The randomized controlled study aimed to examine the efficacy of preoperative ultrasound-guided erector spinae plane (ESP) block combined with ropivacaine in patients undergoing hepatectomy.

The aim of this study is to retrospectively analyze and evaluate the effect of transverse thoracic muscle plane (TTP) block as a routine analgesic strategy for cardiac enhanced recovery after surgery in sternotomy.Patients received TTP block after general anesthesia and tracheal intubation were included in this study. The baseline clinical data of the patients, intraoperative use of sufentanil, internal mammary artery separating time, the postoperative duration of invasive ventilation, visual analogue scale, the compression times of patient-controlled intravenous analgesia in the first 3 days after surgery, and postoperative nausea and vomiting were recorded.A total of 104 cases was included and divided to G group (without TTP block) and TTP group (with TTP). Sufentanil use (sufentanil dose/min, sufentanil dose/kg body weight, sufentanil dose/[min kg]) in TTP group was significantly lower than that of G group. In G group, intraoperative use of sufentanil was correlated to the duration of anesthesia (P = .035). The postoperative visual analogue scale pain scores and the compression times of patient-controlled intravenous analgesia in the TTP group were significantly decreased compared with G group (P < .01). The postoperative duration of invasive ventilation of patients with normal and mildly impaired pulmonary function was significantly correlated to the use of sufentanil (P = .027, .009).TTP block has certain analgesic effect and can reduce sufentanil use in medium-length cardiac surgery and postoperative use of opioids. It is indicated that TTP block can be used as a routine enhanced recovery after surgery strategy for sternotomy in cardiac surgery.

The effects of left bundle branch block (LBBB) on left ventricular myocardial metabolism have not been well investigated. This study evaluated these effects in patients with coronary artery disease (CAD).Sixty-five CAD patients with complete LBBB (mean age, 61.8 ± 9.7 years) and 65 without LBBB (mean age, 59.9 ± 8.4 years) underwent single photon emission computed tomography, positron emission tomography, and contrast coronary angiography. The relationship between myocardial perfusion and metabolism and reverse mismatch score, and that between QRS length and reverse mismatch score and wall motion score were evaluated.The incidence of left ventricular septum and anterior wall reverse mismatching between the two groups was significantly different (P < 0.001 and P = 0.002, respectively). The incidences of normal myocardial perfusion and metabolism in the left ventricular lateral and inferior walls were also significantly different between the two groups (P < 0.001 and P < 0.001, respectively). The incidence of septal reverse mismatching in patients with mild to moderate perfusion was significantly higher among those with LBBB than among those without LBBB (P < 0.001). In CAD patients with LBBB, septal reverse mismatching was significantly more common among those with mild to moderate perfusion than among those with severe perfusion defects (P = 0.002). The correlation between the septal reverse mismatch score and QRS length was significant (P = 0.026).In patients with CAD and LBBB, septal and anterior reverse mismatching of myocardial perfusion and metabolism was frequently present; the septal reverse mismatch score negatively correlated with the QRS interval.

Coronary heart disease (CHD) is a cardiovascular disease which is contributed by abnormal neovascularization. VEGFA (vascular endothelial growth factor A) and VEGFR2 (vascular endothelial growth factor receptor 2) have been revealed to be involved in the pathological angiogenesis. This study was intended to confirm whether single nucleotide polymorphisms (SNPs) of VEGFA and VEGFR2 were associated with CHD in a Chinese population, considering pathological features and living habits of CHD patients.Peripheral blood samples were collected from 810 CHD patients and 805 healthy individuals. Six tag SNPs within VEGFA and VEGFR2 were obtained from HapMap Database. Genotyping of SNPs was performed using SNapShot method (Applied Biosystems, Foster, CA). Odd ratios (ORs) and their 95% confidence intervals (95% CIs) were calculated to evaluate the association between SNPs and CHD risk.Under the allelic model, 6 SNPs of VEGFA and VEGFR2 were remarkably associated with the susceptibility to CHD. Genotype CT of rs3025039, TT of rs2305948, and AA of rs1873077 were associated with a reduced risk of CHD when smoking, alcohol intake and diabetes were considered, while homozygote GG of rs1570360 might elevate the susceptibility to CHD (all P < 0.05) for patients who were addicted to smoking or those with hypertension. All of the combined effects of rs699947 (CC/CA) and rs2305948 (TT), rs3025039 (TT) and rs2305948 (TT), rs3025039 (CT) and rs1870377 (AA) had positive effects on the risk of CHD, respectively (all P < 0.05). By contrast, the synthetic effects of rs69947 (CA/AA) and rs1870377 (TA), rs699947 (CA) and rs7667298 (GG), rs699947 (AA) and rs7667298 (GG), rs1570360 (GG) and rs2305948 (TT), as well as rs1570360 (GG) and rs1870377 (AA) all exhibited adverse effects on the risk of CHD, respectively (all P < 0.05).Six polymorphisms in VEGFA and VEGFR2 may have substantial influence on the susceptibility to CHD in a Han Chinese population. Prospective cohort studies should be further designed to confirm the above conclusions.

Polycyclic aromatic hydrocarbons (PAHs) may be 1 of etiologic factors responsible for congenital heart diseases (CHDs). Variations of the microsomal epoxide hydrolase (EPHX1) gene, as well as their possible interactions with PAHs exposure, may increase susceptibility to CHDs.This case-control study investigated the risk of CHDs in relation to the EPHX1 polymorphisms and assessed the interactions between these polymorphisms and PAHs exposure in 357 mothers of CHDs fetuses and 270 control mothers. Logistic regression models for the risk of CHDs were applied to determine the effect of genetic polymorphisms using additive, recessive, and dominant genetic models, as well as gene-exposure interactions. Multiple testing was adjusted by applying the false discovery rate (FDR).None of the maternal genetic polymorphisms of EPHX1 was associated with CHDs occurrence. Only the single nucleotide polymorphism rs1051740 was associated with an increased risk of right-sided obstructive malformations under the recessive model (adjusted odds ratio [aOR] = 1.852, 95% confidence interval [CI]: 1.065, 3.22) before FDR correction. A possible modifying effect of PAHs exposure on genetic polymorphisms of EPHX1 was found in susceptibility to CHDs, though no multiplicative-scale interactions between maternal exposure to PAHs and polymorphisms of EPHX1 gene were seento affect the risk of CHDs.The role of EPHX1 gene polymorphisms for CHDs need to be further evaluated, in particularly by interacting with PAHs exposure.

The effects of genetic variants on warfarin dosing vary among different ethnic groups, especially in the Chinese population. The objective of this study was to recruit patients through a rigorous experimental design and to perform a comprehensive screen to identify gene polymorphisms that may influence warfarin dosing in northern Han Chinese patients with mechanical heart valve replacement. Consenting patients (n = 183) with a stable warfarin dose were included in this study. Ninety-six single nucleotide polymorphisms (SNPs) in 30 genes involved in warfarin pharmacological pathways were genotyped using the Illumina SNP GoldenGate Assay, and their associations with warfarin dosing were assessed using univariate regression analysis with post hoc comparison using least significant difference analysis. Multiple linear regression was performed by incorporating patients' clinical and genetic data to create a new algorithm for warfarin dosing. From the 96 SNPs analyzed, VKORC1 rs9923231, CYP1A2 rs2069514, CYP3A4 rs28371759, and APOE rs7412 were associated with higher average warfarin maintenance doses, whereas CYP2C9 rs1057910, EPHX1 rs2260863, and CYP4F2 rs2189784 were associated with lower warfarin doses (P < 0.05). Multiple linear regression analysis could estimate 44.4% of warfarin dose variability consisting of, in decreasing order, VKORC1 rs9923231 (14.2%), CYP2C9*3 (9.6%), body surface area (6.7%), CYP1A2 rs2069514 (3.7%), age (2.7%), CYP3A4 rs28371759 (2.5%), CYP4F2 rs2108622 (1.9%), APOE rs7412 (1.7%), and VKORC1 rs2884737 (1.4%). In the dosing algorithm we developed, we confirmed the strongest effects of VKORC1, CYP2C9 on warfarin dosing. In the limited sample set, we also found that novel genetic predictors (CYP1A2, CYP3A4, APOE, EPHX1, CYP4F2, and VKORC1 rs2884737) may be associated with warfarin dosing. Further validation is needed to assess our results in larger independent northern Chinese samples.

In recent years, lymphocyte-to-monocyte ratio (LMR) has become a novel indirect marker of inflammation, which has been demonstrated to be associated with poor prognosis of oncology and cardiovascular disease. The aim of the study was to assess the relationship between LMR on admission and in-hospital and long-term major adverse cardiac and cerebrovascular events (MACCE) in patients with ST-elevated myocardial infarction (STEMI) after primary percutaneous coronary intervention (PCI).A total of 306 STEMI patients were enrolled and grouped according to tertiles of LMR from the blood samples obtained in the emergency room on admission. Total white blood cell count, differential count of neutrophil, lymphocyte, monocyte, and other factors were evaluated.The median follow-up period was 21 months (1-36 months). As the LMR decreased, in-hospital nonfatal myocardial infarction and cardiovascular mortality increased (P = .002, P = .009, respectively). And long-term stroke/TIA, TVR, nonfatal myocardial infarction, and cardiovascular mortality also increased with decreasing LMR (P = .012, P = .001, P = .003, P = .002, respectively). The receiver operating characteristic (ROC) curve of LMR for predicting MACCE showed the sensitivity of 76% and specificity of 78% and the optimal cut-off value was determined as 2.62. In multivariate analysis, after adjusting for confounders, LMR was an independent predictor of in-hospital and long-term MACCE (odds ratio [OR] 1.192 [1.069-1.315] P < .001, OR 1.239 [1.125-1.347] P < .001, respectively).The LMR is an independent predictor of in-hospital and long-term MACCE in patients with STEMI after primary PCI. Our results suggest that this simple, inexpensive, relatively available inflammatory marker may have significant effects on the treatment and prognosis in patients with STEMI.

Abnormal development of the atrioventricular ring can lead to the formation of a bypass pathway and the occurrence of Wolff-Parkinson-White (WPW) syndrome. The genetic mechanism underlying the sporadic form of WPW syndrome remains unclear. Existing evidence suggests that both T-box transcription factor 3 (TBX3) and T-box transcription factor 2 (TBX2) genes participate in regulating annulus fibrosus formation and atrioventricular canal development. Thus, we aimed to examine whether single-nucleotide polymorphisms (SNPs) in the TBX3 and TBX2 genes confer susceptibility to WPW syndrome in a Han Chinese Population. We applied a SNaPshot SNP assay to analyze 5 selected tagSNPs of TBX3 and TBX2 in 230 patients with sporadic WPW syndrome and 231 sex- and age-matched controls. Haplotype analysis was performed using Haploview software. Allele C of TBX3 rs1061657 was associated with a higher risk of WPW syndrome (odds ratio [OR] = 1.41, 95% confidence interval [CI]: 1.08-1.83, P = .011) and left-sided accessory pathways (OR = 1.40, 95% CI: 1.07-1.84, P = .016). However, allele C of TBX3 rs8853 was likely to reduce these risks (OR = 0.71, 95% CI: 0.54-0.92, P = .011; OR = 0.70, 95% CI: 0.53-0.92, P = .011, respectively). The data revealed no association between TBX3 rs77412687, TBX3 rs2242442, or TBX2 rs75743672 and WPW syndrome. TBX3 rs1061657 and rs8853 are significantly associated with sporadic WPW syndrome among a Han Chinese population. To verify our results, larger sample sizes are required in future studies.

Although supraclavicular brachial plexus block (SCBPB) was repopularized by the introduction of ultrasound, its usefulness in shoulder surgery has not been widely reported. The objective of this study was to compare motor and sensory blockades, the incidence of side effects, and intraoperative opioid analgesic requirements between SCBPB and interscalene brachial plexus block (ISBPB) in patients undergoing arthroscopic shoulder surgery. Patients were randomly assigned to 1 of 2 groups (ISBPB group: n = 47; SCBPB group: n = 46). The side effects of the brachial plexus block (Horner's syndrome, hoarseness, and subjective dyspnea), the sensory block score (graded from 0 [no cold sensation] to 100 [intact sensation] using an alcohol swab) for each of the 5 dermatomes (C5-C8 and T1), and the motor block score (graded from 0 [complete paralysis] to 6 [normal muscle force]) for muscle forces corresponding to the radial, ulnar, median, and musculocutaneous nerves were evaluated 20 min after the brachial plexus block. Fentanyl was administered in 50 μg increments when the patients complained of pain that was not relieved by the brachial plexus block. There were no conversions to general anesthesia due to a failed brachial plexus block. The sensory block scores for the C5 to C8 dermatomes were significantly lower in the ISBPB group. However, the percentage of patients who received fentanyl was comparable between the 2 groups (27.7% [ISBPB group] and 30.4% [SCBPB group], P = 0.77). SCBPB produced significantly lower motor block scores for the radial, ulnar, and median nerves than did ISBPB. A significantly higher incidence of Horner's syndrome was observed in the ISBPB group (59.6% [ISBPB group] and 19.6% [SCBPB group], P < 0.001). No patient complained of subjective dyspnea. Despite the weaker degree of sensory blockade provided by SCBPB in comparison to ISBPB, opioid analgesic requirements are similar during arthroscopic shoulder surgery under both brachial plexus blocks. However, SCBPB produces a better motor blockade and a lower incidence of Horner's syndrome than ISBPB.

The present study attempted to analyze the clinical characteristics and pathogenesis of Kawasaki disease (KD) in children with hyperbilirubinemia.A total of 390 children with KD hospitalized in our hospital from September 2018 to July 2019 were selected and divided into control (270 cases) and hyperbilirubinemia (120 cases) groups based on the total, direct, and indirect bilirubin values after admission. Clinical data of the inflammatory index and fever process of the 2 groups were analyzed and compared.The difference in sex and age between the 2 groups was statistically nonsignificant (P > .05). In the hyperbilirubinemia group, the white blood cell count, C-reactive protein, hemoglobin, platelet count, erythrocyte sedimentation rate, alanine aminotransferase, aspartate aminotransferase, albumin, and routine urine leucocyte; and incidence of coronary artery expansion, heart injury, and unreactive gamma globulin treatment were higher than those in the control group and the differences were statistically significant (P < .05). In the hyperbilirubinemia group, the mean fever duration before admission was shorter than that in the control group, whereas the fever duration after gamma globulin treatment was longer than that in the control group; these differences were statistically significant (P < .05).Hyperbilirubinemia incidence in children with KD was approximately 30.77% (120 cases), of which increased direct bilirubin was observed in 70.83% (85 cases) and increased indirect bilirubin in 29.17% (35 cases). Children with KD combined with hyperbilirubinemia exhibited a strong inflammatory reaction, which may be due to liver damage or biliary block.

While increased obesity prevalence among persons of African ancestry (AAs) compared to persons of European ancestry (EAs) is linked to social, environmental and behavioral factors, there are no gene variants that are common and significantly associated with obesity in AA populations. We sought to explore the association between ancestry specific renal risk variants in the apolipoprotein L1 (APOL1) gene with obesity related traits in AAs.We conducted a genotype-phenotype association study from 3 electronic medical record linked cohorts (BioMe Biobank, BioVU, nuGENE); randomized controlled trials (genetic testing to understand and address renal disease disparities) and prospective cohort study (Jackson Heart Study). We analyzed association of APOL1 renal risk variants with cross-sectional measures of obesity (average body mass index (BMI), and proportion of overweight and obesity) and with measures of body composition (in Jackson Heart Study).We had data on 11,930 self-reported AA adults. Across cohorts, mean age was from 42 to 49 years and percentage female from 58% to 75.3%. Individuals who have 2 APOL1 risk alleles (14% of AAs) have 30% higher obesity odds compared to others (recessive model adjusted odds ratio 1.30; 95% confidence interval 1.16-1.41; P = 2.75 × 10-6). An additive model better fit the association, in which each allele (47% of AAs) increases obesity odds by 1.13-fold (adjusted odds ratio 1.13; 95% confidence interval 1.07-1.19; P = 3.07 × 10-6) and increases BMI by 0.36 kg/m2 (∼1 kg, for 1.7 m height; P = 2 × 10-4). APOL1 alleles are not associated with refined body composition traits overall but are significantly associated with fat free mass index in women [0.30 kg/m2 increment per allele; P = .03].Thus, renal risk variants in the APOL1 gene, found in nearly half of AAs, are associated with BMI and obesity in an additive manner. These variants could, either on their own or interacting with environmental factors, explain a proportion of ethnic disparities in obesity.

Inflammation plays an important role in the pathogenesis of atherosclerosis. Recent studies indicate that macrophage migration inhibitory factor (MIF) is a potent proinflammatory cytokine which mediates the inflammatory process during atherosclerosis. The polymorphism of MIF gene (rs755622 [-173G/C], rs1007888, and rs2096525) were genotyped by TaqMan single nucleotide polymorphism (SNP) genotyping assay in 320 patients with coronary artery disease (CAD) and 603 controls in a Chinese Kazakh population. Coronary angiography was performed on all CAD patients and Gensini score was used to assess the severity of coronary artery lesions. The frequency of the CC genotype and C allele of rs755622 were significantly higher in CAD patients than that in control subjects (8.4% vs. 5.1%, P < 0.001, 30.3% vs. 22.1%, P < 0.001, respectively). Multivariate logistic regression analysis showed that individuals with CC genotype or C allele had a higher risk for CAD (CC genotype vs. GG genotype, OR = 2.224, 95% CI, 1.239-3.992, P = 0.007, and C allele vs. G allele, OR = 1.473, 95% CI, 1.156-1.876, P = 0.002, respectively). Moreover, CAD patients with rs755622 C allele (CC + CG genotype) have higher levels of Gensini score when compared to C allele noncarriers (32.74 ± 26.66 vs. 21.44 ± 19.40, P < 0.001, adjusted). Our results suggested that the CC genotype and C allele of MIF rs755622 SNP may be a genetic marker for the risk of CAD and potentially predict the severity of CAD in Chinese Kazakh population.

Matrix metalloproteinases-2 (MMP-2) plays an important role in the pathogenesis of type A aortic dissection (AD). The aim of this study was to evaluate the association of 3 single nucleotide polymorphisms (SNPs) in the MMP-2 gene with type A AD risk and aortic diameters in patients. We performed a case-control study with 172 unrelated type A AD patients and 439 controls. Three SNPs rs11644561, rs11643630, and rs243865 were genotyped through the MassARRAY platform. Allelic associations of SNPs and SNP haplotypes with type A AD and aortic diameters in patients were evaluated. The frequency of the G allele of the rs11643630 polymorphism was significantly lower in type A AD patients than in control subjects (odds ratio 0.705, 95% confidence interval 0.545-0.912, P = 0.008). The association remained significant after adjusting for clinical covariates (P = 0.008). Carriers of the GG genotype of the rs11643630 polymorphism had significantly smaller aortic diameters than those with GT genotype or TT genotype (P = 0.02). Further haplotype analysis identified 1 protective haplotype (GC; P = 0.008) for development of type A AD. Again, a significant correlation was observed between haplotype GC and AD size (P = 0.020). Our results suggest that MMP-2 gene polymorphisms contribute to type A AD susceptibility. In addition, MMP-2 gene SNPs are associated with AD size, which could be used as a target for the development of new drug therapy.

Sympathetic hyperactivation is one of the causes of postoperative ileus, which occurs frequently after abdominal surgery and adversely influences the patient's prognosis. We aimed to investigate whether dexmedetomidine (DEX) could attenuate postoperative ileus in patients undergoing laparoscopic gastrectomy. Ninety-two patients were randomized to the control (n = 46) or DEX group (n = 46). DEX was administered at a loading dose of 0.5 μg/kg for 10 minutes, followed by an infusion rate of 0.4 μg/kg/h from insufflation of the pneumoperitoneum to the end of surgery. The primary goal was to compare postoperative bowel movements by evaluating the time to first flatus. The balance of the autonomic nervous system, duration of postoperative hospital stay, and pain scores were assessed. The time to first flatus was shorter in the DEX group compared with the control group (67.2 ± 16.8 hours vs 79.9 ± 15.9 hours, P < 0.001). The low-frequency/high-frequency power ratio during pneumoperitoneum increased in the control group, compared with baseline values and the DEX group. The length of postoperative hospital stay was shorter in the DEX group compared with the control group (5.4 ± 0.7 days vs 5.8 ± 1.1 days, P = 0.04). Patients in the DEX group had lower pain scores and required fewer analgesics at 1 hour postoperatively. DEX facilitated bowel movements and reduced the length of hospital stay in patients undergoing laparoscopic gastrectomy. This may be attributed to the sympatholytic and opioid-sparing effects of DEX.

Kawasaki disease (KD) is a systemic vasculitis of unknown etiology. IFNG gene encoding interferon (IFN)-γ, produced by natural killer cells and T cells, has been suggested to play an important role in the immunopathogenesis of Kawasaki disease. The aim of this study was to examin the correlation of gene polymorphisms of the IFNG gene and plasma levels of IFN-γ in KD patients and their outcomes.A total of 950 subjects (381 KD and 569 controls) were recruited. Three tagging single-nucleotide polymorphisms (rs2069718, rs1861493, rs2069705) were selected for TaqMan allelic discrimination assay. Clinical phenotypes, coronary artery lesions (CAL), coronary artery aneurysms (CAA) and intravenous immunoglobulin (IVIG) treatment outcomes were collected for analysis. Plasma IFN-γ levels were also measured with an enzyme-linked immunosorbent assay.Polymorphisms of the IFNG gene were significantly different between the normal controls and KD patients. The G allele of rs1861493 conferred a better response to IVIG treatment in KD patients. AA allele frequencies of rs1861493 were also associated with a significantly higher risk of CAA in KD patients. Furthermore, the plasma IFN-γ level was lower in the AA allele than in the GG allele of rs1861493 both before and after IVIG treatment in KD patients.This study provides the first evidence supporting an association between IFNG gene polymorphisms, susceptibility of KD, IVIG responsiveness, and plasma IFN-γ levels in KD patients.

Radiofrequency catheter ablation (RFCA) is an established effective method for the treatment of typical cavo-tricuspid isthmus (CTI)-dependent atrial flutter (AFL). The introduction of 3-dimensional electro-anatomic systems enables RFCA without fluoroscopy (No-X-Ray [NXR]). The aim of this study was to evaluate the feasibility and effectiveness of CTI RFCA during implementation of the NXR approach and the maximum voltage-guided (MVG) technique for ablation of AFL.Data were obtained from prospective standardized multicenter ablation registry. Consecutive patients with the first RFCA for CTI-dependent AFL were recruited. Two navigation approaches (NXR and fluoroscopy based as low as reasonable achievable [ALARA]) and 2 mapping and ablation techniques (MVG and pull-back technique [PBT]) were assessed. NXR + MVG (n  =  164; age: 63.7 ± 9.5; 30% women), NXR + PBT (n  =  55; age: 63.9 ± 10.7; 39% women); ALARA + MVG (n  =  36; age: 64.2 ± 9.6; 39% women); and ALARA + PBT (n  =  205; age: 64.7 ± 9.1; 30% women) were compared, respectively. All groups were simplified with a 2-catheter femoral approach using 8-mm gold tip catheters (Osypka AG, Germany or Biotronik, Germany) with 15 min of observation. The MVG technique was performed using step-by-step application by mapping the largest atrial signals within the CTI.Bidirectional block in CTI was achieved in 99% of all patients (P  =  NS, between groups). In NXR + MVG and NXR + PBT groups, the procedure time decreased (45.4 ± 17.6 and 47.2 ± 15.7 min vs. 52.6 ± 23.7 and 59.8 ± 24.0 min, P < .01) as compared to ALARA + MVG and ALARA + PBT subgroups. In NXR + MVG and NXR + PBT groups, 91% and 98% of the procedures were performed with complete elimination of fluoroscopy. The NXR approach was associated with a significant reduction in fluoroscopy exposure (from 0.2 ± 1.1 [NXR + PBT] and 0.3 ± 1.6 [NXR + MVG] to 7.7 ± 6.0 min [ALARA + MVG] and 9.1 ± 7.2 min [ALARA + PBT], P < .001). The total application time significantly decreased in the MVG technique subgroup both in NXR and ALARA (P < .01). No major complications were observed in either groups.Complete elimination of fluoroscopy is feasible, safe, and effective during RFCA of CTI in almost all AFL patients without cardiac implanted electronic devices. The most optimal method for RFCA of CTI-dependent AFL seems to be MVG; however, it required validation of optimal RFCA's parameters with clinical follow-up.

The purpose was to identify the Transient receptor potential (TRP) superfamily gene variants associate with the prognosis of ischemic cardiomyopathy (ICM). A whole-exome sequencing study involving 252 ICM and 252 healthy controls participants enrolled from March 2003 to November 2017. Optimal sequence kernel association test and Cox regression dominant was conducted to identify the cause genes of TRP with ICM and association of common SNPs with prognosis of ICM. Rs224534 was verified in the replication population. Besides, the expression of TRPV1 was detectable in human failed heart ventricular tissues. The TRPs was not associated with the risk of ICM (P > .05). Rs224534 was significantly associated with the prognosis of ICM (Hazard ratio, 2.27, 95%CI: 1.31-3.94; P = 3.7 × 10-3), in the replication cohort, (hazard ratio 1.47, 95%CI: 1.04-2.07; P = 2.9 × 10-2), and in combined cohort hazard ratio 1.62 (95%CI: 1.21-2.18; P = 1.1 × 10-3). The common SNP of TRPV1 (rs224534) is associated with the prognosis of ICM, and homozygote rs224534-AA showed an unfavorable prognosis of ICM in the dominant model tested. Genotyping the variant may benefit to further progress judgment of ICM.

High-sensitivity troponin assay brought new challenges as we detect elevated concentration in many other diseases, and it became difficult to distinguish the real cause of this elevation. In this notion, diagnosis of acute coronary syndrome (ACS) remains a challenge in emergency department (ED). We aim to examine different approaches for rule-in and rule-out of ACS using risk scores, copeptin, and coronary computed tomography angiography (CCTA). A prospective observational study was designed to evaluate chest pain patients. Consecutive adult patients admitted to the ED with a chief complaint of chest pain due to any cause were included. All patients were followed-up for 6 months after discharge for major adverse cardiovascular events and readmissions. Admission data, ED processes, and diagnoses were analyzed. One hundred forty-six patients were included, average age was 63 ± 13.4 years, and 95 (65.1%) were male. Global Registry of Acute Coronary Events (GRACE) and History, ECG, Age, Risk factors, Troponin (HEART) scores showed good prognostic abilities, but HEART combination with copeptin improves diagnoses of myocardial infarction (area under the curve [AUC] 0.764 vs AUC 0.864 P = .0008). Patients with elevated copeptin were older, had higher risk scores, and were more likely to be admitted to hospital and diagnosed with ACS in ED. For copeptin, AUC was 0.715 (95% confidence interval 0.629-0.803), and for combination with troponin, AUC of 0.770 (0.703-0.855) did not improve rule-in of myocardial infarction. High-sensitivity troponin I assay alongside prior stroke, history of carotid stenosis, dyslipidemia, use of diuretics, and electrocardiogram changes (left bundle branch block or ST depression) are good predictors of myocardial infarction (χ² = 52.29, AUC = 0.875 [0.813-0.937], P < .001). The regression analysis showed that combination of copeptin and CCTA without significant stenosis can be used for ACS rule-out (χ² = 26.36, P < .001, AUC = 0.772 [0.681-0.863], negative predictive value of 96.25%). For rule-in of ACS, practitioner should consider not only scores for risk stratification but carefully analyze medical history and nonspecific electrocardiogram changes and even with normal troponin results, we strongly suggest thorough evaluation in chest pain unit. For rule-out of ACS combination of copeptin and CCTA holds great potential.

Disabled-2 (Dab2) is a clathrin and cargo-binding endocytic adaptor protein that plays a role in cellular trafficking of low-density lipoprotein receptor (LDLR). However, little is known about its involvement in coronary artery disease (CAD). Here, we aimed to investigate the association between Dab2 single-nucleotide polymorphisms (SNPs) and CAD in Chinese Han and Uyghur populations.We performed a case-control study in CAD group that consisted of 621 Han and 346 Uygurs, and the age and gender matched control group consisted of 611 Han and 405 Uygurs. The clinicopathological characteristics of these subjects were analyzed. Genotyping of 4 SNPs (rs1050903, rs2855512, rs11959928, and rs2255280) of the Dab2 gene was performed in all subjects with an improved multiplex ligase detection reaction method.The distribution of the genotype, dominant model (AA vs. AC + CC), as well as allele frequencies of both rs2855512 and rs2255280, was significantly different between CAD patients and control subjects in Han population but not in Uyghur population. AA genotype may be a risk factor for CAD. For Han population, statistical significant correlation between dominant model for both SNPs (AA) and CAD was found after multivariate adjustment. After multivariate adjustment in the Han population, we speculate that rs285512 A allele and rs2255280 A allele may be potentially associated with the onset of coronary heart disease. Individuals with the AA genotype had an OR of 1.44 (95% CI: 1.10-1.88, P = .01, rs2855512) and 1.41 (95% CI: 1.08-1.85, P = .01, rs2255280) for CAD compared with individuals with the AC or CC genotype, respectively.Our data indicates that the AA genotype of rs2855512 and rs2255280 in the Dab2 gene may be a genetic marker of CAD risk in Chinese Han population.

Asymptomatic myocardial injury following noncardiac surgery (MINS) is an independent predictor of 30-day mortality and may go unrecognized based on standard diagnostic definition for myocardial infarction (MI). Given lack of published research on MINS in India, our study aims to determine incidence of MINS in patients undergoing noncardiac surgery at our tertiary care hospital, and evaluate the clinical characteristics including 30-day outcome.The prospective observational study included patients >65 years or >45 years with either hypertension (HTN), diabetes mellitus (DM), coronary artery disease (CAD), cerebrovascular accident (CVA), or peripheral arterial disease undergoing noncardiac surgery. MINS was peak troponin level of ≥0.03 ng/dL at 12-hour or 24-hour postoperative. All patients were followed for 30 days postoperatively. Predictors of MINS and mortality were analyzed using multivariate logistic regression. Patients categorized based on peak troponin cut-off values determined by receiver operating characteristic curve were analyzed by Kaplan-Meir test to compare the survival of patients between the groups.Among 1075 patients screened during 34-month period, the incidence of MINS was 17.5% (188/1075). Patients with DM, CAD, or who underwent peripheral nerve block anaesthesia were 1.5 (P < .01), 2 (P < .001), and 12 (P < .001) times, respectively, more likely to develop MINS than others. Patients with heart rates ≥96 bpm before induction of anesthesia were significantly associated with MINS (P = .005) and mortality (P = .02). The 30-day mortality in MINS cohort was 11.7% (22/188, 95% CI 7.5%-17.2%) vs 2.5% (23/887, 95% CI 1.7%-3.9%) in patients without MINS (P < .001). ECG changes (P = .002), peak troponin values >1 ng/mL (P = .01) were significantly associated with mortality. A peak troponin cut-off of >0.152 ng/mL predicted mortality among MINS patients at 72% sensitivity and 58% specificity. Lack of antithrombotic therapy following MINS was independent predictor of mortality (P < .001), with decreased mortality in patients who took post-op ASA (Aspirin) or Clopidogrel. Mortality among MINS patients with post-op ASA intake is 6.7% vs 12.1% among MINS patients without post-op ASA intake. Mortality among MINS patients with post-op Clopidogrel intake is 10.5% vs 11.8% among MINS patients without post-op Clopidogrel intake.A higher (17.5%, 95% CI 15-19%) incidence of MINS was observed in our patient cohort with significant association with 30-day mortality. Serial postoperative monitoring of troponin following noncardiac surgery as standard of care, would identify "at risk" patients translating to improved outcomes.