Search for jet extinction in the inclusive jet-pT spectrum from proton-proton collisions at s=8 TeV

Published by the American Physical Society under the terms of the Creative Commons Attribution 3.0 License. Further distribution of this work must maintain attribution to the author(s) and the published articles title, journal citation, and DOI.The first search at the LHC for the extinction of QCD jet production is presented, using data collected with the CMS detector corresponding to an integrated luminosity of 10.7  fb−1 of proton-proton collisions at a center-of-mass energy of 8 TeV. The extinction model studied in this analysis is motivated by the search for signatures of strong gravity at the TeV scale (terascale gravity) and assumes the existence of string couplings in the strong-coupling limit. In this limit, the string model predicts the suppression of all high-transverse-momentum standard model processes, including jet production, beyond a certain energy scale. To test this prediction, the measured transverse-momentum spectrum is compared to the theoretical prediction of the standard model. No significant deficit of events is found at high transverse momentum. A 95% confidence level lower limit of 3.3 TeV is set on the extinction mass scale

Searches for electroweak neutralino and chargino production in channels with Higgs, Z, and W bosons in pp collisions at 8 TeV

Searches for supersymmetry (SUSY) are presented based on the electroweak pair production of neutralinos and charginos, leading to decay channels with Higgs, Z, and W bosons and undetected lightest SUSY particles (LSPs). The data sample corresponds to an integrated luminosity of about 19.5 fb(-1) of proton-proton collisions at a center-of-mass energy of 8 TeV collected in 2012 with the CMS detector at the LHC. The main emphasis is neutralino pair production in which each neutralino decays either to a Higgs boson (h) and an LSP or to a Z boson and an LSP, leading to hh, hZ, and ZZ states with missing transverse energy (E-T(miss)). A second aspect is chargino-neutralino pair production, leading to hW states with E-T(miss). The decays of a Higgs boson to a bottom-quark pair, to a photon pair, and to final states with leptons are considered in conjunction with hadronic and leptonic decay modes of the Z and W bosons. No evidence is found for supersymmetric particles, and 95% confidence level upper limits are evaluated for the respective pair production cross sections and for neutralino and chargino mass values

Coronary artery calcification score is an independent predictor of the no-reflow phenomenon after reperfusion therapy in acute myocardial infarction

Abundant evidence shows that coronary artery calcification (CAC) is a strong marker of structural and functional changes within the artery wall. Thus far, the implications of CAC in patients with acute coronary syndromes remain unclear. We aimed to investigate whether the CAC score is associated with impaired reperfusion during the acute phase of ST-elevation myocardial infarction (STEMI). We enrolled 60 consecutive STEMI patients to undergo cardiac computed tomography for assessment of the CAC score within 1 week after STEMI. Coronary thrombus burden, coronary blood flow (TIMI flow), and myocardial blush grade (MBG) were evaluated systematically. Patients with maximal TIMI flow and MBG were grouped as optimal reperfusion (n=27) and their counterparts as no-reflow (NR, n=33). There were no differences in the clinical characteristics between groups. Patients in the NR group had higher heart rate, coronary angiographic severity, and CAC score. CAC score greater than 100 was associated independently with the presence of NR (odds ratio 4.4, 95% confidence interval 1.17-16.3). The CAC score of nonculprit coronary arteries was higher in NR individuals than in their counterparts (P=0.04). In addition, the CAC score of the isnfarct-related artery correlated negatively with the TIMI-flow rate (r=-0.54, P<0.001) and with the MBG (r=-0.32, P=0.04). The CAC score is associated with the presence of the NR phenomenon in STEMI patients.Abundant evidence shows that coronary artery calcification (CAC) is a strong marker of structural and functional changes within the artery wall. Thus far, the implications of CAC in patients with acute coronary syndromes remain unclear. We aimed to investigate whether the CAC score is associated with impaired reperfusion during the acute phase of ST-elevation myocardial infarction (STEMI). We enrolled 60 consecutive STEMI patients to undergo cardiac computed tomography for assessment of the CAC score within 1 week after STEMI. Coronary thrombus burden, coronary blood flow (TIMI flow), and myocardial blush grade (MBG) were evaluated systematically. Patients with maximal TIMI flow and MBG were grouped as optimal reperfusion (n=27) and their counterparts as no-reflow (NR, n=33). There were no differences in the clinical characteristics between groups. Patients in the NR group had higher heart rate, coronary angiographic severity, and CAC score. CAC score greater than 100 was associated independently with the presence of NR (odds ratio 4.4, 95% confidence interval 1.17-16.3). The CAC score of nonculprit coronary arteries was higher in NR individuals than in their counterparts (P=0.04). In addition, the CAC score of the isnfarct-related artery correlated negatively with the TIMI-flow rate (r=-0.54, P<0.001) and with the MBG (r=-0.32, P=0.04). The CAC score is associated with the presence of the NR phenomenon in STEMI patients2656256

Mdr-1 C3435t Polymorphism May Affect Blood Pressure In Resistant Hypertensive Patients Independently Of Its Effects On Aldosterone Release

Aldosterone increases plasma volume and may be involved with resistant hypertension. P-glycoprotein is a transporter involved in the distribution and disposition of aldosterone, and is encoded by the MDR-1 gene. MDR-1 has functional polymorphisms that may affect P-glycoprotein expression. We hypothesized that the C3435T polymorphism in MDR-1 could be associated with resistant hypertension and with changes in hypertension-related parameters. We studied 105 healthy volunteers, 137 hypertensive patients responsive to treatment, and 83 resistant hypertensive patients. While we found no association of C3435T genotypes with resistance to treatment (p = 0.31), C allele was associated with hypertension (p = 0.03). Furthermore, the CC genotype was associated with higher systolic blood pressure (p T affects mRNA stability (2005) Pharmacogenet Genomics, 15, pp. 693-704Sissung, T.M., Gardner, E.R., Piekarz, R.L., Impact of ABCB1 allelic variants on QTc interval prolongation (2011) Clin Cancer Res, 17, pp. 937-946Bochud, M., Eap, C.B., Maillard, M., Association of ABCB1 genetic variants with renal function in Africans and in Caucasians (2008) BMC Med Genomics, 1, p. 21Cascorbi, I., Paul, M., Kroemer, H.K., Pharmacogenomics of heart failure - Focus on drug disposition and action (2004) Cardiovasc Res, 64, pp. 32-39Eap, C.B., Bochud, M., Elston, R.C., CYP3A5 and ABCB1 genes influence blood pressure and response to treatment, and their effect is modified by salt (2007) Hypertension, 49, pp. 1007-1014VI Brazilian Guidelines on Hypertension [in Portuguese] (2010) Arq Bras Cardiol, 95, pp. 1-51Taylor, D.W., Sackett, D.L., Haynes, R.B., Compliance with antihypertensive drug therapy (1978) Ann N y Acad Sci, 304, pp. 390-403Morisky, D.E., Green, L.W., Levine, D.M., Concurrent and predictive validity of a self-reported measure of medication adherence (1986) Med Care, 24, pp. 67-74De Souza, W.A., Yugar-Toledo, J.C., Bergsten-Mendes, G., Effect of pharmaceutical care on blood pressure control and health-related quality of life in patients with resistant hypertension (2007) Am J Health Syst Pharm, 64, pp. 1955-1961Zolk, O., Jacobi, J., Pahl, A., MDR1 genotype-dependent regulation of the aldosterone system in humans (2007) Pharmacogenet Genomics, 17, pp. 137-144Manunta, P., Ferrandi, M., Bianchi, G., Endogenous ouabain in cardiovascular function and disease (2009) J Hypertens, 27, pp. 9-18Tripodi, G., Citterio, L., Kouznetsova, T., Steroid biosynthesis and renal excretion in human essential hypertension: Association with blood pressure and endogenous ouabain (2009) Am J Hypertens, 22, pp. 357-363Fromm, M.F., Importance of P-glycoprotein at blood-tissue barriers (2004) Trends Pharmacol Sci, 25, pp. 423-42

Infliximab Reduces Cardiac Output In Rheumatoid Arthritis Patients Without Heart Failure [infliximabe Reduz Débito Cardíaco Em Pacientes Com Artrite Reumatoide Sem Insuficiência Cardíaca]

Objective: Human anti-tumor necrosis factor (TNF-α) monoclonal antibody (infliximab) is used to treat autoimmune diseases such as rheumatoid arthritis (RA). Although the risk of worsening heart failure has been described in patients under chronic treatment, the acute cardiovascular effects of this drug are unknown in RA patients without heart failure. Methods: 14 RA patients with normal echocardiography and no history of heart failure were evaluated during the 2-hour infliximab (3-5 mg/kg) infusion period, using a noninvasive hemodynamic beat-to-beat system (Portapres). Stroke volume (SV); systolic, diastolic and mean blood pressures (SBP, DBP and MBP, respectively); cardiac output (CO); heart rate (HR); and total peripheral vascular resistance (PVR) were recorded. All patients also received saline infusion instead of infliximab as a control. Significant differences in hemodynamic parameters were determined using Tuckey's test. All values were expressed as mean ± standard deviation (SD). Results: Fourteen RA patients (6M/8F) with mean age of 47.2 ± 8.8 years were evaluated. A significant decrease was found in cardiac output and stroke volume (7.04 ± 2.3 to 6.12 ± 2.1 l/min and 91 ± 29.0 to 83 ± 28.8 mL/beat, respectively) after infliximab infusion. Although not statistically significant, a progressive increase was detected in SBP, DBP and total PVR during infusion. Saline infusion did not cause significant hemodynamic changes in the same group of RA patients. No adverse effects were observed during the infusion period. Conclusion: Acute infliximab administration decreased cardiac output due to low stroke volume in RA patients without heart disease. The results also demonstrated that, in spite of its negative inotropic effect, infliximab enhanced BP, probably by increasing PVR. © 2012 Elsevier Editora Ltda. All rights reserved.586698702Smolen, J.S., Aletaha, D., Koeller, M., Weisman, M.H., Emery, P., New therapies for treatment of rheumatoid arthritis (2007) Lancet., 370, pp. 1861-1874Doan, T., Massarotti, E., Rheumatoid arthritis: An overview of new and emerging therapies (2005) J Clin Pharmacol., 45, pp. 751-762Mann, D.L., Inflammatory mediators and the failing heart: Past, present, and the foreseeable future (2002) Circ Res., 91, pp. 988-998Lysander, W.J., van Lieshout, J.J., Non-invasive pulsatile arterial pressure and stroke volume changes from the human finger (2005) Exp Physiol., 90, pp. 437-446Wallberg-Jonsson, S., Johansson, H., Ohman, M.L., Rantapaa-Dahlqvist, S., Extent of inflammation predicts cardiovascular disease and overall mortality in seropositive rheumatoid arthritis. A retrospective cohort study from disease onset (1999) J Rheumatol., 26, pp. 2562-2571Wolfe, F., Flowers, N., Burke, T.A., Arguelles, L.M., Pettitt, D., Increase in lifetime adverse drug reactions, service utilization, and disease severity among patients who will start COX-2 specific inhibitors: Quantitative assessment of channeling bias and confounding by indication in 6689 patients with rheumatoid arthritis and osteoarthritis (2002) J Rheumatol., 29, pp. 1015-1022Bértolo, M.B., Brenol, C.V., Schainberg, C.G., Neubarth, F., Lima, F.A.C., Laurindo, I.M., Atualização do consenso brasileiro no diagnóstico e tratamento da artrite reumatóide (2007) Rev Bras Reumatol., 47, pp. 151-159Aletaha, D., Neogi, T., Silman, A.J., Funovits, J., Felson, D.T., Bingham III, C.O., 2010 rheumatoid arthritis classification criteria: An American College of Rheumatology/European League Against Rheumatism collaborative initiative (2010) Arthritis Rheum., 62, pp. 2569-2581Lang, E.A., Recommendations for chamber quantification: A report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group (2005) J Am Soc Echocardiogr., 18, pp. 1440-1463El Assaad, M.A., Topouchian, J.A., Darne, B.M., Asmar, R.G., Validation of the Omron HEM-907 device for blood pressure measurement (2002) Blood Press Monit., 7, pp. 237-241Chobanian, A.V., Bakris, G.L., Black, H.R., Cushman, W.C., Green, L.A., Izzo Jr., J.L., The Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 report (2003) JAMA., 289, pp. 2560-2572Langewouters, G.J., Settels, J.J., Roelandt, R., Wesseling, K.H., Why use Finapres or Portapres rather than intra-arterial or intermittent non-invasive techniques of blood pressure measuremant? (1998) J Med Eng Technol., 22, pp. 37-43Jansen, J.R.C., Schreuder, J.J., Mulier, J.P., Smith, N.T., Settels, J.J., Wesseling, K.H., A comparison of cardiac output derived from the arterial pressure wave against thermodilution in cardiac surgery patients (2001) Br J Anaesth., 87, pp. 212-222Leonetti, P., Audat, F., Girard, A., Laude, D., Lefrère, F., Elghozi, J., Stroke volume monitored by modeling flow from finger arterial pressure waves mirrors blood volume withdrawn by phlebotomy (2004) Clin Auton Res., 14, pp. 176-181Ramey, D.R., Raynauld, J.P., Fries, J.F., The health assessment questionnaire 1992: Status and review (1992) Arthritis Care Res., 5, pp. 119-129Wolfe, F., A reappraisal of HAQ disability in rheumatoid arthritis (2000) Arthritis Rheum., 43, pp. 2751-2761Kumar, A., Anel, R., Bunnell, E., Habet, K., Neumann, A., Wolff, D., Effect of large volume infusion on left ventricular volumes, performance and contractility parameters in normal volunteers (2004) Intensive Care Med., 30, pp. 1361-1369Ku, I.A., Imboden, J.B., Hsue, P.Y., Ganz, P., Rheumatoid arthritis: Model of systemic inflammation driving atherosclerosis (2009) Circ J., 73, pp. 977-985van de Putte, L.B., Atkins, C., Malaise, M., Sany, J., Russell, A.S., van Riel, P.L., Efficacy and safety of adalimumab as monotherapy in patients with rheumatoid arthritis for whom previous disease modifying antirheumatic drug treatment has failed (2004) Ann Rheum Dis., 63, pp. 508-516Weinblatt, M.E., Keystone, E.C., Furst, D.E., Moreland, L.W., Weisman, M.H., Birbara, C.A., Adalimumab, a fully human anti-tumor necrosis factor alpha monoclonal antibody, for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate: The ARMADA trial (2003) Arthritis Rheum., 48, pp. 35-45Mann, D.L., McMurray, J.J., Packer, M., Swedberg, K., Borer, J.S., Colucci, W.S., Targeted anticytokine therapy in patients with chronic heart failure: Results of the Randomized Etanercept Worldwide Evaluation (RENEWAL) (2004) Circulation., 109, pp. 1594-1602Chung, E.S., Packer, M., Lo, K.H., Fasanmade, A.A., Willerson, J.T., Randomized, double-blind, placebo-controlled, pilot trial of infliximab, a chimeric monoclonal antibody to tumor necrosis factor-alpha, in patients with moderate-to-severe heart failure: Results of the anti-TNF Therapy Against Congestive Heart Failure (ATTACH) trial (2003) Circulation., 107, pp. 3133-3140Kubota, T., Bounoutas, G.S., Miyagishima, M., Kadokami, T., Sanders, V.J., Bruton, C., Soluble tumor necrosis factor receptor abrogates myocardial inflammation but not hypertrophy in cytokine-induced cardiomyopathy (2000) Circulation., 101, pp. 2518-2525Kadokami, T., Frye, C., Lemster, B., Wagner, C.L., Feldman, A.M., McTiernan, C.F., Anti-tumor necrosis factor-alpha antibody limits heart failure in a transgenic model (2001) Circulation., 104, pp. 1094-1097Zink, A., Strangfeld, A., Schneider, M., Herzer, P., Hierse, F., Stoyanova-Scholz, M., Effectiveness of tumor necrosis factor inhibitors in rheumatoid arthritis in an observational cohort study: Comparison of patients according to their eligibility for major randomized clinical trials (2006) Arthritis Rheum., 54, pp. 3399-3407Khaper, N., Bryan, S., Dhingra, S., Singal, R., Bajaj, A., Pathak, C.M., Targeting the vicious inflammation-oxidative stress cycle for the management of heart failure (2010) Antioxid Redox Signal., 13, pp. 1033-1049Giordano, F.J., Oxygen, oxidative stress, hypoxia, and heart failure (2005) J Clin Invest., 115, pp. 500-508Matsuzawa, A., Ichijo, H., Redox control of cell fate by MAP kinase: Physiological roles of ASK1-MAP kinase pathway in stress signaling (2008) Biochim Biophys Acta., 1780, pp. 1325-1336Scallon, B.J., Moore, M.A., Trinh, H., Knight, D.M., Ghrayeb, J., Chimeric anti-TNFalpha monoclonal antibody cA2 binds recombinant transmembrane TNFalpha and activates immune effector functions (1995) Cytokine., 7, pp. 251-25

Elevated Cetp Activity During Acute Phase Of Myocardial Infarction Is Independently Associated With Endothelial Dysfunction And Adverse Clinical Outcome

Objective: Recent data suggests that cholesteryl ester transfer protein (CETP) activity may interact with acute stress conditions via inflammatory-oxidative response and thrombogenesis. We investigated this assumption in patients with ST-elevation myocardial infarction (STEMI). Methods: Consecutive patients with STEMI (n=116) were enrolled &lt;24-hof symptoms onset and were followed for 180 days. Plasma levels of C-reactive protein (CRP), interleukin-2 (IL-2), tumor necrosis factor (TNFα), 8-isoprostane, nitric oxide (NOx) and CETP activity were measured at enrollment (D1) and at fifth day (D5). Flow-mediated dilation (FMD) was assessed by ultrasound and coronary thrombus burden (CTB) was evaluated by angiography. Results: Neither baseline nor the change of CETP activity from D1 to D5 was associated with CRP, IL-2, TNFα, 8-isoprostane levels or CTB. The rise in NOx from D1 to D5 was inferior [3.5(-1; 10) vs. 5.5(-1; 12); p&lt;0.001] and FMD was lower [5.9(5.5) vs. 9.6(6.6); p=0.047] in patients with baseline CETP activity above the median value than in their counterparts. Oxidized HDL was measured by thiobarbituric acid reactive substances (TBARS) in isolated HDL particles and increased from D1 to D5, and remaining elevated at D30. The change in TBARS content in HDL was associated with CETP activity (r=0.72; p=0.014) and FMD (r=-0.61; p=0.046). High CETP activity at admission was associated with the incidence of sudden death and recurrent MI at 30 days (OR 12.8; 95% CI 1.25-132; p=0.032) and 180 days (OR 3.3; 95% CI 1.03-10.7; p=0.044). Conclusions: An enhanced CETP activity during acute phase of STEMI is independently associated with endothelial dysfunction and adverse clinical outcome.2372777783Cazita, P.M., Barbeiro, D.F., Moretti, A.I., Quintao, E.C., Soriano, F.G., Human cholesteryl ester transfer protein expression enhances the mouse survival rate in an experimental systemic inflammation model: a novel role for CETP (2008) Shock, 30 (5), pp. 590-595Deguchi, H., Fernandez, J.A., Griffin, J.H., Plasma cholesteryl ester transfer protein and blood coagulability (2007) Thromb. Haemost., 98 (6), pp. 1160-1164Grion, C.M., Cardoso, L.T., Perazolo, T.F., Garcia, A.S., Barbosa, D.S., Morimoto, H.K., Lipoproteins and CETP levels as risk factors for severe sepsis in hospitalized patients (2010) Eur. J. Clin. Investig., 40 (4), pp. 330-338Frangogiannis, N.G., Smith, C.W., Entman, M.L., The inflammatory response in myocardial infarction (2002) Cardiovasc. Res., 53 (1), pp. 31-47Campo, G., Valgimigli, M., Ferraresi, P., Malagutti, P., Baroni, M., Arcozzi, C., Tissue factor and coagulation factor VII levels during acute myocardial infarction: association with genotype and adverse events (2006) Arterioscler. Thromb. Vasc. Biol., 26 (12), pp. 2800-2806Minnema, M.C., Peters, R.J., de Winter, R., Lubbers, Y.P., Barzegar, S., Bauer, K.A., Activation of clotting factors XI and IX in patients with acute myocardial infarction (2000) Arterioscler. Thromb. Vasc. Biol., 20 (11), pp. 2489-2493Sposito, A.C., Carvalho, L.S., Cintra, R.M., Araujo, A.L., Ono, A.H., Andrade, J.M., Rebound inflammatory response during the acute phase of myocardial infarction after simvastatin withdrawal (2009) Atherosclerosis, 207 (1), pp. 191-194Lagrost, L., Determination of the mass concentration and the activity of the plasma cholesteryl ester transfer protein (CETP) (1998) Methods Mol. 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Res., 99 (12), pp. e88-99Fang, C., Yoon, S., Tindberg, N., Jarvelainen, H.A., Lindros, K.O., Ingelman-Sundberg, M., Hepatic expression of multiple acute phase proteins and down-regulation of nuclear receptors after acute endotoxin exposure (2004) Biochem. Pharmacol., 67 (7), pp. 1389-1397Luo, Y., Tall, A.R., Sterol upregulation of human CETP expression invitro and in transgenic mice by an LXR element (2000) J.Clin. Investig., 105 (4), pp. 513-520Christison, J.K., Rye, K.A., Stocker, R., Exchange of oxidized cholesteryl linoleate between LDL and HDL mediated by cholesteryl ester transfer protein (1995) J.Lipid Res., 36 (9), pp. 2017-2026Matsunaga, T., Hokari, S., Koyama, I., Harada, T., Komoda, T., NF-kappa B activation in endothelial cells treated with oxidized high-density lipoprotein (2003) Biochem. Biophys. Res. 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