Displaying publications 61 - 80 of 114 in total

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  1. Krackhardt F, Waliszewski M, Wan Ahmad WA, Kočka V, Toušek P, Janek B, et al.
    PLoS One, 2020;15(1):e0226606.
    PMID: 31929543 DOI: 10.1371/journal.pone.0226606
    BACKGROUND: The objective of this study was to assess regional and ethnic differences in an unselected patient population treated with polymer-free sirolimus-eluting stents (PF-SES) in Asia and Europe.

    METHODS: Two all-comers observational studies based on the same protocol (ClinicalTrials.gov Identifiers: NCT02629575 and NCT02905214) were combined for data analysis to assure sufficient statistical power. The primary endpoint was the accumulated target lesion revascularization (TLR) rate at 9-12 months.

    RESULTS: Of the total population of 7243 patients, 44.0% (3186) were recruited in the Mediterranean region and 32.0% (2317) in central Europe. The most prominent Asian region was South Korea (17.6%, 1274) followed by Malaysia (5.7%, 413). Major cardiovascular risk factors varied significantly across regions. The overall rates for accumulated TLR and MACE were low with 2.2% (140/6374) and 4.4% (279/6374), respectively. In ACS patients, there were no differences in terms of MACE, TLR, MI and accumulated mortality between the investigated regions. Moreover, dual antiplatelet therapy (DAPT) regimens were substantially longer in Asian countries even in patients with stable coronary artery disease as compared to those in Europe.

    CONCLUSIONS: PF-SES angioplasty is associated with low clinical event rates in all regions. Further reductions in clinical event rates seem to be associated with longer DAPT regimens.

    Matched MeSH terms: Platelet Aggregation Inhibitors
  2. Amin AM, Sheau Chin L, Teh CH, Mostafa H, Mohamed Noor DA, Abdul Kader MASK, et al.
    Eur J Pharm Sci, 2018 May 30;117:351-361.
    PMID: 29526765 DOI: 10.1016/j.ejps.2018.03.011
    Dual antiplatelet therapy (DAPT) of clopidogrel and aspirin is crucial for coronary artery disease (CAD) patients undergoing percutaneous coronary intervention (PCI). However, some patients may endure clopidogrel high on treatment platelets reactivity (HTPR) which may cause thromboembolic events. Clopidogrel HTPR is multifactorial with some genetic and non-genetic factors contributing to it. We aimed to use nuclear magnetic resonance (1H NMR) pharmacometabolomics analysis of plasma to investigate this multifactorial and identify metabolic phenotypes and pathways associated with clopidogrel HTPR. Blood samples were collected from 71 CAD patients planned for interventional angiographic procedure (IAP) before the administration of clopidogrel 600 mg loading dose (LD) and 6 h after the LD. Platelets function testing was done 6 h post-LD using VerifyNow® P2Y12 assay. Pre-dose and post-dose plasma samples were analysed using 1H NMR. Multivariate statistical analysis was used to indicate the discriminating metabolites. Two metabotypes, each with 34 metabolites (pre-dose and post-dose) were associated with clopidogrel HTPR. Pathway analysis of these metabotypes revealed that aminoacyl-tRNA biosynthesis, nitrogen metabolism and glycine-serine-threonine metabolism are the most perturbed metabolic pathways associated with clopidogrel HTPR. Furthermore, the identified biomarkers indicated that clopidogrel HTPR is multifactorial where the metabolic phenotypes of insulin resistance, type two diabetes mellitus, obesity, gut-microbiota and heart failure are associated with it. Pharmacometabolomics analysis of plasma revealed new insights on the implicated metabolic pathways and the predisposing factors of clopidogrel HTPR.
    Matched MeSH terms: Platelet Aggregation Inhibitors/adverse effects; Platelet Aggregation Inhibitors/blood; Platelet Aggregation Inhibitors/therapeutic use*
  3. Sharma AK, Khanna D, Balakumar P
    Int J Cardiol, 2014 Mar 15;172(2):530-2.
    PMID: 24495652 DOI: 10.1016/j.ijcard.2014.01.053
    Matched MeSH terms: Platelet Aggregation Inhibitors/administration & dosage*
  4. Periayah MH, Halim AS, Hussein AR, Saad AZ, Rashid AH, Noorsal K
    Int J Biol Macromol, 2013 Jan;52:244-9.
    PMID: 23063426 DOI: 10.1016/j.ijbiomac.2012.10.001
    Chitosan-derived hemostatic agents with various formulations may have distinct potential in hemostasis. This study assessed the ability of different grades and forms of chitosan derivatives as hemostatic agents to enhance platelet adhesion and aggregation in vitro. The chitosan derivatives utilized were 2% NO-CMC, 7% NO-CMC (with 0.45 mL collagen), 8% NO-CMC, O-C 52, 5% O-CMC-47, NO-CMC-35, and O-C 53. Samples of chitosan derivatives weighing 5mg were incubated at 37°C with 50 μL of phosphate buffer saline (PBS) (pH 7.4) for 60 min. The morphological features of the platelets upon adherence to the chitosan were viewed using scanning electron microscope (SEM), and the platelet count was analyzed with an Automated Hematology Analyzer. For platelet aggregation, we added an adenosine diphosphate (ADP) agonist to induce the chitosan-adhered platelets. O-C 52 bound with platelets exhibited platelet aggregates and clumps on the surface of the membrane layer with approximately 70-80% coverage. A statistically significant correlation (p<0.01) for the platelet count was identified between the baseline value and the values at 10 min and 20 min. The results indicate that O-C 53 and O-C 52 were able to promote clotting have the potential to induce the release of platelets engaged in the process of hemostasis.
    Matched MeSH terms: Platelet Aggregation/drug effects*
  5. Norlinah MI, Shahizon AM
    Med J Malaysia, 2008 Dec;63(5):410-2.
    PMID: 19803303 MyJurnal
    Secondary paroxysmal dyskinesias (PxD) have been previously reported in patients with multiple sclerosis, lacunar infarcts, head trauma, metabolic disorders such as hyperglycaemia, hypocalcaemia, migraine and central nervous system (CNS) infections. The causative lesions typically involve the basal ganglia structures, medulla and rarely the spinal cord. We report two patients who presented with paroxysmal dyskinesias as the only manifestation of subcortical white-matter ischaemia. Patient 1 presented with 3-year history of paroxysmal kinesigenic dyskinesia (PKD) and patient 2 with 6-month history of paroxysmal nonkinesigenic dyskinesia (PNKD). All investigations, including CSF oligoclonal bands were negative, except for a brain MRI which showed multiple, non-enhancing subcortical white matter lacunar infarcts. Therefore, subcortical white matter ischaemia should also be included in the differential diagnosis of PxD.
    Matched MeSH terms: Platelet Aggregation Inhibitors/therapeutic use
  6. Jantan I, Raweh SM, Sirat HM, Jamil S, Mohd Yasin YH, Jalil J, et al.
    Phytomedicine, 2008 Apr;15(4):306-9.
    PMID: 17913483
    Twelve compounds isolated from Alpinia mutica Roxb., Kaempferia rotunda Linn., Curcuma xanthorhiza Roxb., Curcuma aromatica Valeton and Zingiber zerumbet Smith (Family: Zingiberaceae) and three synthesized derivatives of xanthorrhizol were evaluated for their ability to inhibit arachidonic acid- (AA), collagen- and ADP-induced platelet aggregation in human whole blood. Antiplatelet activity of the compounds was measured in vitro by the Chrono Log whole blood aggregometer using an electrical impedance method. Among the compounds tested, curcumin from C. aromatica, cardamonin, pinocembrine and 5,6-dehydrokawain from A. mutica and 3-deacetylcrotepoxide from K. rotunda showed strong inhibition on platelet aggregation induced by AA with IC(50) values of less than 84 microM. Curcumin was the most effective antiplatelet compound as it inhibited AA-, collagen- and ADP-induced platelet aggregation with IC(50) values of 37.5, 60.9 and 45.7 microM, respectively.
    Matched MeSH terms: Platelet Aggregation/drug effects*
  7. Foo LC, Roshidah I, Aimy MB
    Thromb. Haemost., 1991 Mar 4;65(3):317-9.
    PMID: 2048056 DOI: 10.1055/s-0038-1648142
    Platelet aggregation to collagen, and productions of 6-keto-prostaglandin-F1-alpha and thromboxane B2 during aggregation were measured after an overnight fast, involving both food and cigarettes, in 19 clinically healthy habitual smokers (10 or more cigarettes/day) and 23 non-smokers receiving the same diet. The subjects (all males; ages = 21-30 years) were residents of a school hostel. Mean platelet aggregation was significantly lower in smokers than non-smokers (23.2 ohms vs 31.5 ohms, p less than 0.005). Non-smokers had significantly higher mean concentration of 6-keto-prostaglandin-F1-alpha than smokers (109.8 pmol/l vs 92.3 pmol/l, p less than 0.05). The level of thromboxane B2 did not differ significantly between the two groups. These observations suggest that the role of smoking as a risk factor for ischaemic heart disease is unlikely to be related to a direct enhancement of aggregation. On the contrary, the observations seem to suggest that habitual smoking may directly reduce platelet aggregability.
    Matched MeSH terms: Platelet Aggregation/drug effects*
  8. Vallance TM, Ravishankar D, Albadawi DAI, Layfield H, Sheard J, Vaiyapuri R, et al.
    Sci Rep, 2019 12 03;9(1):18258.
    PMID: 31796818 DOI: 10.1038/s41598-019-54617-w
    Platelets are small circulating blood cells that play essential roles in the maintenance of haemostasis via blood clotting. However, they also play critical roles in the regulation of innate immune responses. Inflammatory receptors, specifically Toll-like receptor (TLR)-4, have been reported to modify platelet reactivity. A plethora of studies have reported controversial functions of TLR4 in the modulation of platelet function using various chemotypes and preparations of its ligand, lipopolysaccharide (LPS). The method of preparation of LPS may explain these discrepancies however this is not fully understood. Hence, to determine the impact of LPS on platelet activation, we used ultrapure preparations of LPS from Escherichia coli (LPSEC), Salmonella minnesota (LPSSM), and Rhodobacter sphaeroides (LPSRS) and examined their actions under diverse experimental conditions in human platelets. LPSEC did not affect platelet activation markers such as inside-out signalling to integrin αIIbβ3 or P-selectin exposure upon agonist-induced activation in platelet-rich plasma or whole blood whereas LPSSM and LPSRS inhibited platelet activation under specific conditions at supraphysiological concentrations. Overall, our data demonstrate that platelet activation is not largely influenced by any of the ultrapure LPS chemotypes used in this study on their own except under certain conditions.
    Matched MeSH terms: Platelet Aggregation/drug effects
  9. Wong WT, Ismail M, Imam MU, Zhang YD
    BMC Complement Altern Med, 2016 Jul 28;16:252.
    PMID: 27465266 DOI: 10.1186/s12906-016-1223-9
    Rice bran is bioactive-rich and has proven health benefits for humans. Moreover, its source, the brown rice has antioxidant, hypolipidemic and other functional properties that are increasingly making it a nutritional staple especially in Asian countries. This study investigated the antiplatelet aggregation mechanisms of crude hexane/methanolic rice bran extract, in which policosanol was the targeted bioactive. Platelets play a vital role in pathogenesis of atherosclerosis and cardiovascular diseases, and their increased activities could potentially cause arterial thrombus formation or severe bleeding disorders. Thus, in this study, platelet aggregation and adhesion of platelets to major components of basal lamina were examined in vitro. In addition, cellular protein secretion was quantified as a measurement of platelet activation.
    Matched MeSH terms: Platelet Aggregation/drug effects*
  10. Law ZK, Desborough M, Roberts I, Al-Shahi Salman R, England TJ, Werring DJ, et al.
    J Am Heart Assoc, 2021 02;10(5):e019130.
    PMID: 33586453 DOI: 10.1161/JAHA.120.019130
    Background Antiplatelet therapy increases the risk of hematoma expansion in intracerebral hemorrhage (ICH) while the effect on functional outcome is uncertain. Methods and Results This is an exploratory analysis of the TICH-2 (Tranexamic Acid in Intracerebral Hemorrhage-2) double-blind, randomized, placebo-controlled trial, which studied the efficacy of tranexamic acid in patients with spontaneous ICH within 8 hours of onset. Multivariable logistic regression and ordinal regression were performed to explore the relationship between pre-ICH antiplatelet therapy, and 24-hour hematoma expansion and day 90 modified Rankin Scale score, as well as the effect of tranexamic acid. Of 2325 patients, 611 (26.3%) had pre-ICH antiplatelet therapy. They were older (mean age, 75.7 versus 66.5 years), more likely to have ischemic heart disease (25.4% versus 2.7%), ischemic stroke (36.2% versus 6.3%), intraventricular hemorrhage (40.2% versus 27.5%), and larger baseline hematoma volume (mean, 28.1 versus 22.6 mL) than the no-antiplatelet group. Pre-ICH antiplatelet therapy was associated with a significantly increased risk of hematoma expansion (adjusted odds ratio [OR], 1.28; 95% CI, 1.01-1.63), a shift toward unfavorable outcome in modified Rankin Scale (adjusted common OR, 1.58; 95% CI, 1.32-1.91) and a higher risk of death at day 90 (adjusted OR, 1.63; 95% CI, 1.25-2.11). Tranexamic acid reduced the risk of hematoma expansion in the overall patients with ICH (adjusted OR, 0.76; 95% CI, 0.62-0.93) and antiplatelet subgroup (adjusted OR, 0.61; 95% CI, 0.41-0.91) with no significant interaction between pre-ICH antiplatelet therapy and tranexamic acid (P interaction=0.248). Conclusions Antiplatelet therapy is independently associated with hematoma expansion and unfavorable functional outcome. Tranexamic acid reduced hematoma expansion regardless of prior antiplatelet therapy use. Registration URL: https://www.isrctn.com; Unique identifier: ISRCTN93732214.
    Matched MeSH terms: Platelet Aggregation Inhibitors/adverse effects*
  11. Akkaif MA, Ng ML, Sk Abdul Kader MA, Daud NAA, Sha'aban A, Ibrahim B
    Pharmacol Rep, 2021 Dec;73(6):1551-1564.
    PMID: 34283374 DOI: 10.1007/s43440-021-00309-0
    BACKGROUND: Ticagrelor is an oral antiplatelet drug that can reversibly bind to the platelet P2Y12 receptor. Ticagrelor is metabolized mainly by CYP3A4 and produces a rapid blood concentration-dependent platelet inhibitory effect. Unlike other P2Y12 receptor antagonists, many clinical features of ticagrelor are not related to P2Y12 receptor antagonism.

    PURPOSE: This review aims to gather existing literature on the clinical effects of ticagrelor after inhibiting adenosine uptake.

    METHODOLOGY: The current study reviewed literature related to the effects of ticagrelor on adenosine metabolism. The review also examined the drug's biological effects and clinical characteristics to see how it could be used in a clinical setting.

    RESULTS: Many studies have shown that ticagrelor can inhibit equilibrative nucleoside transporter 1 (ENT1). This inhibition leads to intracellular adenosine uptake, increased adenosine half-life and plasma concentration levels and an enhanced adenosine-mediated biological effect.

    CONCLUSIONS: Based on the studies reviewed, it was found that ticagrelor essentially inhibits adenosine absorption of adenosine into cells through ENT1, which increases the concentration in the blood and subsequently increases the protection of the heart muscle by adenosine. It also prevents platelet aggregation, and extends the biological effects of coronary arteries. Moreover, it leads to a lower mortality rate in acute coronary syndrome (ACS) patients.

    Matched MeSH terms: Platelet Aggregation Inhibitors/pharmacology
  12. Ishak R, Mohamed AB, Hassan K
    Malays J Reprod Health, 1990 Jun;8(1):1-4.
    PMID: 12316339
    A study was conducted on a total of 100 women attending the Family Planning Clinic in Kuala Lumpur. 50 took combined low-dose estrogen and progesterone pills for a year or more and the other 50 used different methods of birth control. Platelet aggregation, ATP release, Thromboxane B2, and 6-keto-prostaglandin F1alpha estimations were made to evaluate the effect of oral contraceptives (OCs) on platelet function and prostanoid production. The results showed no significant differences in the parameters measured in the 2 groups investigated. These findings are comparable to those reported by other studies, suggesting relatively low risk, if any, of thrombosis in OC users.
    Matched MeSH terms: Platelet Aggregation*
  13. Gan YL, Fu JY, Lai OM, Chew BH, Yuen KH, Teng KT, et al.
    Sci Rep, 2017 09 14;7(1):11542.
    PMID: 28912593 DOI: 10.1038/s41598-017-11813-w
    Tocotrienols, the unsaturated form of vitamin E, were reported to modulate platelet aggregation and thrombotic mechanisms in pre-clinical studies. Using a Food and Drug Administration (FDA)-approved cartridge-based measurement system, a randomised, double-blind, crossover and placebo-controlled trial involving 32 metabolic syndrome adults was conducted to investigate the effect of palm-based tocotrienols and tocopherol (PTT) mixture supplementation on platelet aggregation reactivity. The participants were supplemented with 200 mg (69% tocotrienols and 31% α-tocopherol) twice daily of PTT mixture or placebo capsules for 14 days in a random order. After 14 days, each intervention was accompanied by a postprandial study, in which participants consumed 200 mg PTT mixture or placebo capsule after a meal. Blood samples were collected on day 0, day 14 and during postprandial for the measurement of platelet aggregation reactivity. Subjects went through a 15-day washout period before commencement of subsequent intervention. Fasting platelet aggregation reactivity stimulated with adenosine diphosphate (ADP) did not show substantial changes after supplementation with PTT mixture compared to placebo (p = 0.393). Concomitantly, changes in postprandial platelet aggregation reactivity remained similar between PTT mixture and placebo interventions (p = 0.408). The results of this study highlight the lack of inhibitory effect on platelet aggregation after short-term supplementation of PTT mixture in participants with metabolic syndrome.
    Matched MeSH terms: Platelet Aggregation/drug effects*
  14. Amin AM, Sheau Chin L, Mohamed Noor DA, Mostafa H, Abdul Kader MASK, Kah Hay Y, et al.
    Thromb Res, 2017 10;158:22-24.
    PMID: 28802144 DOI: 10.1016/j.thromres.2017.07.032
    Matched MeSH terms: Platelet Aggregation Inhibitors/pharmacology*
  15. Hwong WY, Abdul Aziz Z, Sidek NN, Bots ML, Selvarajah S, Kappelle LJ, et al.
    BMC Neurol, 2017 Nov 23;17(1):203.
    PMID: 29169331 DOI: 10.1186/s12883-017-0984-1
    BACKGROUND: Evaluation of secondary stroke prevention in low and middle-income countries remains limited. This study assessed the prescription of secondary preventive drugs among ischemic stroke patients upon hospital discharge in Malaysia and identified factors related to the prescribing decisions.

    METHODS: From Malaysian National Stroke Registry, we included patients with non-fatal ischemic stroke. Prescriptions of antiplatelet, anticoagulants, antihypertensive drugs and lipid-lowering drugs were assessed. Multi-level logistic regressions were performed to determine the relation between potential factors and drug prescriptions.

    RESULTS: Of 5292 patients, 48% received antihypertensive drugs, 88.9% antiplatelet and 88.7% lipid-lowering drugs upon discharge. Thirty-three percent of patients with an indication for anticoagulants (n = 391) received it. Compared to patients <=50 years, patients above 70 years were less likely to receive antiplatelet (OR: 0.72, 95% CI: 0.50-1.03), lipid-lowering drugs (OR: 0.66, 95% CI: 0.45-0.95) and anticoagulants (OR: 0.27, 95% CI: 0.09-0.83). Patients with moderate to severe disability upon discharge had less odds of receiving secondary preventive drugs; an odds ratio of 0.57 (95% CI: 0.45-0.71) for antiplatelet, 0.86 (95% CI: 0.75-0.98) for antihypertensive drugs and 0.78 (95% CI: 0.63-0.97) for lipid-lowering drugs in comparison to those with minor disability. Having prior specific comorbidities and drug prescriptions significantly increased the odds of receiving these drugs. No differences were found between sexes and ethnicities.

    CONCLUSIONS: Prescription of antihypertensive drugs and anticoagulants among ischemic stroke patients in Malaysia were suboptimal. Efforts to initiate regular clinical audits to evaluate the uptake and effectiveness of secondary preventive strategies are timely in low and middle-income settings.

    Matched MeSH terms: Platelet Aggregation Inhibitors/therapeutic use
  16. Berwanger O, Abdelhamid M, Alexander T, Alzubaidi A, Averkov O, Aylward P, et al.
    Clin Cardiol, 2018 Oct;41(10):1322-1327.
    PMID: 30098028 DOI: 10.1002/clc.23043
    Primary percutaneous coronary intervention (PCI) is the preferred reperfusion method in patients with ST-segment elevation myocardial infarction (STEMI). In patients with STEMI who cannot undergo timely primary PCI, pharmacoinvasive treatment is recommended, comprising immediate fibrinolytic therapy with subsequent coronary angiography and rescue PCI if needed. Improving clinical outcomes following fibrinolysis remains of great importance for the many patients globally for whom rapid treatment with primary PCI is not possible. For patients with acute coronary syndrome who underwent primary PCI, the PLATO trial demonstrated superior efficacy of ticagrelor relative to clopidogrel. Results in the predefined subgroup of patients with STEMI were consistent with the overall PLATO trial. Patients who received fibrinolytic therapy in the 24 hours before randomization were excluded from PLATO, and there is thus a lack of data on the safety of using ticagrelor in conjunction with fibrinolytic therapy in the first 24 hours after STEMI. The TREAT study addresses this knowledge gap; patients with STEMI who had symptom onset within the previous 24 hours and had received fibrinolytic therapy (of whom 89.4% had also received clopidogrel) were randomized to treatment with ticagrelor or clopidogrel (median time between fibrinolysis and randomization: 11.5 hours). At 30 days, ticagrelor was found to be non-inferior to clopidogrel for the primary safety outcome of Thrombolysis in Myocardial Infarction (TIMI)-defined first major bleeding. Considering together the results of the PLATO and TREAT studies, initiating or switching to treatment with ticagrelor within the first 24 hours after STEMI in patients receiving fibrinolysis is reasonable.
    Matched MeSH terms: Platelet Aggregation Inhibitors/therapeutic use
  17. Williams HF, Mellows BA, Mitchell R, Sfyri P, Layfield HJ, Salamah M, et al.
    PLoS Negl Trop Dis, 2019 Jan;13(1):e0007041.
    PMID: 30695027 DOI: 10.1371/journal.pntd.0007041
    Snakebite is a major neglected tropical health issue that affects over 5 million people worldwide resulting in around 1.8 million envenomations and 100,000 deaths each year. Snakebite envenomation also causes innumerable morbidities, specifically loss of limbs as a result of excessive tissue/muscle damage. Snake venom metalloproteases (SVMPs) are a predominant component of viper venoms, and are involved in the degradation of basement membrane proteins (particularly collagen) surrounding the tissues around the bite site. Although their collagenolytic properties have been established, the molecular mechanisms through which SVMPs induce permanent muscle damage are poorly understood. Here, we demonstrate the purification and characterisation of an SVMP from a viper (Crotalus atrox) venom. Mass spectrometry analysis confirmed that this protein is most likely to be a group III metalloprotease (showing high similarity to VAP2A) and has been referred to as CAMP (Crotalus atrox metalloprotease). CAMP displays both collagenolytic and fibrinogenolytic activities and inhibits CRP-XL-induced platelet aggregation. To determine its effects on muscle damage, CAMP was administered into the tibialis anterior muscle of mice and its actions were compared with cardiotoxin I (a three-finger toxin) from an elapid snake (Naja pallida) venom. Extensive immunohistochemistry analyses revealed that CAMP significantly damages skeletal muscles by attacking the collagen scaffold and other important basement membrane proteins, and prevents their regeneration through disrupting the functions of satellite cells. In contrast, cardiotoxin I destroys skeletal muscle by damaging the plasma membrane, but does not impact regeneration due to its inability to affect the extracellular matrix. Overall, this study provides novel insights into the mechanisms through which SVMPs induce permanent muscle damage.
    Matched MeSH terms: Platelet Aggregation/drug effects
  18. Ahrens I, Averkov O, Zúñiga EC, Fong AYY, Alhabib KF, Halvorsen S, et al.
    Clin Cardiol, 2019 Oct;42(10):1028-1040.
    PMID: 31317575 DOI: 10.1002/clc.23232
    Clinical guidelines for the treatment of patients with non-ST-segment elevation myocardial infarction (NSTEMI) recommend an invasive strategy with cardiac catheterization, revascularization when clinically appropriate, and initiation of dual antiplatelet therapy regardless of whether the patient receives revascularization. However, although patients with NSTEMI have a higher long-term mortality risk than patients with ST-segment elevation myocardial infarction (STEMI), they are often treated less aggressively; with those who have the highest ischemic risk often receiving the least aggressive treatment (the "treatment-risk paradox"). Here, using evidence gathered from across the world, we examine some reasons behind the suboptimal treatment of patients with NSTEMI, and recommend approaches to address this issue in order to improve the standard of healthcare for this group of patients. The challenges for the treatment of patients with NSTEMI can be categorized into four "P" factors that contribute to poor clinical outcomes: patient characteristics being heterogeneous; physicians underestimating the high ischemic risk compared with bleeding risk; procedure availability; and policy within the healthcare system. To address these challenges, potential approaches include: developing guidelines and protocols that incorporate rigorous definitions of NSTEMI; risk assessment and integrated quality assessment measures; providing education to physicians on the management of long-term cardiovascular risk in patients with NSTEMI; and making stents and antiplatelet therapies more accessible to patients.
    Matched MeSH terms: Platelet Aggregation Inhibitors/therapeutic use*
  19. Moharam BA, Jantan I, Jalil J, Ahmad F
    Phytother Res, 2012 May;26(5):687-91.
    PMID: 22002630 DOI: 10.1002/ptr.3620
    Phytochemical investigation on the bark of Goniothalamus tapis Miq. and G. uvaroides King has resulted in the isolation of eight styryl-lactones, (-)-cryptomeridiol, liriodenine, 3-methyl-1H-benz[f]indole-4,9-dione, (-)-stigmasterol and dimethyl terephthalate. The structures of the compounds were elucidated by spectroscopic techniques. The compounds were evaluated for their effect on platelet-activating factor (PAF) receptor binding on rabbit platelets using (3) H-PAF as a ligand. Among the compounds tested, (-)-cryptomeridiol, (+)-goniothalamin and (+)-isoaltholactone exhibited a significant and concentration-dependent inhibitory effect on PAF receptor binding, with inhibitory concentration (IC)(50) values of 17.5, 19.7 and 46.5 µm, respectively. The inhibitory effects of the first two compounds were comparable to that obtained from the positive control, cedrol. The results indicated that these compounds were strong PAF receptor binding inhibitors.
    Matched MeSH terms: Platelet Aggregation/drug effects; Platelet Aggregation Inhibitors/isolation & purification; Platelet Aggregation Inhibitors/pharmacology*; Platelet Aggregation Inhibitors/chemistry
  20. Hassan Y, Al-Jabi SW, Aziz NA, Looi I, Zyoud SH
    Basic Clin Pharmacol Toxicol, 2012 Apr;110(4):370-7.
    PMID: 22023326 DOI: 10.1111/j.1742-7843.2011.00825.x
    There has been recent interest in combining antiplatelets, angiotensin-converting enzyme inhibitors (ACEIs) and statins in primary and secondary ischaemic stroke prevention. This observational study was performed to evaluate the impact of adding ACEIs and/or statins to antiplatelets on post-stroke in-hospital mortality. Ischaemic stroke patients attending a hospital in Malaysia over an 18-month period were evaluated. Patients were categorized according to their vital status at discharge. Data included demographic information, risk factors, clinical characteristics and previous medications with particular attention on antiplatelets, ACEIs and statins. In-hospital mortality was compared among patients who were not taking antiplatelets, ACEIs or statins before stroke onset versus those who were taking antiplatelets alone or in combination with either ACEIs, statins or both. Data analysis was performed using SPSS version 15. Overall, 637 patients met the study inclusion criteria. After controlling for the effects of confounders, adding ACEIs or statins to antiplatelets significantly decreased the incidence of death after stroke attack by 68% (p = 0.036) and 81% (p = 0.010), respectively, compared to patients on antiplatelets alone or none of these medications. Additionally, the addition of both ACEIs and statins to antiplatelet medication resulted in the highest reduction (by 94%) of the occurrence of death after stroke attack (p < 0.001). Our results suggest that adding ACEIs and/or statins to antiplatelets for patients at risk of developing stroke, either as a primary or as a secondary preventive regimen, was associated with a significant reduction in the incidence of mortality after ischaemic stroke than antiplatelets alone. These results might help reduce the rate of ischaemic stroke morbidity and mortality by enhancing the application of specific therapeutic and management strategies for patients at a high risk of acute stroke.
    Matched MeSH terms: Platelet Aggregation Inhibitors/administration & dosage; Platelet Aggregation Inhibitors/therapeutic use*
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