Pathophysiology Of Acute Coronary Syndromes Research Articles

Study of Immature Platelet Fraction, Mean Platelet Volume and Interleukin-6 in Acute Coronary Syndrome: A Study at a Tertiary Care Hospital in India

Background: In the pathophysiology of acute coronary syndrome (ACS), platelets play a key role. The immature platelet fraction (IPF) is thought to be a possible indicator of activation of platelets and turnover processes. Younger platelets have a higher thrombotic potential and combine with collagen faster, which might compromise their ability to maintain hemostasis and lead to the development of thrombus. MPV measurements show platelet activation. IL-6 plasma levels seem to indicate the degree of latent plaque inflammation and, thus, may indicate susceptibility to plaque rupture. Aims and Objectives: To estimate the levels of IPF, MPV and IL-6 in ACS and to find out the association and correlation of IPF, MPV and IL-6 with ACS. Material and Method: Seventy patients of ACS fitting the Universal criteria of Myocardial infarction as cases and 70 healthy controls were included in the study. MPV, IPF, and IL6 were analyzed in all the cases and controls using various statistical tools. Result: MPV (fl) was the best predictor among all parameters at a cutoff point of >4.2, with an AUC of 0.855 for correctly predicting STEMI. IPF came out to be a reasonably good marker for predicting STEMI, with a mean of 8.71 ± 5.39. IL-6 in NSTEMI was significantly higher than in controls ( P = .004) and was comparable with UA ( P = .09). Conclusion: The current study’s findings seem to confirm that elevated MPV and IPF are important ancillary indicators in the assessment of ACS.

Novel Biomarkers and Their Role in the Diagnosis and Prognosis of Acute Coronary Syndrome.

The burden of cardiovascular diseases and the critical role of acute coronary syndrome (ACS) in their progression underscore the need for effective diagnostic and prognostic tools. Biomarkers have emerged as crucial instruments for ACS diagnosis, risk stratification, and prognosis assessment. Among these, high-sensitivity troponin (hs-cTn) has revolutionized ACS diagnosis due to its superior sensitivity and negative predictive value. However, challenges regarding specificity, standardization, and interpretation persist. Beyond troponins, various biomarkers reflecting myocardial injury, neurohormonal activation, inflammation, thrombosis, and other pathways are being explored to refine ACS management. This review article comprehensively explores the landscape of clinically used biomarkers intricately involved in the pathophysiology, diagnosis, and prognosis of ACS (i.e., troponins, creatine kinase MB (CK-MB), B-type natriuretic peptides (BNP), copeptin, C-reactive protein (CRP), interleukin-6 (IL-6), d-dimers, fibrinogen), especially focusing on the prognostic role of natriuretic peptides and of inflammatory indices. Research data on novel biomarkers (i.e., endocan, galectin, soluble suppression of tumorigenicity (sST2), microRNAs (miRNAs), soluble oxidized low-density lipoprotein receptor-1 (sLOX-1), F2 isoprostanes, and growth differentiation factor 15 (GDF-15)) are further analyzed, aiming to shed light on the multiplicity of pathophysiologic mechanisms implicated in the evolution of ACS. By elucidating the complex interplay of these biomarkers in ACS pathophysiology, diagnosis, and outcomes, this review aims to enhance our understanding of the evolving trajectory and advancements in ACS management. However, further research is necessary to establish the clinical utility and integration of these biomarkers into routine practice to improve patient outcomes.

Predictors of Intracoronary Heavy Thrombus Burden in Patients with ST Elevation Myocardial Infarction Undergoing Primary PCI within 12 Hours from Chest Pain Onset

Abstract Background ST segment elevation myocardial infarction (STEMI) comprises approximately 25-40% of myocardial infarction (MI) presentation. The pathophysiology of acute coronary syndrome (ACS) is rupture or erosion of the fibrous cap overlying lipid rich plaques within the arterial tree. This event exposes pro-inflammatory substances, ultimately resulting in platelet aggregation and formation of obstructive thrombus. Aim of the Work Identify predictors of heavy thrombus burden in patients with STEMI undergoing primary percutaneous coronary intervention (PCI) within 12 hours from onset of chest pain. Patients and Methods Our study included 200 consecutive patients who presented with STEMI and were managed by primary PCI within 12 hours from onset of chest pain. All patients were subjected to thorough history taking ] e.g. Age, HTN, family history of premature coronary artery disease (CAD) and pain to balloon time [, clinical examination, electrocardiogram (ECG), biochemical biomarkers, PCI and transthoracic echocardiography (TTE). Results Our study showed that there was significant positive correlation between grading of thrombus burden with age (rho = 0.165; P = 0.020), HTN (rho = 0.143; P = 0.043), number of risk factors (rho = 0.253; P < 0.001), Killip classification (rho = 0.211; P = 0.003), pain to balloon time (rho = 0.453; P < 0.001), ST elevation score (rho = 0.185; P = 0.009), RDW (rho = 0.878; P < 0.001), TLC (rho = 0.445; P < 0.001), troponin (rho = 0.600; P < 0.001), CK-MB (rho = 0.661; P < 0.001) and CPK(rho = 0.533; P < 0.001) and N/L ratio (rho=0.563 ; P = <0.001) also, there was significant negative correlation between grading of thrombus burden with EF (rho = -0.397; P < 0.001). Conclusion There was significant positive correlation between age, number of cardiovascular risk factor, pain to balloon time, Killip classification, RDW, TLC, N/L ratio and grading of thrombus burden. Only pain to balloon and RDW were considered as independent predictors of heavy thrombus burden

The Pathophysiology of Acute Coronary Syndrome

The Pathophysiology of Acute Coronary Syndrome

Uric acid plasma levels are associated with C-reactive protein concentrations and the extent of coronary artery lesions in patients with acute coronary syndromes.

Many studies have pointed out that inflammation plays a pivotal role in pathophysiology of acute coronary syndromes (ACS) because several inflammatory molecules impair the endothelial functions in the coronary circulation and promote atherothrombotic events. Recently, many clinical/experimental evidences indicate that elevated plasma levels of uric acid (UA) might be considered a risk factor for developing ACS. It has been reported that elevated UA doses impair physiologic functions of endothelial cells, shifting them toward a pro atherothrombotic phenotype. In the present manuscript, we investigated the relationship between UA plasma levels, inflammatory burden, and extension of coronary atherosclerotic disease in patients with ACS. Patients with a clinical presentation of ACS (ST-elevated and non-ST-elevated myocardial infarction) admitted to the Vanvitelli Catheterization Laboratory at Monaldi Hospital in 2019, before the COVID-19 pandemia, were retrospectively analyzed. Biochemical profile, type of ACS presentation, as well as extension of coronary atherosclerosis were assessed. A total of 132 ACS patients were included in the analysis, and grouped into 3 tertiles according to the UA values (UA < 4.72mg/dl, UA between 4.72 and 6.15mg/dl, and UA > 6.15mg/dl). Patients with UA plasma levels ≥ 6.15mg/dL showed higher levels of C-reactive protein (mean of 5.1mg/dL) as compared to patients with lower UA plasma levels. Moreover, the former group of patients showed higher levels of cardiac troponin and CPK, and presented more often with multivessel disease and complex coronary stenosis (type C of Ellis classification). Even though monocentric and with limited sample size, the present study shows that plasma levels of UA and hs-CRP are elevated in ACS patients and are associated with a more severe coronary disease, suggesting a potential role of UA in the pathophysiology of acute coronary events.

Current Role of Intracoronary Imaging for Implementing Risk Stratification and Tailoring Culprit Lesion Treatment: A Narrative Review.

Our understanding of the pathophysiology of acute coronary syndrome and of the vascular biology of coronary atherosclerosis has made enormous progress with the implementation of intravascular imaging. Intravascular imaging contributes to overcoming the known limitations of coronary angiography and allows for the in vivo discrimination of plaque morphology giving insight into the underlying pathology of the disease process. The possibility of using intracoronary imaging to characterize lesion morphologies and correlate them with clinical presentations may influence the treatment of patients and improve risk stratification, offering the opportunity for tailored management. This review examines the current role of intravascular imaging and describes how intracoronary imaging represents a valuable tool for modern interventional cardiology in order to improve diagnostic accuracy and offer a tailored approach to the treatment of patients with coronary artery disease, especially in the acute setting.

Role of combined use of mean platelet volume-to-lymphocyte ratio and monocyte to high-density lipoprotein cholesterol ratio in predicting patients with acute myocardial infarction

BackgroundAtherosclerosis and thrombosis play important roles in the pathophysiology of acute coronary syndrome, with platelet activation and inflammation as the key and initiative factors. Recently mean platelet volume-to-lymphocyte ratio (MPVLR) and monocyte to high-density lipoprotein cholesterol ratio (MHR) have emerged as new prognostic indicators of cardiovascular diseases. However, the predicting effect of the combination of MPVLR and MHR in myocardial infarction has not been reported.ObjectiveThe aim of this study was to investigate the usefulness of combination of MPVLR and MHR in predicting patients with AMI.Methods375 patients who had chest pain or stuffiness were retrospectively enrolled in this study. According to the results of coronary angiography and cardiac troponin, patients were divided into AMI group (n = 284) and control group (n = 91). MPVLR, MHR, Gensini score and Grace score were calculated.ResultsMPVLR and MHR were significantly higher in AMI group than that in control group (6.47 (4.70–9.58) VS 4.88 (3.82–6.44), 13.56 (8.44–19.01) VS 9.14 (7.00–10.86), P < 0.001, respectively). Meanwhile, both were positively correlated with Gensini score and Grace score. Patients with a high level of MPVLR or MHR had an increased risk for AMI (odds ratio (OR) = 1.2, 95% confidence interval (CI) 1.1–1.4, OR = 1.2, 95% CI 1.2–1.3). Combination of MPVLR and MHR identified a greater ROC area than its individual parameters (P < 0.001).ConclusionBoth MPVLR and MHR are independent predictors of AMI. Combination of MPVLR and MHR had higher predicting value in AMI, and thus appears to be a new risk factor and biomarker in the evaluation of risk and severity of atherosclerosis in AMI.

New Concepts on the Pathophysiology of Acute Coronary Syndrome

Acute coronary syndrome (ACS) is the most severe form of ischemic heart disease. Although it is caused by atherosclerotic plaque thrombosis or nonatherosclerotic causes, its pathophysiological mechanism of ACS is not fully understood, and its concept is constantly updated and developed. At present, the main pathophysiological mechanisms include plaque rupture, plaque erosion, calcified nodules (CN) and non-atherosclerotic causes such as coronary vasospasm and myocardial bridging (MB). These mechanisms may overlap and coexist in some ACS patients. Therefore, the pathophysiological mechanism of ACS is complex, and is of great significance for the diagnosis and treatment of ACS. This review will discuss the pathophysiological mechanisms of ACS to provide new thoughts on the pathogenesis, diagnosis and treatment of ACS.

Role of oxidase and antioxidant enzymes in neutrophils and blood circulation in patients with acute coronary syndrome

Acute coronary syndrome (ACS), a subcategory of cardiovascular diseases, has become a major cause of mortality and morbidity worldwide. Oxidative stress resulting from increased production of reactive oxygen species and decreased antioxidants plays a major role in the pathophysiology of ACS. This study evaluated the activities of certain oxidase and antioxidant enzymes in circulation and neutrophils to determine their roles in increased oxidative stress in patients with ACS. A total of 52 patients with ACS admitted in the coronary care unit of two tertiary hospitals and 52 healthy controls were enrolled. Blood samples were collected from all subjects, and various oxidase and antioxidant enzymes in neutrophils and circulation were assayed. The patients had significantly higher white blood cell and neutrophil counts than the controls. In patients, the mean (±SD) serum activities of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (12.83±6.6 U/L) and superoxidase dismutase (4.34±1.41 U/mL) were significantly higher than in the control group (4.88±3.03 U/L and 3.02±1.7 U/mL, respectively) while the catalase had significantly lower activities (33.36±13.16 U/mL vs. 63.98±31.86 U/mL). In neutrophils, the activities of myeloperoxidase, NADPH oxidase and catalase were significantly higher in ACS patients, while superoxidase dismutase was significantly lower. Further, significant positive correlations were found between activities of myeloperoxidase and catalase, and NADPH oxidase and superoxidase dismutase in neutrophils of ACS patients. These findings revealed that higher activities of myeloperoxidase and NADPH oxidase, both in serum and neutrophils, lead to increased oxidative stress and form the inflammatory basis of ACS, and the antioxidant enzymes combat the events.

Simultaneous total occlusion due to spasm of 2 main coronary arteries: A case report.

Coronary artery spasm (CAS) defined by severe reversible focal or diffuse vasoconstriction, plays an essential role in the pathophysiology of acute coronary syndrome but is not very common in the clinic. Due to its transience, it is difficult to diagnose CAS directly, many patients are diagnosed by clinical experience. Here, we report the diagnosis and treatment of a rare case of simultaneous total occlusion due to spasm of the two main coronary arteries by coronary angiography (CAG). A 47-year-old man with no medical history was admitted to our emergency room complaining of sudden-onset chest pain lasting 3 hours. Emergency CAG showed total occlusion of the proximal left anterior descending artery and right coronary artery. Acute myocardial infarction caused by CAS was diagnosed, according to CAG findings and test results. Intracoronary injection of nitroglycerin and anti-spasm medication. The patient was discharged on the 8th day with complete resolution of symptoms and normalization of the electrocardiography findings. No ischemic events occurred during a follow-up for 27 months. This case highlights the significance of identifying CAS in patients with acute myocardial infarction and avoiding blind interventional stent therapy, which requires closer attention from clinicians.

Unique crosstalk between platelet and leukocyte counts during treatment for acute coronary syndrome: A retrospective observational study

In the pathophysiology of acute coronary syndrome (ACS), platelet (PLT) and neutrophil (Neu) crosstalk may be important for activating coagulation and inflammation. It has been speculated that PLTs and Neu may affect each other's cell counts; however, few studies have investigated this hypothesis. In this study, we measured changes in blood cell counts in 245 patients with ACS during treatment and investigated the mutual effects of each blood cell type. Path diagrams were drawn using structural equation modeling, and temporal changes in the count of each blood cell type and the relevance of these changes were analyzed. Throughout the treatment period, the numbers of all blood cell types (red blood cells [RBCs], leukocytes, and PLTs) were associated with each other before and after treatment. A detailed examination of the different cell types revealed that the PLT count at admission had a significant positive effect on the leukocyte (especially Neu) count after treatment. Conversely, the leukocyte (especially Neu) count at admission had a significant positive effect on the PLT count after treatment. During ACS, PLTs and leukocytes, especially Neu, stimulate each other to increase their numbers. The formation of a PLT-leukocyte complex may increase coagulation activity and inflammation, which can lead to a further increase in the counts of both blood cell types.

Predicting protective gene biomarker of acute coronary syndrome by the circRNA-associated competitive endogenous RNA regulatory network.

Background: The mortality and disability rates of acute coronary syndrome (ACS) are quite high. Circular RNA (circRNA) is a competitive endogenous RNA (ceRNA) that plays an important role in the pathophysiology of ACS. Our goal is to screen circRNA-associated ceRNA networks for biomarker genes that are conducive to the diagnosis or exclusion of ACS, and better understand the pathology of the disease through the analysis of immune cells. Materials and methods: RNA expression profiles for circRNAs (GSE197137), miRNAs (GSE31568), and mRNAs (GSE95368) were obtained from the GEO database, and differentially expressed RNAs (DEcircRNAs, DEmiRNAs, and DEmRNAs) were identified. The circRNA-miRNA and miRNA-mRNA regulatory links were retrieved from the CircInteractome database and TargetScan databases, respectively. As a final step, a regulatory network has been designed for ceRNA. On the basis of the ceRNA network, hub mRNAs were verified by quantitative RT-PCR. Hub genes were validated using a third independent mRNA database GSE60993, and ROC curves were used to evaluate their diagnostic values. The correlation between hub genes and immune cells associated with ACS was then analyzed using single sample gene set enrichment analysis (ssGSEA). Results: A total of 17 DEcircRNAs, 229 DEmiRNAs, and 27 DEmRNAs were found, as well as 52 circRNA-miRNA pairings and 10 miRNA-mRNA pairings predicted. The ceRNA regulatory network (circRNA-miRNA-mRNA) was constructed, which included 2 circRNA (hsa_circ_0082319 and hsa_circ_0005654), 4 miRNA (hsa-miR-583, hsa-miR-661, hsa-miR-671-5p, hsa-miR-578), and 5 mRNA (XPNPEP1, UCHL1, DBNL, GPC6, and RAD51). The qRT-PCR analysis result showed that the XPNPEP1, UCHL1, GPC6 and RAD51 genes had a significantly decreased expression in ACS patients. Based on ROC curve analysis, we found that XPNPEP1 has important significance in preventing ACS occurrence and excluding ACS diagnosis. ACS immune infiltration analysis revealed significant correlations between the other 3 hub genes (UCHL1, GPC6, RAD51) and the immune cells (Eosinophils, T folliculars, Type 2T helper cells, and Imumature dendritic cells). Conclusion: Our study constructed a circRNA-related ceRNA network in ACS. The XPNPEP1 gene could be a protective gene biomarker for ACS. The UCHL1, GPC6 and RAD51 genes were significantly correlated with immune cells in ACS.

Genetic variants, gene expression, and soluble CD36 analysis in acute coronary syndrome: Differential protein concentration between ST-segment elevation myocardial infarction and unstable angina.

BackgroundAtherosclerosis plays an important role in the pathophysiology of acute coronary syndrome (ACS). CD36 is a scavenger receptor involved in lipid metabolism. Some single‐nucleotide variants in the non‐coding region could indirectly alter the expression and the function of the protein.ObjectiveThe aim of this study was to investigate the gene and protein expression associated with CD36 variants (rs1194182;C > G; rs1049654;C > A, rs1334512;G > T, and rs3211892;G > A) in ACS patients from the western Mexican population.MethodsWe recruited 310 ACS patients and 308 subjects in the control group (CG). Genotyping was determined by TaqMan SNP genotyping assays. CD36 expression at the mRNA level was quantified by TaqMan gene expression assays. Soluble CD36 (sCD36) was measured by enzyme‐linked immunosorbent assay.ResultsWe show that rs1194182G > C variant provides a protective effect with a 1.7‐fold lower susceptibility to develop ACS (p = 0.03); however, this association was masked by diabetes and dyslipidemia. We observed a higher sCD36 concentration in patient with ST‐segment elevation myocardial infarction (STEMI) compared with patients with unstable angina (UA) (p = 0.038). Likewise, in diabetic patients versus non‐diabetic (p < 0.001). We observed in patients an increase in CD36 mRNA expression (1.91 times higher) than in the CG (p = 0.02).ConclusionThe rs1194182 seems to be associated with diabetes in a risky manner, in ACS patients and protective for dyslipidemia in both groups. The concentration of sCD36 seems to be associated with the clinical spectrum of the ACS patients and the presence of diabetes, since patients with STEMI present significantly elevated level compared with UA.

IL-6, IL-1β and MDA correlate with Thrombolysis in Myocardial Infarction (TIMI) risk score in patients with Acute Coronary Syndrome.

Inflammation plays a significant role in the pathophysiology of Acute Coronary Syndrome (ACS) but is not included in current risk stratification. To determine the association between Thrombolysis in Myocardial Infarction (TIMI) risk score and inflammatory biomarkers in the ACS, including unstable angina (UA), non-ST segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). We hypothesized that including inflammatory biomarkers could add prognostic value to the TIMI risk score. In this cross-sectional study, serum levels of interleukins (IL)-6 and IL-1β and MDA (malondialdehyde) were quantified by ELISA and colorimetry, respectively , patients with ACS (n = 48; 31.3% with UA, 33.3% with NSTEMI, and 35.4% with STEMI) and healthy controls (n = 43). We assessed the TIMI scores in the first 24 h after symptom onset. The results showed that patients with ACS had significantly higher levels (p<0.05) of the inflammatory biomarkers IL-6, IL-1β, and MDA compared to the control group. However, we found no significant differences in IL-6, IL-1β, and MDA levels among the patients with ACS according to their classification as UA, NSTEMI, and STEMI. Positive correlations were observed between TIMI and IL-6 (r=0.68), IL-1β (r= 0.53), and MDA (r=0.58) in patients with UA and between TIMI and IL-1β (r= 0.62) in STEMI patients. These data suggest the presence of a pro-inflammatory profile in patients with ACS as well as positive correlations between TIMI scores and the inflammatory biomarkers IL-6, IL-1β, and MDA in patients with UA and between TIMI scores and IL-1β in patients with STEMI. Combining inflammatory biomarkers with the TIMI risk score could provide better insight into the processes involved in ACS.

Role of complete blood count, antioxidants, and total antioxidant capacity in the pathophysiology of acute coronary syndrome

Role of complete blood count, antioxidants, and total antioxidant capacity in the pathophysiology of acute coronary syndrome

Biomarkers of Inflammation and Oxidative stress in the Prediction and Management of Acute Coronary Syndrome

The assessment of patients presenting with chest pain or symptoms indicative of cardiac ischemia remains a diagnostic challenge. Many types of research have focused on the search for ideal biological markers for the rapid detection of cardiac cell injuries. Markers of inflammation and oxidative stress are the way forward. At present, the biomarker most widely used for diagnosing acute coronary syndrome is cardiac troponin though it has some limitations. Apart from cardiac troponin, several other biomarkers, especially inflammation and oxidative stress markers in acute coronary syndrome, have been investigated. However, most of them still require validation in further studies. As markers of inflammation and oxidative stress address a particular aspect of the pathophysiology of acute coronary syndrome, these biomarkers may provide unique information to the managing clinician separate from that of markers of myocyte necrosis. Serum markers of inflammation and oxidative stress appear before cardiac necrosis markers and are valuable targets for early and timely diagnosis of an acute cardiac event. Using these markers in combination with biomarkers of plaque formation, unstable plaque development, plaque rupture, thrombosis, and myocardial necrosis (multimarker approach) could increase their diagnostic and prognostic value.

Screening Analysis of Platelet miRNA Profile Revealed miR-142-3p as a Potential Biomarker in Modeling the Risk of Acute Coronary Syndrome.

Transcriptome analysis constitutes one of the major methods of elucidation of the genetic basis underlying the pathogenesis of various diseases. The post-transcriptional regulation of gene expression is mainly provided by microRNAs. Their remarkable stability in biological fluids and their high sensitivity to disease alteration indicates their potential role as biomarkers. Given the high mortality and morbidity of cardiovascular diseases, novel predictive biomarkers are sorely needed. Our study focuses for the first time on assessing potential biomarkers of acute coronary syndrome (ACS) based on the microRNA profiles of platelets. The study showed the overexpression of eight platelet microRNAs in ACS (miR-142-3p; miR-107; miR-338-3p, miR-223-3p, miR-21-5p, miR-130b-3p, miR-301a-3p, miR-221-3p) associated with platelet reactivity and functionality. Our results show that the combined model based on miR-142-3p and aspartate transaminase reached 82% sensitivity and 88% specificity in the differentiation of the studied groups. Furthermore, the analyzed miRNAs were shown to cluster into two orthogonal groups, regulated by two different biological factors. Bioinformatic analysis demonstrated that one group of microRNAs may be associated with the physiological processes of platelets, whereas the other group may be linked to platelet–vascular environment interactions. This analysis paves the way towards a better understanding of the role of platelet microRNAs in ACS pathophysiology and better modeling of the risk of ACS.

Effects of colchicine on tissue factor in oxLDL-activated T-lymphocytes.

Several studies have shown that T-cells might be involved in pathophysiology of acute coronary syndromes (ACS). Tissue factor (TF) plays a key role in ACS. Many evidences have indicated that some statins reduce TF expression in several cell types. However, literature about rosuvastatin and TF and about statins effects on T-cells is still scanty. Colchicine is an anti-inflammatory drug recently proven to have beneficial effects in ACS via unknown mechanisms. This study investigates the effects of colchicine and rosuvastatin on TF expression in oxLDL-activated T-cells. T-cells, isolated from buffy coats of healthy volunteers, were stimulated with oxLDL (50µg/dL). T-cells were pre-incubated with colchicine (10µM) or rosuvastatin (5µM) for 1h and then stimulated with oxLDL (50μg/mL). TF gene (RT-PCR), protein (western blot), surface expression (FACS) and procoagulant activity (FXa generation assay) were measured. NF-κB/IκB axis was examined by western blot analysis and translocation assay. Colchicine and rosuvastatin significantly reduced TF gene, and protein expression and procoagulant activity in oxLDL stimulated T-cells. This effect was associated with a significant reduction in TF surface expression as well as its procoagulant activity. These phenomena appear modulated by drug effects on the transcription factor NF-kB. Rosuvastatin and colchicine prevent TF expression in oxLDL-stimulated T-cells by modulating the NF-κB/IκB axis. Thus, we speculate that this might be another mechanism by which these drugs exert benefic cardiovascular effects.

Leuko-platelet index as an independent predictor of in-hospital events in patients with non-ST elevation acute coronary syndrome

Abstract Background Platelet activation and aggregation plays a fundamental role in the pathophysiology of acute coronary syndrome (ACS). Added to this is the activation of the coagulation cascade and a local and systemic inflammatory response. Both the white blood cell count and the platelet count were associated with a worse prognosis in ACS. The leuko-platelet index (LPI) combines the platelet and white blood cell count and has been described as a prognostic marker in these patients. Purpose The aim of this study is to evaluate if LPI is a predictor of in-hospital events and mortality in patients with non-ST elevation ACS (NSTEACS). Materials and methods A retrospective analysis of a multicentre registry of 25 coronary units of Argentina was performed. It was included patients witch diagnostic of NSTEACS. GRACE score and LPI was calculated with admission data. For LPI it was used the following formula: white blood cell count x platelet count/108. The upper quartile of LPI was chosen as the cut-off point for the LPI (LPI&amp;gt;24). According to GRACE and LPI was divided in 4 groups: Group 1 (GRACE&amp;lt;140 and LIP&amp;lt;24), Group 2 (GRACE&amp;lt;140 and LPI&amp;gt;24), group 3 (GRACE &amp;gt;140 and LPI&amp;lt;24) and group 4 (GRACE &amp;gt;140 and LPI &amp;gt;24). In-hospital follow-up was performed and was considered the combined end point of death from any cause, heart failure, and shock as primary end point and in-hospital mortality as secondary end point. Univariate and multivariate analysis was performed by logistic regression. Results 2170 patients with an age 65±11 years were included, 27.3% women, 63% non-ST infarction and 37% unstable angina, 37% had GRACE&amp;gt;140 (n=803) and 25% had LPI&amp;gt;24 (n=542). The combined end point was presented in 9.3% (n=203) with a in hospital mortality of 2.3% (n=50). The figure 1 shows the gradient of events according to the groups with GRACE 140 and ILP 24 (chi of trend: p=0.001 of combined end point and p=0.01 for in-hospital mortality). In the multivariate analysis, the LPI &amp;gt;24 and the GRACE score were independent predictors of the combined end point (OR 1.48 (95% CI 1.04–2.09), p=0.02 and OR 1.02 (95% CI 1.01–1.03), p&amp;lt;0.001; respectively) and mortality (OR 1.29 (95% CI 1.01–1.72), p=0.03 and OR 1.01 (1.003–1.03), p&amp;lt;0.001; respectively). C-Statistic of LPI and GRACE were similar both for the combined end point (LPI: 0.73 versus GRACE: 0.72, p=0.3) and for mortality (LPI: 0.70 versus GRACE: 0.73, p=0.4). Conclusions The LPI was an independent predictor of the combined point and in-hospital mortality, with a similar discrimination capacity as the GRACE score. The presence of LPI&amp;gt;24 in patients with GRACE&amp;gt;140 identifies a very high-risk subgroup. LPI is a very easily obtained marker that could be useful in risk stratification in patients with NSTEACS. Funding Acknowledgement Type of funding sources: None. Gradient of events according groups

The healed plaque: tale of a story with good ending - with practical implications

Acute coronary syndromes have heterogeneous clinical presentations, features and prognosis. They can also occur without angiographic evidence of significant coronary artery stenosis, based on multiple causes. We report on the diagnostic and therapeutic management of a 56-year-old man with an acute coronary syndrome and angiographic evidence of non-obstructive coronary artery disease. In addition to the basic angiographic evaluation, intracoronary imaging was here helpful to understand the underlying mechanism, prompting a tailored therapeutic strategy and avoiding inappropriate treatment with percutaneous coronary intervention and stenting. This clinical case here described offers the opportunity to briefly recapitulate the most meaningful milestones in the progress in the pathophysiology of acute coronary syndromes, also focusing on myocardial infarction non-obstructive coronary artery, and to appreciate the occurrence of rare cases and consequent lessons.