 50%) had a lower incidence of EI (3.3% vs 26.7%, P = .03). There was no significant difference in the percentage of first-pass PVI between the AI-400 group and the AI-350 group (left PVI: 80% vs 73.4%, P = .54; right PVI: 80% vs 60%, P = .1). Neither ablation time nor fluoroscopy time was significantly different between the AI-400 group and the AI-350 group. Conclusions AF ablation guide by AI target value of 350 may reduce esophageal thermal injury and has a similar efficiency on the acute success rate of first-pass PVI compared with an AI target value of 400 at the posterior wall.

Background Contrast induced diabetic nephropathy (CIN) is an important cause of hospital-acquired acute renal failure. Our aim was to observe the effect of protein kinase C β2 (PKCβ2) knockdown on human proximal tubular epithelial cells (HK-2 cells) against meglumine diatrizoate and advanced glycation end products (AGEs)-induced apoptosis and autophagy. Methods Cell viability was detected using cell counting kit-8 (CCK-8) assay in HK-2 cells after disposal with meglumine diatrizoate and AGEs with or without PKCβ2 siRNA/inhibitor LY333531. Flow cytometry and western blot were used to test cell apoptosis and the related protein levels in meglumine diatrizoate and AGEs co-treated HK-2 cells with or without PKCβ2 siRNA/inhibitor LY333531. Autophagy related proteins were detected using western blot. Immunofluorescence staining was used to examine the autophagy-specific protein light chain 3 (LC3), and autophagosome and autolysosome formation was observed under a transmission electron microscopy. Results CCK-8 assay results showed that meglumine diatrizoate inhibited AGEs-induced HK-2 cell viability. Furthermore, meglumine diatrizoate promoted cell apoptosis and the expression level of caspase3 in AGEs-induced HK-2. Western blot results showed that meglumine diatrizoate elevated the expression levels of PKCβ2 and p-PKCβ2 in AGEs-induced HK-2 cells, and up-regulated the expression level of Beclin-1 and the ratio of LC3 II/LC3 I, and down-regulated the expression level of p62 in AGEs-induced HK-2 cells. We found that PKCβ2 knockdown alleviated meglumine diatrizoate and AGEs-induced HK-2 cell apoptosis and autophagy. Intriguingly, PKCβ2 inhibitor LY333531 reversed 3-methyladenine (3-MA)-induced autophagy inhibition in meglumine diatrizoate and AGEs-induced HK-2 cells. Conclusions Our findings reveal that inhibiting PKCβ2 protects HK-2 cells against meglumine diatrizoate and AGEs-induced apoptosis and autophagy, which provide a novel therapeutic insight for CIN in diabetic patients.

We construct a divergence-free HDG scheme for the Cahn-Hilliard-Navier-Stokes phase field model. The scheme is robust in the convection-dominated regime, produce a globally divergence-free velocity approximation, and can be efficiently implemented via static condensation. Two numerical benchmark problems, namely the rising bubble problem, and the Rayleigh-Taylor instability problem are used to show the good performance of the proposed scheme., 15 pages

Background Atherosclerosis is associated with chronic inflammation and lipid metabolism. The neutrophil to lymphocyte ratio (NLR) as an indicator of inflammation has been confirmed to be associated with cardiovascular disease prognosis. However, few studies have explored the effects of blood lipid variability on NLR. We aimed to explore the relationship between variability in blood lipid levels and NLR. Methods The association between variability in blood lipids and NLR was assessed with both univariate and multivariate linear regression. Multivariate linear regression was also performed for a subgroup analysis. Results The variability of HDL-C ([ꞵ] 4.008, SE 0.503, p-value

BACKGROUND Contraction of the esophagus was observed during cryoablation for paroxysmal atrial fibrillation (PAF). The purpose of this study is to investigate the mechanism of esophageal contraction and the correlation between the contraction and esophageal thermal lesions. METHODS This prospective study enrolled 64 patients with PAF undergoing second-generation cryoballoon (CB2) ablation for pulmonary vein isolation (PVI). During PVI for the left inferior pulmonary vein, contrast esophagography was performed before and during cryoablation. The sample population was divided into two groups: A (31 patients) and B (33 patients). Group A consisted of patients in whom the distal half of the CB was in proximity to the esophagus, while for group B the esophagus was away from the distal half of the CB. Esophageal contraction was recorded as a variation in the width of the esophageal lumen during PVI. Postablation esophageal endoscopy was done on all patients. RESULTS The reduction in the width of the esophageal lumen in group A was greater than in group B during freezing (40.12 ± 23.24% vs 8.14 ± 10.35%, P

Background: Serum uric acid (SUA) is strongly associated with hypertension and is associated with a variety of cardiovascular diseases. In this study we aimed to investigate the predictive effect of SUA and blood pressure on the left atrial (LA) size in Chinese south population. Methods: In this cross-sectional study, we investigated the association between SUA and LA diameter and studied the risk of LA enlargement among subjects with and without hyperuricemia (HU) in different grades of blood pressure in a single-center database (n=5392). Results: The LA diameter was significantly correlated with SUA(r=0.31, P

Background and aims Human vascular smooth muscle cells (HA-VSMCs) are an important cell type involved in atherosclerosis. Low density lipoprotein (LDL) is a lipoprotein particle that carries cholesterol into peripheral tissue cells, and oxidized modified LDL (ox-LDL) is a well-known inducer of the atherosclerosis-related phenotype switch in VSMCs, leading to the occurrence of atherosclerosis. Accumulating studies have revealed that long non-coding RNAs (lncRNAs) mediate the effect of ox-LDL on the atherosclerosis-related biological activities of HA-VSMCs, including proliferation, migration, and apoptosis. However, the mechanism of small nucleolar RNA host gene 12 (SNHG12) in ox-LDL-induced phenotype switch of VSMCs remains unclear. Thus, this research dug in whether SNHG12 mediated the influence of ox-LDL on HA-VSMCs and the potential mechanism. Methods Fundamental experiments and functional assays were performed to measure the function of SNHG12 on HA-VSMCs. Then, mechanism assays and rescue assays were performed to study the regulatory mechanism of SNHG12 in HA-VSMCs. Results SNHG12 reversed the influence of ox-LDL treatment in enhancing cell proliferative and migratory abilities and weakening apoptotic ability in HA-VSMCs. SNHG12 was a competitive endogenous RNA (ceRNA) competing with sprouty RTK signaling antagonist 2 (SPRY2) to bind to miR-1301-3p, thus up-regulating SPRY2 expression in ox-LDL-treated HA-VSMCs. Besides, SNHG12 recruited serine and arginine rich splicing factor 1 (SRSF1) to stabilize negative regulator of ubiquitin like proteins 1 (NUB1) expression. Conclusions This study illustrated that SNHG12 inhibited cell proliferation, migration and facilitated cell apoptosis in ox-LDL-induced HA-VSMCs by up-regulating SPRY2 and NUB1.

We present a reduced order method (ROM) based on proper orthogonal decomposition (POD) for the viscous Burgers' equation and the incompressible Navier-Stokes equations discretized using an implicit-explicit hybrid discontinuous Galerkin/discoutinuous Galerkin (IMEX HDG/DG) scheme. A novel closure model, which can be easily computed offline, is introduced. Numerical results are presented to test the proposed POD model and the closure model., Comment: 19 pages

The auxiliary space preconditioning (ASP) technique is applied to the HDG schemes for three different elliptic problems with a parameter dependent low order term, namely, a symmetric interior penalty HDG scheme for the scalar reaction-diffusion equation, a divergence-conforming HDG scheme for a vectorial reaction-diffusion equation, and a C 0 -continuous interior penalty HDG scheme for the generalized biharmonic equation with a low order term. Uniform preconditioners are obtained for each case and the general ASP theory by J. Xu [21] is used to prove the optimality with respect to the mesh size and uniformity with respect to the low order parameter., Comment: 22 pages

Additional file 1: Table S1. Adjusted odds ratio of postoperative atrial fibrillation in sensitivity analysis.

We present a new set of basis functions for H(curl)-conforming, H(div)-conforming, and L2 -conforming finite elements of arbitrary order on a tetrahedron. The basis functions are expressed in terms of Bernstein polynomials and augment the natural H1 -conforming Bernstein basis. The basis functions respect the differential operators, namely, the gradients of the high-order H1 -conforming Bernstein-Bezier basis functions form part of the H(curl)-conforming basis, and the curl of the high-order, non-gradients H(curl)-conforming basis functions form part of the H(div)-conforming basis, and the divergence of the high-order, non-curl H(div)-conforming basis functions form part of the L2-conforming basis. Procedures are given for the efficient computation of the mass and stiffness matrices with these basis functions without using quadrature rules for (piece-wise) constant coefficients on affine tetrahedra. Numerical results are presented to illustrate the use of the basis to approximate representative problems., Comment: 27 pages

Objective It is controversial whether preprocedural elevated high sensitivity C-reactive protein (CRP) could increase the incidence of periprocedural myocardial infraction (PMI) of higher risk stratifications. The primary aim of this study was to evaluate whether preoperative elevated CRP level was related to the incidence of PMI in patients who underwent percutaneous coronary intervention (PCI). Methods A total of 4,426 patients [66 y (59, 75); 72.3% males] with normal preprocedural cardiac enzymes were prospectively divided into two groups; the elevated CRP group was defined as CRP >3 mg/L, which was approximately 30.4% of the patients. The relationship between CRP and the incidence of PMI was established by multivariate logistic regression analysis, and multivariate linear regression analysis was used to assess the correlation between CRP and the severity of myocardial injury. Results The incidence rates were similar between the two groups with periprocedural myocardial minor necrosis (34.23% versus 32.74%, p=0.607), but significantly differed based on the 2007 (defined as cardiac enzymes >3-fold elevations), 31.25% in high CRP group versus 26.25% in low group [odds ratio (OR) 1.19; p=0.046] and the 2012 universal PMI (defined as cardiac enzymes >5-fold elevations with at least one clinical evidence, such as chest pain, ECG changes or imaging diagnosis of heart ischemia), 19.79% versus 15.35% (OR 1.26, p=0.023); besides, the PMI ratios increased in line with the elevation of CRP (p=0.006 for the 2007 and p=0.011 for the 2012 universal PMI). However, no significant linear relationship was found between CRP and high sensitivity cardiac troponin I peak post-PCI. Conclusion Elevated baseline CRP was an independent risk factor for the incidence of the 2007 and the 2012 universal PMI rather than minor necrosis. However, CRP may not correlate with the severity of minor myocardial necrosis in patients with PMI.