Diabetic conditions promote drug coating degradation but prevent endothelial coverage after stenting.

The endothelialization of drug-eluting stents is delayed after implantation in patients with diabetes. Although numerous factors were implicated in hyperglycemia-induced endothelial dysfunction, the effects of stent drug coating degradation on endothelial dysfunction remains unclear. We hypothesized that diabetic conditions promote drugcoating degradation and enhance antiproliferative agent release, but that the rapid release of these antiproliferative agents inhibits endothelial cell proliferation leading to poor reendothelialization post-stenting. To verify this hypothesis, a dynamic hyperglycemic circulation system was introduced to measure the profile of drugcoating degradation in vitro. Flow cytometry and RNA sequencing were performed to evaluate endothelial cell proliferation. Moreover, a Type 1 diabetic rabbit model was generated and a rescue experiment conducted to evaluate the effects of rapid drugcoating elution on endothelial coverage in vivo. The main findings were as follows: 1) diabetic conditions promoted drugcoating degradation and increased antiproliferative agent release; 2) this increase in antiproliferative agent release inhibited endothelial cell proliferation and delayed endothelial coverage; and 3) strict glycemic control attenuated drugcoating degradation and promoted endothelial coverage post-stenting. This is the first study to illustrate rapid drugcoating degradation and its potential effects on endothelial recovery under diabetic conditions, highlighting the importance of strict glycemic management in patients with diabetes after drug-eluting stent implantation. STATEMENT OF SIGNIFICANCE: Diabetic conditions promote drug coating degradation and increase the release of antiproliferative agents. Rapid drug coating degradation under diabetic conditions inhibits endothelial cell proliferation and delays endothelialization. Strict glycemic control attenuates drug coating degradation and promotes endothelialization.

The left adrenal vein: An important direction for right adrenal venous sampling.

This study aimed to evaluate the guiding role of left adrenal vein (LAV) for right adrenal venous sampling (AVS). A total of 347 patients who were diagnosed with primary aldosteronism (PA) and underwent successful AVS procedures from January 2020 to July 2021 were retrospectively analyzed. According to the different quadrant position of the orifice of right adrenal vein (RAV), the area where the orifice of RAV is located is divided into three areas: A, B, and C and the area A is further subdivided into A1, A2, and A3 areas. By counting the area where the orifice of RAV is located, the guiding role of the LAV on the RAV is determined. Most of the orifice of RAV are located in area A, and the proportions of areas A, B, and C was 96.8%, 1.4%, and 1.7%, respectively. In area A, areas A1, A2, and A3 account for 80.9%, 17.0%, and 2.1%, respectively. High body mass index, female and smaller the angle between the LAV and horizontal line was associated with the closer positional relationship between the LAV on the RAV. These findings suggest that most of the horizontal position of the RAV orifice is close to the horizontal position of the most distal end of the LAV, which indicate that the LAV location can play an important role on the guiding for right AVS. Additionally, body mass index, sex, and the angle of the LAV was largely related to location of the orifice of the RAV.

Corroded iron stent increases fibrin deposition and promotes endothelialization after stenting.

Poststent restenosis is caused by insufficient endothelialization and is one of the most serious clinical complications of stenting. We observed a rapid endothelialization rate and increased fibrin deposition on the surfaces of the corroded iron stents. Thus, we hypothesized that corroded iron stents would promote endothelialization by increasing fibrin deposition on rough surfaces. To verify this hypothesis, we conducted an arteriovenous shunt experiment to analyze fibrin deposition in the corroded iron stents. We implanted a corroded iron stent in both the carotid and iliac artery bifurcations to elucidate the effects of fibrin deposition on endothelialization. Co-culture experiments were conducted under dynamic flow conditions to explore the relationship between fibrin deposition and rapid endothelialization. Our findings indicate that, from the generation of corrosion pits, the surface of the corroded iron stent was rough, and numerous fibrils were deposited in the corroded iron stent. Fibrin deposition in corroded iron stents facilitates endothelial cell adhesion and proliferation, which, in turn, promotes endothelialization after stenting. Our study is the first to elucidate the role of iron stent corrosion in endothelialization, pointing to a new direction for preventing clinical complications caused by insufficient endothelialization.

Iron corroded granules inhibiting vascular smooth muscle cell proliferation.

In-stent restenosis after interventional therapy remains a severe clinical complication. Current evidence indicates that neointimal hyperplasia induced by vascular smooth muscle cell (VSMC) proliferation is a major cause of restenosis. Thus, inhibiting VSMC proliferation is critical for preventing in-stent restenosis. The incidence of restenosis was reduced in nitrided iron-based stents (hereafter referred to as iron stents). We hypothesized that the corroded granules produced by the iron stent would prevent in-stent restenosis by inhibiting VSMC proliferation. To verify this hypothesis, we introduced a dynamic circulation device to analyze the components of corroded granules. To investigate the effects of corroded granules on VSMC proliferation, we implanted the corroded iron stent into the artery of the atherosclerotic artery stenosis model. Moreover, we explored the mechanism underlying the inhibition of VSMC proliferation by iron corroded granules. The results indicated that iron stent produced the corroded granules after implantation, and the main component of the corrosion granules was iron oxide. Remarkably, the corroded granules reduced the neointimal hyperplasia in an atherosclerotic artery stenosis model, and iron corroded granules decreased the neointimal hyperplasia by inhibiting VSMC proliferation. In addition, we revealed that corroded granules reduced VSMC proliferation by activating autophagy through the AMPK/mTOR signaling pathway. Importantly, safety of iron corroded granules was evaluated and proved to be satisfactory hemocompatibility in rabbit model. Overall, the role of corroded granules in restenosis prevention was described for the first time. This finding highlighted the implication of corroded granules produced by iron stent in inhibiting VSMC proliferation, pointing to a new direction to prevent in-stent restenosis.

Clinical Features Differ Between Patients With Vertigo Attack Only and Weakness Attack Accompanying Vertigo Before Vertebrobasilar Stroke: A Retrospective Study.

Objective: To determine the different clinical features of patients with vertigo attacks alone and of those with weakness accompanying vertigo attacks before the vertebrobasilar ischemic stroke. Methods: In this 4-year retrospective study, we manually screened the medical records of 209 patients, hospitalized with vertigo attack as the main complaint who were finally diagnosed with acute vertebrobasilar ischemic stroke. Patients were divided into two groups according to their symptoms: patients who only experienced vertigo attacks prior to the vertebrobasilar stroke (VO group) and patients who had both vertigo and weakness attacks (VW group) prior to the stroke. Clinical parameters, such as infarction site and volume, relative risk factors, ABCD2 score, and medical intervention, were compared between the two groups. Results: The prevalence of hypertension was higher in the Vertigo attacks only (VO) group (42.2 vs. 29.0%, p < 0.05). The total cerebral infarction volume in the VO group was larger than the Vertigo and weakness attacks (VW) group (4.44 vs. 2.12 cm3, p < 0.05). Additionally, the cerebellum was more likely to be affected in the VO group. In contrast, patients in the VW group had higher carotid stenosis (14.2 vs. 27.2%, p < 0.05) and ABCD2 score (2.1 ± 1.2 vs. 3.6 ± 1.5, p = 0.02). The percentage of patients with medullary infarctions also increased in the VW group. Vertigo attack events occurred more frequently in the VW group (median 2.4 vs. 4.3, p < 0.04). We also found that the patients in the VW group were more likely to seek medical intervention after vertigo. Conclusions: Clinical parameters, such as infarction location, relative risk factors, and ABCD2 score, differed between patients with vertigo symptoms with or without weakness attacks. These findings highlight the different clinical features of patients with vertigo attack only and those with weakness attacks accompanying vertigo prior to vertebrobasilar ischemic stroke.

Transcriptome Analysis Reveals the Role of Cellular Calcium Disorder in Varicella Zoster Virus-Induced Post-Herpetic Neuralgia.

As a typical neuropathic pain, post-herpetic neuralgia (PHN) is a common complication of herpes zoster (HZ), which seriously affects the normal life and work of patients. The unclear pathogenesis and lack of effective drugs make the clinical efficacy of PHN unsatisfactory. Here, we obtained the transcriptome profile of neuroblastoma cells (SH-SY5Y) and DRG in rats infected with varicella zoster virus (VZV) by transcriptome sequencing (RNA-Seq) combined with publicly available gene array data sets. Next, the data processing of the transcriptome map was analyzed using bioinformatics methods, including the screening of differentially expressed genes (DEGs), Gene Ontology (GO), and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Finally, real-time fluorescent quantitative PCR (qRT-PCR) was used to detect the expression of calcium-related genes, and calcium fluorescent probes and calcium colorimetry were used to evaluate the distribution and content of calcium ions in cells after VZV infection. Transcriptome data analysis (GO and KEGG enrichment analysis) showed that calcium disorder played an important role in SH-SY5Y cells infected by VZV and dorsal root ganglion (DRG) of the PHN rat model. The results of qRT-PCR showed that the expression levels of calcium-related genes BHLHA15, CACNA1F, CACNG1, CHRNA9, and STC2 were significantly upregulated, while the expression levels of CHRNA10, HRC, and TNNT3 were significantly downregulated in SH-SY5Y cells infected with VZV. Our calcium fluorescent probe and calcium colorimetric test results showed that VZV could change the distribution of calcium ions in infected cells and significantly increase the intracellular calcium content. In conclusion, our results revealed that the persistence of calcium disorder caused by VZV in nerve cells might be a crucial cause of herpetic neuralgia, and a potential target for clinical diagnosis and treatment of PHN.

Immune Checkpoint Inhibitors Combined With Chemotherapy Compared With Chemotherapy Alone for Triple-Negative Breast Cancer: A Systematic Review and Meta-Analysis.

BACKGROUND: It is still controversial whether immune checkpoint inhibitors (ICIs) can improve the curative effect when added to original standard chemotherapy treatment for triple-negative breast cancer (TNBC). We compared their antitumor efficacy and adverse effects (AEs) to make a better clinical decision. METHODS: Seven databases were searched for eligible articles. Progression-free survival (PFS), overall survival (OS), and AEs were measured as the primary outcomes. RESULTS: Nine randomized controlled trials (RCTs) involving 4,501 patients were included. ICI+chemotherapy treatment achieved better PFS (hazard ratio [HR]: 0.78, [0.70-0.86], p < 0.00001), OS (HR: 0.86, [0.74-0.99], p = 0.04), and complete response (584/1,106 vs. 341/825, risk ratio [RR]: 1.38, [1.01-1.89], p = 0.04). With the prolongation of survival, the survival advantage of ICI+chemotherapy increased compared with chemotherapy. Subgroup analysis suggested that the addition of ICIs might not have a better effect in Asian patients, patients with locally advanced disease, or patients with brain metastases. In the toxicity analysis, more Grade 3-5 AEs and serious AEs were found in the ICI+chemotherapy group. For Grade 3-5 AEs, more cases of diarrhea, severe skin reactions, pneumonitis, hepatitis, and adrenal insufficiency were related to the ICI+chemotherapy group. CONCLUSIONS: ICI+chemotherapy appears to be better than chemotherapy alone for TNBC treatment, with better OS and PFS. However, its high rates of serious AEs need to be taken seriously. SYSTEMATIC REVIEW REGISTRATION: PROSPERO Registration: CRD42021276394.

ICAM-1 deletion delays the repair process in aging diabetic mice.

BACKGROUND: The delayed repair process in the aging diabetic population is becoming an alarming public health concern. ICAM-1 plays an important role in orchestrating the repair process by mediating neutrophil recruitment and phagocytosis. However, little is known about the role of ICAM-1 in aging diabetic repair. METHODS: By causing injury in aging diabetic mice with ICAM-1 deletion (AD-ICAM-1-/-), we found that AD-ICAM-1-/- mice exhibited a delayed repair process with incomplete re-epithelialization and reduced angiogenesis. Additionally, high-throughput Illumina sequencing was performed to evaluate the microbiota of such mice. RESULTS: The results indicate that the microbiota of the AD-ICAM-1-/- injury site differed taxonomically at both the phylum and genus levels. Neutrophil recruitment and phagocytic function were also reduced in the AD-ICAM-1-/- group. Notably, major inflammatory biomarker expression was also detected in AD-ICAM-1-/- injured tissue. CONCLUSIONS: Overall, this study demonstrated that AD-ICAM-1-/- mice exhibit delayed repair. In addition, neutrophil recruitment and phagocytic activity were impaired in the AD-ICAM-1-/- group, which may have allowed microbes to colonize the injury site.

Hyperglycemia Decreases Epithelial Cell Proliferation and Attenuates Neutrophil Activity by Reducing ICAM-1 and LFA-1 Expression Levels.

Delayed repair is a serious public health concern for diabetic populations. Intercellular adhesion molecule 1 (ICAM-1) and Lymphocyte function-associated antigen 1 (LFA-1) play important roles in orchestrating the repair process. However, little is known about their effects on endothelial cell (EC) proliferation and neutrophil activity in subjects with hyperglycemia (HG). We cultured ECs and performed a scratch-closure assay to determine the relationship between ICAM-1 and EC proliferation. Specific internally labeled bacteria were used to clarify the effects of ICAM-1 and LFA-1 on neutrophil phagocytosis. Transwell assay and fluorescence-activated cell sorting analysis evaluated the roles of ICAM-1 and LFA-1 in neutrophil recruitment. ICAM-1+/+ and ICAM-1-/- mice were used to confirm the findings in vivo. The results demonstrated that HG decreased the expression of ICAM-1, which lead to the low proliferation of ECs. HG also attenuated neutrophil recruitment and phagocytosis by reducing the expression of ICAM-1 and LFA-1, which were strongly associated with the delayed repair.

Association between Radiation Exposure and Endothelium-Dependent Vasodilation: Results from Clinical and Experimental Studies.

PURPOSE: The association between occupational radiation exposure and endothelium-dependent vasodilation (EDV) remains unclear. This study evaluated the association between radiation exposure and EDV among fluoroscopy-guided interventional procedure specialists and explored the possible mechanisms. MATERIALS AND METHODS: Brachial flow-mediated dilation was compared in 21 interventional cardiologists (the radiation group) and 15 noninterventional cardiologists (the nonradiation group). Animal radiation experiments were also performed to observe the impact of radiation on EDV. RESULTS: Flow-mediated dilation in both the left (radiation group, 3.63% vs. nonradiation group, 6.77%; P < .001) and right brachial arteries (5.36% vs. 7.33%, respectively; P = .04) and serum nitric oxide (NO) level (343.69 vs. 427.09 µmol/L, respectively; P = .02) were significantly reduced in the radiation group compared to those in the nonradiation group. EDV was significantly impaired in acetylcholine concentrations of 3 × 10-6 mol/L and 10-5 mol/L (60.09% vs.74.79%, respectively; P = .03; and 62.73% vs. 80.56%, respectively; P = .002), and reactive oxygen species levels in the aorta intima and media layers were significantly increased in mice after a single x-ray exposure, which could be partly rescued by pretreatment with folic acid (P < .05). CONCLUSIONS: Radiation exposure can lead to impairment of flow-mediated vasodilation in human or EDV in mice. In mice acutely exposed to radiation, folic acid alleviated radiation-induced EDV impairment by possible reduction of reactive oxidative species.

Genetic analysis of porcine productive and respiratory syndrome virus between 2013 and 2014 in Southern parts of China: identification of several novel strains with amino acid deletions or insertions in nsp2.

BACKGROUND: Porcine respiratory and reproductive syndrome virus (PRRSV) is one of the most economically significant pathogens in the Chinese swine industry. ORF5 and nsp2 are highly variable regions of the PRRSV genome. Therefore, nsp2 and GP5 are often selected for investigation of variations and phylogenetic analyses for their genetic diversities. Knowledge of the molecular evolution of PRRSV field strains may contribute to the control of PRRS in China. RESULTS: The results of multiple sequence alignments of GP5 showed that there is 84.5-100% aa identity among the 56 strains in this study. These strains shared 84.5-99.0% aa identity with the prototypical type 2 PRRSV VR-2332 and 56.6-59.2% with strain LV, prototypical type 1 PRRSV. Phylogenetic analysis showed there is considerable diversity among PRRSV ORF5 and the existence of two lineages (5 and 8). Most of the strains were classified into lineage 8 with multiple sub-lineages (3, 4 and 6). Moreover, PRRSV strains with 5 novel patterns of deletions or insertions in the nsp2 region were found. CONCLUSIONS: Phylogenetic analysis based on ORF5 sequences indicated the diversity of PRRSV in southern parts of China and the strains with 30 aa deletion in nsp2 are dominant in the porcine population. Also, new PRRSV strains with different patterns of deletions or insertions in nsp2 are emerging. The data presented here constitute a useful basis for further epidemiological studies regarding the heterogeneity of PRRSV strains in China and provide a basis for the prevention of PRRS in southern parts of China.

Relationship of obesity to adverse events in myocardial infarction patients without primary percutaneous coronary intervention: results from the Occluded Artery Trial (OAT).

Objective: Our goal was to investigate the "obesity paradox" in myocardial infarction populations without primary percutaneous coronary intervention (PPCI).Methods: The Occluded Artery Trial (OAT, Clinicaltrials.gov: NCT00004562) is a randomized, multicenter study to investigate the influence of routine percutaneous coronary intervention (PCI) on the clinical outcomes of myocardial infarction patients without PPCI. We stratified these patients into three groups according to body mass index (BMI): normal, 18.5 kg/m2 ≤ BMI < 25 kg/m2; overweight, 25 kg/m2 ≤ BMI < 30 kg/m2; obese, BMI ≥ 30 kg/m2. The purpose of our study was to investigate the effects of BMI on the primary endpoint (all-cause mortality) and the secondary endpoint (cardiac death, non-cardiac death or New York Heart Association [NYHA] class IV heart failure) in the population enrolled in the OAT.Results: A total of 2153 patients (99.4%) constituted the final study population. We found that obese patients were younger and were more likely to have cardiovascular risk factors compared with other BMI groups. A U-shaped relationship was observed between BMI and all-cause mortality. The adjusted hazard ratios (HRs) were 0.892 (95% CI: 0.658-1.210, p = .460) for normal weight patients and 0.671 (95% CI: 0.508-0.888, p = .013) for overweight patients compared with obese patients. The same pattern was also observed for non-cardiac death. The adjusted HRs were 0.919 (95% CI: 0.601-1.40, p = .663) for normal weight patients and 0.524 (95% CI: 0.346-0.792, p = .004) for overweight patients compared with obese patients. We did not find any statistical differences among BMI categories in terms of cardiac death or NYHA class IV heart failure.Conclusions: A U-shaped relationship was observed between BMI and all-cause mortality or non-cardiac death. Overweight patients have the lowest risk of all-cause mortality, which may be attributed to their having the lowest risk of non-cardiac death of the groups studied.

Diagnostic performance of qfr for the evaluation of intermediate coronary artery stenosis confirmed by fractional flow reserve

Abstract Introduction: Quantitative flow ratio (QFR) is a novel method enabling efficient computation of FFR from three-dimensional quantitative coronary angiography (3D QCA) and thrombolysis in myocardial infarction (TIMI) frame counting. We decided to perform a systematic review and quantitative meta-analysis of the literature to determine the correlation between the diagnosis of functionally significant stenosis obtained by QFR versus FFR and to determine the diagnostic accuracy of QFR for intermediate coronary artery stenosis. Methods: We searched PubMed, Embase, and Web of Science for studies concerning the diagnostic performance of QFR. Our meta-analysis was performed using the DerSimonian and Laird random effects model to determine sensitivity, specificity, positive likelihood ratio (LR+), negative likelihood ratio (LR-), and diagnostic odds ratio (DOR). The sROC was used to determine diagnostic test accuracy. Results: Nine studies consisting of 1175 vessels in 1047 patients were included in our study. The pooled sensitivity, specificity, LR+, LR-, and DOR for QFR were 0.89 (95% CI: 0.86-0.92), 0.88 (95% CI: 0.86-0.91), 6.86 (95% CI,: 5.22-9.02), 0.14 (95% CI: 0.10-0.21), and 53.05 (95% CI: 29.75-94.58), respectively. The area under the summary receiver operating characteristic (sROC) curve for QFR was 0.94. Conclusion: QFR is a simple, useful, and noninvasive modality for diagnosis of functional significance of intermediate coronary artery stenosis.

Weight change is associated with increased all-cause mortality and non-cardiac mortality among patients with type 2 diabetes mellitus.

BACKGROUND: It is unclear whether changes in weight affect subsequent adverse events in patients with type 2 diabetes mellitus (T2DM) already at high risk of cardiovascular disease (CVD). METHODS AND RESULTS: This is a post hoc analysis of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study data to examine the relationship between changes in weight and adverse events. Patients were divided into groups based on changes in body mass index (BMI): stable weight, gain or loss of BMI ≤1.5 kg/m2; moderate weight gain, BMI gain of 1.5-5 kg/m2; pronounced weight gain, BMI gain >5 kg/m2; moderate weight loss, BMI loss of 1.5-5 kg/m2; and pronounced weight loss, BMI loss >5 kg/m2. The primary endpoint of the present study was all-cause mortality. Secondary endpoints were cardiac death, non-fatal myocardial infarction (MI), and non-cardiac mortality. A total of 9372 T2DM patients with a mean follow-up of 8.08 ± 3.00 years were included for analysis. The average change in weight across the entire study population was 1.80 ± 9.00%, representing ~0.448 ± 2.98 kg/m2. Patients with pronounced weight loss had the highest risk of all-cause mortality (hazard ratio (HR) 2.07, 95% confidence interval (CI): 1.68-2.55), followed by patients with pronounced weight gain (HR 1.23, 95% CI: 1.02-1.56); patients with stable weight had the lowest risk. An asymmetric V-shaped relationship was observed between changes in BMI and all-cause mortality and non-cardiac mortality. Although no statistical significance was observed in terms of cardiac death and non-fatal MI, a flat V-shaped relationship may exist. CONCLUSIONS: Weight was stable in most T2DM patients with high risk of CVD. Weight loss and gain is associated with increased all-cause mortality and non-cardiac mortality. Pronounced weight loss and weight gain is associated with a slight increase in cardiac death and non-fatal MI incidence, which does not reach statistical significance.

Diagnostic Performance of QFR for the Evaluation of Intermediate Coronary Artery Stenosis Confirmed by Fractional Flow Reserve.

INTRODUCTION: Quantitative flow ratio (QFR) is a novel method enabling efficient computation of FFR from three-dimensional quantitative coronary angiography (3D QCA) and thrombolysis in myocardial infarction (TIMI) frame counting. We decided to perform a systematic review and quantitative meta-analysis of the literature to determine the correlation between the diagnosis of functionally significant stenosis obtained by QFR versus FFR and to determine the diagnostic accuracy of QFR for intermediate coronary artery stenosis. METHODS: We searched PubMed, Embase, and Web of Science for studies concerning the diagnostic performance of QFR. Our meta-analysis was performed using the DerSimonian and Laird random effects model to determine sensitivity, specificity, positive likelihood ratio (LR+), negative likelihood ratio (LR-), and diagnostic odds ratio (DOR). The sROC was used to determine diagnostic test accuracy. RESULTS: Nine studies consisting of 1175 vessels in 1047 patients were included in our study. The pooled sensitivity, specificity, LR+, LR-, and DOR for QFR were 0.89 (95% CI: 0.86-0.92), 0.88 (95% CI: 0.86-0.91), 6.86 (95% CI,: 5.22-9.02), 0.14 (95% CI: 0.10-0.21), and 53.05 (95% CI: 29.75-94.58), respectively. The area under the summary receiver operating characteristic (sROC) curve for QFR was 0.94. CONCLUSION: QFR is a simple, useful, and noninvasive modality for diagnosis of functional significance of intermediate coronary artery stenosis.

Effects of ischaemic postconditioning on outcomes of patients with ST-segment elevation myocardial infarction who underwent primary percutaneous coronary intervention: a meta-analysis.

OBJECTIVE: The aim of this meta-analysis was to evaluate the effects of ischaemic postconditioning (IPC) therapy on hard clinical endpoints in ST-segment elevation myocardial infarction (STEMI) patients who underwent primary percutaneous coronary intervention (PPCI). DESIGN: Systematic review and meta-analysis to evaluate the effects of IPC on the outcomes of patients with STEMI. DATA SOURCES: PubMed, Embase and the Cochrane Library were systematically searched for relevant articles published prior to May 1, 2018. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Randomised trials comparing conventional PPCI to PPCI combined with IPC in STEMI patients were included. The primary endpoint was heart failure. Secondary endpoints were all-cause mortality and major adverse cardiac events (MACE), including cardiac death, heart failure and MI. The Cochrane Reviewer's Handbook 4.2 was used to assess the risk of bias. DATA EXTRACTION AND SYNTHESIS: Relevant data were extracted by two independent investigators. We derived pooled risk ratios (RRs) with random effects models. Sensitivity and subgroup analyses were performed. RESULTS: Ten studies that had enrolled 3137 patients were included. PPCI combined with IPC failed to reduce heart failure (RR: 0.88, 95% CI: 0.61 to 1.26, p=0.47; absolute risk: 3.64% in the IPC group and 4.11% in the PPCI only group), all-cause mortality (RR: 0.94, 95% CI: 0.69 to 1.27, p=0.68; absolute risk: 5.07% in the IPC group and 5.27% in the PPCI onlygroup), MACE (RR: 1.05, 95% CI: 0.83 to 1.32, p=0.69; absolute risk: 9.37% in the IPC group and 8.93% in the PPCI only group), cardiac death (RR: 1.28, 95% CI: 0.85 to 1.93, p=0.24; absolute risk: 4.28% in the IPC group and 3.25% in the PPCI only group) and MI (RR: 1.08, 95% CI: 0.38 to 3.12, p=0.88; absolute risk: 3.61% in the IPC group and 3.44% in the PPCI only group). CONCLUSIONS: IPC combined with PPCI does not reduce heart failure, MACE and all-cause mortality compared with traditional PPCI in patients with STEMI. TRIAL REGISTRATION NUMBER: CRD42017063959.

Risk assessment model for predicting ventricular tachycardia or ventricular fibrillation in ST-segment elevation myocardial infarction patients who received primary percutaneous coronary intervention.

Ventricular tachycardia/ventricular fibrillation (VT/VF) is a kind of malignant arrhythmia in ST-segment elevation myocardial infarction (STEMI) patients who received primary percutaneous coronary intervention (PPCI). However, there are no risk assessment tools to anticipate the occurrence of VT/VF.This study is to build a risk assessment model to predict the possibility of VT/VF onset in STEMI patients undergoing PPCI.A retrospective study was conducted to analyze the patients who underwent PPCI from January 2006 to May 2015. Subjects were divided into VT/VF group and no VT/VF group based on whether VT/VF had occurred or not. In addition, the VT/VF group was further separated into early-onset group (from the time that symptoms began to before the end of PPCI) and late-onset group (after the end of PPCI) based on the timing of when VT/VF happened. Multivariate regression analysis was carried out to distinguish the independent risk factors of VT/VF and an additional statistical method was executed to build the risk assessment model.A total of 607 patients were enrolled in this study. Of these patients, 67 cases (11%) experienced VT/VF. In addition, 91% (61) of patients experienced VT/VF within 48 h from the time that the symptoms emerged. Independent risk factors include: age, diabetes mellitus, heart rate, ST-segment maximum elevation, ST-segment total elevation, serum potassium, left ventricular ejection fraction (LVEF), culprit artery was right coronary artery, left main (LM) stenosis, Killip class > I class, and pre-procedure thrombolysis in myocardial infarction (TIMI) flow zero grade. Risk score model and risk rank model have been established to evaluate the possibility of VT/VF. Class I: ≤ 4 points; Class II: > 4 points, ≤ 5.5 points; Class III: > 5.5 points, < 6.5 points; and Class IV ≥ 6.5 points. The higher the class, the higher the risk.The incidence of VT/VF in STEMI patients undergoing PPCI is 11% and it occurs more frequently from the time that symptoms begin to before the end of PPCI, which, in most cases, occurs within 48 h of the event. Our risk assessment model could predict the possible occurrence of VT/VF.

Relationship of Obesity to Adverse Events Among Patients With Mean 10-Year History of Type 2 Diabetes Mellitus: Results of the ACCORD Study.

Background Recent evidence from cohort studies and meta-analyses suggests that the obesity paradox phenomenon may exist in patients with diabetes mellitus. The goal of this study was to assess the association between adverse events and obesity by using 2 different measures of obesity, body mass index (BMI; kg/m2) and waist circumference, in patients with a mean 10-year history of type 2 diabetes mellitus. Methods and Results We used data from the ACCORD (the Action to Control Cardiovascular Risk in Diabetes) study to evaluate the relationship between obesity and adverse events in patients with a mean 10-year history of type 2 diabetes mellitus. The primary outcome of this study was all-cause mortality. Secondary outcomes were cardiac death, nonfatal myocardial infarction, and stroke. Patients who were class III obese with BMI ≥40 had the highest risk of all-cause mortality, followed by patients with class II obesity, whereas overweight patients had the lowest risk. We found significant correlations between BMI and waist circumference ( r=0.802). We observed that the relationships between waist circumference and primary and second end points were much like the relationships between BMI and primary and second end points (J-shaped relationship for all-cause mortality, V-shaped relationship for cardiac death, U-shaped relationship for nonfatal myocardial infarction, and reverse linear relationship for noncardiac death). Conclusions No evidence of the obesity paradox was observed in patients with a 10-year history of diabetes mellitus. Class III obese patients showed the highest risk of adverse events (all-cause mortality, cardiac death, nonfatal myocardial infarction, and noncardiac death). BMI and waist circumference showed similar relationships with adverse events. Clinical Trial Registration URL : http://www.clinicaltrials.gov . Unique identifier: NCT 00000620.

Aortic stenosis complicated by cardiogenic shock treated by transcatheter aortic valve replacement with extracorporeal membrane oxygenation: A case report.

RATIONALE: Cardiogenic shock secondary to aortic stenosis (AS) is a challenging problem owing to the high mortality associated with treatment, and successful treatment of such patients has been rare. PATIENT CONCERNS: A 77-year-old man presented with exercise intolerance and progressive exertional dyspnea and chest pain. The patient was suffered from cardiogenic shock after percutaneous coronary intervention. DIAGNOSIS: He was diagnosed by transthoracic echocardiography (TTE) and coronary angiogram. His main diagnose was AS and coronary artery disease. INTERVENTION: The patient received venoarterial extracorporeal membrane oxygenation (VA-ECMO) and transcatheter aortic valve replacement (TAVR). OUTCOME: As of the 5-month follow-up, the patient was well, and capable of basic independent living. The TTE suggested that the left ventricular end-diastolic volume had decreased from 66 to 45 mm and the left ventricular ejection fraction had risen from 20% to 50%. LESSONS: Patients with cardiogenic shock secondary to AS are very difficult to treat medically. ECMO with TAVR may be a reasonable strategy.