Uncovering the flip side of immune checkpoint inhibitors: a comprehensive review of immune-related adverse events and predictive biomarkers.

Immune checkpoint inhibitors (ICIs) have generated considerable excitement as a novel class of immunotherapeutic agents due to their remarkable efficacy in treating various types of cancer. However, the widespread use of ICIs has brought about a number of safety concerns, especially the development of immune-related adverse events (irAEs). These serious complications could result in treatment discontinuation and even life-threatening consequences, making it critical to identify high-risk groups and predictive markers of irAEs before initiating therapy. To this end, the current article examines several potential predictive markers of irAEs in important organs affected by ICIs. While retrospective studies have yielded some promising results, limitations such as small sample sizes, variable patient populations, and specific cancer types and ICIs studied make it difficult to generalize the findings. Therefore, prospective cohort studies and real-world investigations are needed to validate the potential of different biomarkers in predicting irAEs risk. Overall, identifying predictive markers of irAEs is a crucial step towards improving patient safety and enhancing the management of irAEs. With ongoing research efforts, it is hoped that more accurate and reliable biomarkers will be identified and incorporated into clinical practice to guide treatment decisions and prevent the development of irAEs in susceptible patients.

Acute pulmonary embolism presenting with electrocardiographic signs and serum biomarkers of ST-segment elevation myocardial infarction: a case report.

Acute pulmonary embolism (APE) with ST-segment elevation and an upward T-wave is rare, and only a few cases have been reported to date. We herein present a case involving a man in his early 70s with an 8-hour history of dyspnea. Serial electrocardiography (ECG) demonstrated ST-segment elevation in leads V1 to V3 with an upward T-wave, laboratory tests revealed a high serum concentration of high-sensitivity cardiac troponin I, and signs of acute myocardial infarction were present. However, emergency coronary angiography revealed normal coronary arteries. A subsequent computed tomography scan of the pulmonary arteries showed findings consistent with APE. The patient's chest tightness was relieved after catheter-directed thrombolysis. Postoperative ECG showed that the ST-segment in leads V1 to V3 had fallen back and that the T-wave was inverted. The patient was discharged on rivaroxaban therapy. Clinically, the ECG findings of ST-segment elevation and an upward T-wave in APE can be easily misdiagnosed as acute myocardial infarction. Physicians should maintain clinical suspicion through risk stratification to identify APE.

Efficacy and safety of self-administered acupressure on symptoms, quality of life and nasal mucosal function in patients with perennial allergic rhinitis: study protocol for a randomized controlled exploratory trial.

INTRODUCTION: Allergic rhinitis is a global health problem that can potentially be managed through acupressure. Our clinical observations have identified Allergic Rhinitis Acupressure Therapeutic (ARAT) as a novel acupressure treatment acting on specific acupoints, which may enhance the effectiveness of acupressure. Therefore, we propose a three-arm randomized controlled trial will be conducted to investigate the efficacy and safety of ARAT for perennial allergic rhinitis (PAR). METHODS/DESIGN: In this trial, eligible 111 participants diagnosed with PAR will be randomly assigned to one of three groups: the ARAT group, the non-specific acupoints group, or the blank control group. The primary outcome will be the change in the total nasal symptom score, and the secondary outcomes will include: 1) changes in the scores of the standard version of Rhinoconjunctivitis Quality of Life Questionnaire (RQLQs); 2) acoustic rhinometry and anterior rhinomanometry; 3) changes in the scores of relief medication usage; 4) incidence of adverse events. Additionally, we will measure and compare the changes in cytokine levels (IL-5, IL-13, IFN-γ, and TSLP) in nasal secretions. The RQLQs and primary outcomes will be assessed at the beginning, middle, and end stages of the treatment period, with monthly follow-ups conducted over a total of three months. The secondary outcomes and biomarkers in nasal secretions will be measured at the beginning and end of the treatment period. Any adverse events or need for rescue medication will be carefully noted and recorded. DISCUSSION: This study may produce a new acupressure treatment prescription that is easy to learn, more targeted, and adaptable. This trial represents the first clinical investigation comparing ARAT treatment for PAR with the non-specific acupoints group and blank control group. Our data is expected to provide evidence demonstrating the safety and efficacy of ARAT for PAR patients, while also exploring the functional mechanism underlying ARAT treatment, moreover, the results offer valuable insights for healthcare professionals in managing PAR symptoms. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR2300072292. Registered on June 08, 2023.

Aldehyde dehydrogenase 2 and NOD-like receptor thermal protein domain associated protein 3 inflammasome in atherosclerotic cardiovascular diseases: A systematic review of the current evidence.

Inflammation and dyslipidemia underlie the pathological basis of atherosclerosis (AS). Clinical studies have confirmed that there is still residual risk of atherosclerotic cardiovascular diseases (ASCVD) even after intense reduction of LDL. Some of this residual risk can be explained by inflammation as anti-inflammatory therapy is effective in improving outcomes in subjects treated with LDL-lowering agents. NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome activation is closely related to early-stage inflammation in AS. Aldehyde dehydrogenase 2 (ALDH2) is an important enzyme of toxic aldehyde metabolism located in mitochondria and works in the metabolism of toxic aldehydes such as 4-HNE and MDA. Despite studies confirming that ALDH2 can negatively regulate NLRP3 inflammasome and delay the development of atherosclerosis, the mechanisms involved are still poorly understood. Reactive Oxygen Species (ROS) is a common downstream pathway activated for NLRP3 inflammasome. ALDH2 can reduce the multiple sources of ROS, such as oxidative stress, inflammation, and mitochondrial damage, thereby reducing the activation of NLRP3 inflammasome. Further, according to the downstream of ALDH2 and the upstream of NLRP3, the molecules and related mechanisms of ALDH2 on NLRP3 inflammasome are comprehensively expounded as possible. The potential mechanism may provide potential inroads for treating ASCVD.

Disaster Nursing Competency of Intensive Care Nurses in Jinan, China: A Multicenter Cross-Sectional Study.

BACKGROUND: Patients in disaster areas require the most urgent assistance. In recent large-scale natural disasters, intensive care nurses have served as an important reserve component of disaster response teams. In disaster nursing, ability and attitude directly affect the quality and effectiveness of disaster rescues. However, few studies have examined the disaster nursing competency of intensive care nurses in China. PURPOSE: This study was designed to describe the current status of disaster nursing competency among intensive care nurses, analyze the related factors affecting the disaster response effectiveness, and evaluate the values of disaster nursing continuing education and training in cultivating professional personnel with disaster emergency rescue competence. METHODS: This cross-sectional study was conducted at six tertiary general government hospitals in Jinan, Shandong Province, China. A convenience sampling method was adopted, and the Wenjuanxing website was used to compile the network questionnaire, which participants completed via a WeChat group. Descriptive, correlation, and regression analyses were performed using SPSS software. RESULTS: The participants in this study included 285 registered intensive care nurses employed at six hospitals in Jinan. Most were female (77.9%), and the mean age was 29.9 years. The mean total disaster nursing ability score was 122.98 (SD = 31.70), and the average scores for each item ranged from 2.78 to 3.70. The incident command system item earned the highest mean score (3.70, SD = 1.22), followed by triage (3.24, SD = 0.93). The biological preparedness item earned the lowest mean score (2.78, SD = 1.04). Being male, being < 30 years old, having an understanding of disaster nursing, having previously participated in disaster emergency simulation drills or training, and having a higher self-evaluation of rescue competence were all associated with higher disaster-nursing knowledge scores. Multiple linear regression analyses indicated that understanding of disaster nursing and experience participating in disaster emergency rescue drills or training had the most significant influence on the disaster nursing emergency knowledge score, followed by positive self-evaluation of disaster nursing ability and demand for training. CONCLUSIONS/IMPLICATIONS FOR PRACTICE: The findings of this study indicate that the participants had a moderate disaster-nursing competency and that this competency may be improved through disaster-related continuing education and training. The cognitive attitude of disaster nursing was found to correlate positively with self-efficacy. Simulated emergency drills may effectively improve the disaster nursing competency of critical care nurses. The findings emphasize that experiences other than direct clinical practice such as specialized simulated emergency drills and training as well as willingness for such training are stronger factors for identifying and developing overall disaster nursing competency.

Intracoronary Glycoprotein IIb/IIIa Inhibitors Improve Short-Term Mortality and Reinfarction in East Asian Patients with ST-Segment Elevation Myocardial Infarction after Thrombus Aspiration: A Meta-Analysis.

OBJECTIVE: Intracoronary (IC) glycoprotein IIb/IIIa inhibitors (GPIs) after thrombus aspiration (TA) for patients with ST-segment elevation myocardial infarction (STEMI), as compared with percutaneous coronary interventions (PCI) alone, is still on debate. To address this issue, we performed a meta-analysis of results from prospective or randomized controlled trials on the topic. METHODS: We searched electronic and printed sources (up to June 20, 2016) according to the selection criteria. Data were abstraction and meta-analysis was performed using RevMan 5.3 software. RESULTS: The cohorts involved 14 articles describing 1,918 participants were included. The incidence of the short-term major adverse cardiac events (MACE) was significantly reduced with intracoronary GPIs after TA (odds ratio [OR]: 0.29; 95% confidence interval [CI]: 0.13 to 0.65, p=0.003). Benefits were noted for short-term mortality (OR: 0.31; 95% CI: 0.17 to 0.57, p=0.0002) and reinfarction (OR: 0.28; 95% CI: 0.10 to 0.78, p=0.01) in subjects who received intracoronary GPIs after TA. Moreover, the Thrombolysis in Myocardial Infarction (TIMI) trial grade 3 postprocedure (OR: 2.29; 95% CI: 1.72 to 3.04, P<0.00001) and complete ST-segment resolution (STR) rate (OR: 2.68; 95% CI: 1.85 to 3.87, P<0.00001) were both improved with intracoronary GPIs after TA. As a result, left ventricular ejection fraction (LVEF) at short-term follow-up showed a significant difference (OR: 7.33; 95% CI: 5.60 to 9.06, p<0.0001) in favor of the TA and intracoronary GPIs administration. CONCLUSIONS: Our study demonstrates that intracoronary GPIs may have a synergistic effect with thrombus aspiration on short-term mortality, reinfarction, and cardiac functional recovery.

Association of serum levels of AngII, KLK1, and ACE/KLK1 polymorphisms with acute myocardial infarction induced by coronary artery stenosis.

INTRODUCTION: The study aims to confirm the association of acute myocardial infarction (AMI) with serum angiotensin II (AngII), kallikrein1 (KLK1), and ACE/KLK1 polymorphisms. MATERIALS AND METHODS: Serum AngII/KLK1 levels and ACE and KLK1 genotypes were determined in 208 patients with AMI and 216 normal controls. Binary logistic regression was used for data analysis. RESULTS: The differences in serum AngII levels were statistically significant between the groups. After adjusting for potential confounding factors, high serum levels of AngII and KLK1 significantly increased the risk of AMI. The individuals with ACE DD and KLK1 GG genotypes significantly increased the risk of AMI compared with those harboring the ACE II and KLK1 AA genotypes (OR = 8.77, 95% CI = 1.74-44.16). CONCLUSIONS: (1) Increasing the serum levels of AngII increased the risk of AMI. (2) The risk of AMI increased significantly when the serum levels of AngII and KLK1 simultaneously increased. (3) Individuals with the combined genotypes of ACE DD and KLK1 GG showed significantly increased risk of AMI compared with those with the combined genotypes of ACE II and KLK1 AA.

Expression of molecular factors correlated with metastasis in small cell lung cancer and their significance.

Distant metastasis continues to be a fatal threat to quality of life in patients with small cell lung caner (SCLC). The purpose of this work is to analyze the expressions of chemokine receptor four (CXCR4), matrix metalloproteinase-9 (MMP-9), transforming growth factor-b1 (TGF-ß1), N-cadherin and vascular endothelial growth factor (VEGF) in small cell lung caner (SCLC), and to explore their correlations with the prognosis and metastasis. Sixty-five consecutive patients with stage I-III SCLC who received operation in our hospital from Jan 2003 to Oct 2009 were retrospectively analyzed. The expression of CXCR4 was found significantly correlated with bone metastasis (P = 0.004), and were marginally correlated with brain metastasis (P = 0.068) and lymph node metastasis (P = 0.085). The expression of MMP-9 was significantly associated with pathological staging (P = 0.048). Univariate analysis suggested surgical approach, clinical stage, lymph node metastasis were significantly associated with OS and PFS (P < 0.05), high expression of CXCR4 was significantly correlated with worse OS (P = 0.004) and PFS (P = 0.005). Multivariate analysis suggested surgical approach, TGF-ß1, CXCR4 and lymph node metastasis were independent prognostic factor for PFS. In conclusion, High expression of CXCR4, MMP-9, TGF-ß1 and VEGF were found in SCLC. High expression of MMP-9 was significantly associated with pathological staging, and high expression of CXCR4 was correlated with bone metastasis and also might correlate with brain metastasis. CXCR4 were independent prognostic factor for survival in SCLC and expanded samples should be further explored in the future.

Circulating CD36 and fractalkine levels are associated with vulnerable plaque progression in patients with unstable angina pectoris.

The chemokine, fractalkine, independently enhances the vulnerability of coronary atherosclerotic plaques. The present study investigated the combined effects of CD36 and fractalkine on coronary plaque progression in patients with unstable angina pectoris. In the present study, 120 unstable angina pectoris patients undergoing coronary angiography and intravascular ultrasound were divided into two groups: an intermediate lesion group (lumen diameter stenosis 50-70%, 80 patients) and a severe lesion group (at least one lesion with lumen diameter stenosis > 70%, 40 patients). The control group consisted of 40 healthy age- and sex-matched subjects. Concentrations of CD36 and fractalkine were measured by enzyme-linked immunosorbent assay. Major adverse cardiovascular events were monitored over a 2-year follow up. Intravascular ultrasound showed that patients with severe lesions had more calcified and mixed plaques, and a larger plaque area and plaque burden than patients with intermediate lesions (P < 0.05-0.01). More patients with severe lesions underwent stent deployment (P < 0.05) than those with intermediate lesions. CD36 and fractalkine concentrations were significantly higher in the severe lesion patients (P < 0.05), and both had significant positive correlations (P < 0.05) with the plaque burden of atherosclerotic lesions. Using the matched nested case-control study, we found that CD36 and fractalkine levels were higher in patients with recurrent major adverse cardiovascular events than controls (P < 0.05). In conclusion, CD36 and fractalkine both promote, and might synergistically enhance, the progression of coronary atherosclerotic plaques.

Alpha-lipoic acid ameliorates oxidative stress by increasing aldehyde dehydrogenase-2 activity in patients with acute coronary syndrome.

Aldehyde dehydrogenase-2 (ALDH2) is the main enzyme responsible for acetaldehyde oxidation in ethanol metabolism and also provides protection against oxidative stress. Alpha-lipoic acid (α-LA), a natural dithiol compound with antioxidant properties, has been reported to increase ALDH2 activity in cultured cells. We analyzed the therapeutic efficacy of α-LA in 63 patients with confirmed acute coronary syndrome (ACS). These patients (52 men and 11 women, with age range 49-72 years) were randomized into two groups: untreated group (n = 30) and α-LA group (n = 33). Patients in the α-LA group were given an intravenous injection of 600 mg α-LA every day for 5 days while the patients in the untreated group were given saline. An isoprostane, 8-iso-prostaglandin F2α (8-iso-PGF2α), one product of arachidonic acid metabolism, was measured as a marker for oxidative stress. The serum levels of 8-iso-PGF2α and ALDH2 activity were determined at admission to the hospital (time 0), and at 24 hours and 1 week after treatment. At 24 hours and 1 week after treatment, ALDH2 activity was significantly higher in the α-LA group than in the untreated group (P < 0.05), whereas the levels of 8-iso-PGF2α were significantly lower in the α-LA group than in the untreated group (all P < 0.05). Importantly, the decrease of 8-iso-PGF2α levels correlated with the increased ALDH2 activity at both 24 hours (r = 0.6234, P < 0.001) and 1 week after treatment (r = -0.3941, P = 0.0014). α-LA may ameliorate oxidative stress through up-regulating ALDH2 activity in patients with ACS.

[Significance of expression of chemokine receptor and matrix metalloproteinase in small cell lung cancer].

OBJECTIVE: To explore the expressions of CXC chemokine receptor 4 (CXCR4) and matrix metalloproteinase-9 (MMP-9) and examine their correlations with metastasis and prognosis in small cell lung cancer (SCLC). METHODS: Immunohistochemistry was employed to detect the expressions of CXCR4 and MMP-9 in the tissue samples from 65 SCLC patients treated in Cancer Institute and Hospital Attached to Tianjin Medical University from January 2003 to October 2009. And their correlations with metastasis and prognosis were analyzed by Chi-square test and Kaplan-Meier method and Cox regression. RESULTS: The positive expression rates of CXCR4 and MMP-9 were 100.0% (65/65) and 87.7% (57/65) in SCLC tissues respectively. Significant difference of the expression rate of CXCR4 was found between patients undergoing bone metastasis or not (P = 0.004). But the differences were not significant between brain metastasis or not (P = 0.068) and lymph node metastasis or not (P = 0.085). A high expression rate of MMP-9 was significantly associated with pathological staging (P = 0.048). But the difference between lymph node metastasis or not was not significant (P = 0.085). Univariate analysis suggested that a high expression rate of CXCR4 was significantly correlated with the disease-free survival (DFS) of SCLC patients (P = 0.005). But a high expression rate of MMP-9 was not associated with DFS (P = 0.341). Multivariate analysis suggested that a high expression rate of CXCR4 was an independent prognostic factor for DFS in SCLC. CONCLUSIONS: The elevated levels of CXCR4 and MMP-9 are found in SCLC tissues. And the expression rate of CXCR4 may be correlated with bone metastasis, but the correlation is not notable for MMP-9. The expression rate of CXCR4 is an independent prognostic factor for DFS in SCLC.

Role of aldehyde dehydrogenase 2 Glu504lys polymorphism in acute coronary syndrome.

This study aimed to investigate the association of the aldehyde dehydrogenase 2 (ALDH2) Glu504Lys polymorphism, which exists in 30-50% of East Asians, and risk of acute coronary syndrome (ACS). We enrolled 1092 unrelated Han Chinese, including 546 with ACS and 546 age- and sex-matched controls. Subjects with ALDH2 mutant genotypes showed significantly higher ACS than did controls (46.7% versus 31.9%, P < 0.001). Logistic regression analysis revealed the ALDH2 mutant independently associated with ACS (odds ratio [OR] 1.95, 95% confidence interval [CI]: 1.31-2.92, P = 0.001), but the association was weaker on adjusting for alcohol consumption (OR 1.82, 95% CI: 1.23-2.70, P = 0.003). Similar results were found in a subgroup analysis of patients with primary ST-segment elevation myocardial infarction (STEMI). The ALDH2 mutant was significantly associated with level of high-sensitivity C-reactive protein (hs-CRP) in patients with ACS (P = 0.002) and in controls (P = 0.009) and number of circulating endothelial progenitor cells (EPCs) (P = 0.032); furthermore, inclusion of hs-CRP level and EPCs number as independent variables in regression analysis reduced the importance of ALDH2 polymorphism in ACS or primary STEMI. However, ALDH2 polymorphism was not associated with number of coronary arteries with significant stenosis, Gensini score or flow-mediated dilation of the brachial artery. Our results suggest that ALDH2 mutation is a genetic risk marker for ACS, which is explained in part by alcohol consumption, inflammation and number of circulating EPCs.

The polymorphism in acetaldehyde dehydrogenase 2 gene, causing a substitution of Glu > Lys(504), is not associated with coronary atherosclerosis severity in Han Chinese.

Alcohol consumption has an important effect on coronary atherosclerotic heart disease (CAD). Acetaldehyde dehydrogenase 2 (ALDH2) is a key enzyme in alcohol metabolism. A G-to-A missense mutation of ALDH2 gene, which causes a Glu > Lys(504) substitution, was recently shown to be associated with carotid atherosclerosis; however, its relationship with coronary atherosclerosis has not been well studied. We, therefore, investigated this relationship in Han Chinese. There are two ALDH2 alleles (1 and 2) and their combination: 1/1 (GG, typical homozygote), 1/2 (GA, heterozygote) and 2/2 (AA, atypical homozygote) in the population. Successive Han Chinese, including 89 with myocardial infarction (MI) and 142 with unstable angina, were recruited, and underwent coronary angiography and gene sequencing. Coronary atherosclerosis severity was expressed by the number of lesioned coronary arteries (>or=50% diameter stenosis) and Gensini score, calculated based on the luminal narrowing degree and its geographic importance, as assessed by angiography. Based on their ALDH2 genotypes, the 231 patients were divided into wild-type (1/1, n = 145) and mutation groups (1/2 and 2/2, n = 86). There were no significant differences in basic clinical data between the two groups; however, the mutation group had significantly higher rates of diabetes mellitus and MI, and lower prevalence of alcohol consumption than wild-type group. Yet, the two groups were not significantly different in coronary atherosclerosis severity. Multiple regression analysis has shown that the ALDH2 genotype 1/2 or 2/2 is an independent risk factor for MI, but is not associated with coronary atherosclerosis severity in Han Chinese.

Multivessel percutaneous coronary intervention in Chinese patients with acute myocardial infarction and simple nonculprit arteries.

BACKGROUND: Multivessel percutaneous coronary intervention (PCI) for patients during acute myocardial infarction (AMI) is currently controversial. In this study, we investigated the significance of multivessel PCI in Chinese patients with ST-segment elevation AMI and relatively simple lesions in nonculprit arteries. METHODS: We reviewed all consecutive primary PCI of ST-segment elevation AMI in our hospital between 2002 and 2005. The patients with multivessel disease and ACC/AHA type A/B1 lesions in nonculprit arteries who underwent multivessel PCI were identified (n = 105, multivessel PCI group), and 120 patients with single-vessel disease and treatment with primary PCI were enrolled as control subjects (single-vessel PCI group). The primary end points were the occurrences of 6-month major adverse cardiac events (cardiogenic death, nonfatal reinfarction, and target vessel revascularization). The secondary end points included procedure time, angiographic success rate, TIMI grade, reperfusion arrhythmia, ST-segment resolution, and left ventricular ejection fraction. RESULTS: All patients with multivessel PCI tolerated the operations well and had similar TIMI 3 and angiographic success rates but longer procedure times than those patients with single-vessel PCI. There were no significant differences in reperfusion arrhythmia, ST-segment resolution, left ventricular ejection fraction, or 6-month MACEs between both groups. CONCLUSIONS: This study suggests that multivessel PCI is effective and safe for Chinese patients with ST-segment elevation AMI and simple lesions in nonculprit arteries.

Facilitated PCI in younger Chinese patients with AMI.

Presently, facilitated percutaneous coronary intervention (PCI) in patients remains controversial. We evaluated the efficacy and safety of facilitated PCI, intravenous low-dose rt-PA administration prior to urgent PCI, in Chinese patients < 70 years of age with ST-segment elevation myocardial infarction. Our results suggest that the age and dosage of thrombolytics should be noticed seriously when considering facilitated PCI.

Effect of aspirin plus clopidogrel on inflammatory markers in patients with non-ST-segment elevation acute coronary syndrome.

BACKGROUND: Aspirin can inhibit inflammatory reactions and platelet aggregation, but little is known about the effects of the combination of aspirin plus clopidogrel, a new antiplatelet agent, on inflammation. The purpose of this study was to determine whether aspirin plus clopidogrel can further suppress inflammation in patients with non-ST-segment elevation acute coronary syndrome (NSTEACS). METHODS: One hundred and fifteen patients with NSTEACS were randomized into two groups: group A (aspirin alone, n =58) and group B (aspirin plus clopidogrel, n =57). Patients in group A received a loading dose of 300 mg aspirin, then 100 mg per day. The patients in group B received a loading dose of 300 mg aspirin and 300 mg clopidogrel, then 100 mg aspirin and 75 mg clopidogrel per day. Serum high sensitivity C-reactive protein (hs-CRP) and tumor necrosis factor-alpha (TNF-alpha) were measured in all patients at baseline prior to any drug treatment after admission, and at 7 and 30 days after beginning drug treatment. Thirty healthy volunteers on no medications were enrolled as controls (group C). RESULTS: Baseline levels of hs-CRP and TNF-alpha in group A and group B were significantly higher than those in group C. Seven days after administration, the levels of hs-CRP in both group A and group B decreased significantly [Group A: (6.15 +/- 1.39) mg/L vs (9.18 +/- 1.62) mg/L, P <0.01; Group B:(4.99 +/- 1.62) mg/L vs (10.29 +/- 1.47) mg/L, P <0.01]. Similarly, levels of TNF- alpha in both groups decreased at 7 days compared to baseline [Group A: (90.99 +/- 28.91) pg/ml vs (117.20 +/- 37.13) pg/ml, P <0.01; Group B: (74.32 +/- 21.83) pg/ml vs (115.27 +/- 32.11) pg/ml, P <0.01]. Thirty days after administration, the levels of hs-CRP in both group A and group B decreased further to (3.49 +/- 1.53) mg/L, and (2.40 +/- 1.17) mg/L respectively (P <0.01 for both comparisons). Levels of TNF-alpha in groups A and B also decreased significantly between 7 and 30 days, to 63.28 +/- 29.01 pg/ml (group A) and (43.95 +/- 17.10) pg/ml (group B; P <0.01 for both comparisons). Significantly lower levels of hs-CRP and TNF-alpha were observed in group B compared to Group A at thirty days after initiating drug treatment (P <0.05). CONCLUSIONS: Aspirin plus clopidogrel treatment reduced levels of serum hs-CRP and TNF-alpha in patients with NSTEACS significantly more than aspirin alone. Because both aspirin and clopidogrel produce important anti-inflammatory effects, these results suggest the possibility that long-term treatment with aspirin plus clopidogrel may produce greater clinical benefits compared to treatment with aspirin alone.