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A total of 139 patients (Rapid ATT group) received antithrombotic therapy before 24 h of thrombolysis, and 33 patients (Standard ATT group) after 24 h. The brain parenchyma and vessel status were assessed using simple CT scan on admission, multimodal CT scan at the end of thrombolysis, and angio-CT/MRI scan at day 3. Functional outcome was scored using the modified Rankin Scale (mRS) at day 90.
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Bevezetés: Korábban már leírták a clopidogrelkezelés hatékonyságát akut ischaemiás cerebrovascularis eseményen átesett betegek körében rövid távon. Célkitűzés: A szerzők célja a betegek egyéves utánkövetési adatainak bemutatása. Módszer: A vizsgálatban 100, akut stroke-on/tranziens ischaemiás attakon átesett beteg vett részt. A betegek az első 48 órában aszpirinkezelésben, majd clopidogrelkezelésben részesültek. A kezelés hatékonyságát a gyógyszeres terápia bevezetését követően 7 és 28 nap, majd 3, 6 és 12 hónap után ellenőrizték. A betegeket két csoportra osztották optikai aggregometriás leletük alapján (clopidogrelérzékeny és -rezisztens). A két csoport kockázati profilját, gyógyszereit, laboratóriumi paramétereit és a klinikai kimenetelt elemezték. Eredmények: A clopidogrelkezelés esetében szoros összefüggés mutatkozott az aktuális vérnyomás, a vércukor- és vérzsíranyagcsere-paraméterek, az ultraszenzitív C-reaktív protein szintje és a thrombocytaaggregációs értékek között (p<0,05). Erélyes szekunder prevenciós kezelés hatására a fent jelzett paraméterek normalizálásával párhuzamosan a thrombocytaaggregáció-gátló kezelés hatékonysága is növelhető volt, hosszabb távon rezisztens beteg nem volt. Az egyéves utánkövetés során a kezdetben rezisztens betegek esetében több volt a vascularis események aránya (4 kezdeti clopidogrelérzékeny [4,5%] vs. 2 kezdeti clopidogrelrezisztens [18,1%], p<0,01), ugyanakkor a rezisztencia jelensége nem bizonyult a későbbi kedvezőtlen kimenetel független kockázati faktorának a multivariációs analízis során. Következtetések: Jelen vizsgálat eredményei alapján igen komolyan felvetődik az erélyes szekunder prevenciós kezelés szerepe a thrombocytaaggregáció-gátló terápia hatékonyságának hátterében. Orv. Hetil., 2015, 156(2), 53–59.
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Apparent permeability coefficient (Papp) and diffusion profiles obtained with EGS and Sartorius SM 16750 apparatus were similar for diclofenac and metformin, whereas, we noticed significant differences (p ≤ 0.05), for tramadol, doxycycline, clopidogrel and chlorothiazide.
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Baseline neutrophil count was measured in 2865 patients in CLARITY-TIMI 28, a randomized trial of clopidogrel vs. placebo in STEMI patients undergoing fibrinolysis. Angiography was performed at 2-8 days following enrollment. Analyses were adjusted for demographics, time from symptom onset, Killip class, peak CK-MB, and therapies received. A baseline neutrophil count in the highest quartile was independently associated with the risk of cardiovascular (CV) death [adj (adjusted) OR (odds ratio) 5.8, P < 0.001] and congestive heart failure (adj OR 3.0, P = 0.009) at 30 days. Patients with higher neutrophil counts were less likely to achieve complete ST-segment resolution (adj OR 0.76, P = 0.03) or TIMI myocardial perfusion grade 2/3 (adj OR 0.71, P = 0.017). Clopidogrel had a lesser effect on reducing the odds of a closed infarct-related artery, or death or MI before angiography, in patients with a neutrophil count above the median (adjusted OR 0.83, 0.61-1.13) vs. in those below the median (adjusted OR 0.46, 0.33-0.64) (Pinteraction = 0.008).
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Five randomized controlled trials were reviewed, including 1 trial of dabigatran, 2 trials of rivaroxaban, and 2 trials of apixaban. These studies were conducted in patients with a recent acute coronary syndrome, so most patients were receiving aspirin and clopidogrel as dual antiplatelet therapy in addition to a therapeutic dose of one of the anticoagulants. The 3 Phase 2 dose-ranging trials (1 each of dabigatran, rivaroxaban, and apixaban) found an increasing risk of major and clinically relevant nonmajor bleeding with increasing doses of the anticoagulants. The Phase 3 trial of apixaban was terminated early due to an excess of bleeding events, and the trial of rivaroxaban also found an increased risk of bleeding.
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Some studies have recently suggested a potential pharmacodynamic interaction between aspirin and some non-selective non-steroidal anti-inflammatory drugs (NSAIDs). We have evaluated the reality of this pharmacodynamic interaction and analyse its clinical pertinence.
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The aim of this prospective trial was to assess whether platelet reactivity to clopidogrel assessed with multiple electrode platelet aggregometry (MEA) correlates with the risk of early drug-eluting stent thrombosis (ST).
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Median pre- and postprocedural stenosis rate was 65.4 ± 1% vs 25.1 ± 1%. Technical success rate was 100%. Major procedural complications occurred in 16 patients (8.1%). Combined neurological morbidity and mortality rate at 30 days was 2 patients (0.9%). In 174 stenoses (83%) angiographic follow-up was obtained (mean, 10.2 months). A restenosis (>50%) was observed in 43 (24.7%) cases after 4.2 months (mean) with 4 (9.3%) symptomatic lesions. Incidence of recurrent ischemia related to the stented artery was 2.2% during 10.2 months of mean follow-up.
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Aspirin, clopidogrel, prasugrel and ticagrelor are antiplatelet agents for the prevention of ischemic events in patients with acute coronary syndromes (ACS), percutaneous coronary intervention (PCI) and other indications. Variability in response is observed to different degrees with these agents, which can translate to increased risks for adverse cardiovascular events. As such, potential pharmacogenetic determinants of antiplatelet pharmacokinetics, pharmacodynamics and clinical outcomes have been actively studied.
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Selection Large randomized placebo controlled trials of dual antiplatelet therapy in acute coronary syndromes. Data Extraction From original trials.
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Combined aspirin and clopidogrel were used in 3268 patients (22%). Compared with aspirin alone, aspirin plus clopidogrel was associated with reductions of in-hospital mortality (0.95% vs 1.78%; adjusted odds ratio: 0.50; 95% confidence interval: 0.25, 0.99) and bleeding events (4.19% vs 5.17%; adjusted odds ratio: 0.70; 95% confidence interval: 0.51, 0.97). Ischemic or thrombotic events were not significantly different (1.29% vs 1.53%; adjusted odds ratio, 0.99; 95% confidence interval: 0.59, 1.64). The relative effect of combined treatment did not differ between on-pump and off-pump coronary artery bypass grafting.
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The C3435T polymorphism of the MDR-1 gene influences ADP dependent platelet reactivity in patients with acute coronary syndrome but does not affect mid-term prognosis in this population.
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Patients with intermittent claudication show a wide variability in their response to clopidogrel. While a small proportion of these patients shows no response at all, another small group appears to respond excessively to clopidogrel. Clinical studies are required to identify whether hyper-responders are at increased risk of bleeding complications and whether hyporesponders are at a higher risk of thrombotic events.
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The aim of this study was to assess, in clopidogrel nonresponders undergoing elective percutaneous coronary intervention (PCI), the benefit of adjusted antiplatelet therapy with glycoprotein (GP) IIb/IIIa antagonist administration during PCI for 1-month clinical outcome.
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In contrast to using genome-wide association studies to discover associations between genes or single-nucleotide polymorphisms in the genome with disease status or outcome, some recent pharmacogenomic studies have focused on whether polymorphisms in genes involved in metabolizing drugs significantly impact their efficacy. Whether a drug starts as an active compound and gets metabolized and eliminated from the body or starts as an inactive compound and gets metabolized to an active form, patients in subgroups separated by polymorphism of a gene needed to metabolize the drug might derive differential benefit from that drug. With the use of the Clopidogrel in Unstable Angina to Prevent Recurrent Events trial for Plavix as an example, this article proposes Multiple Comparisons with Control (Subgroup) and Multiple Comparisons with the Best (Subgroup) as methods to infer whether some subgroups of patients derive more or less benefit than wild-type patients and which subgroup or subgroups of patients derive maximum benefit or practically maximum benefit from the drug.
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We were able to determine the characteristics, treatments and in-hospital outcomes of patients hospitalized with ACS in our region. There is room for improvement in using medications, reducing needle to door time and utilizing more cardiac catheterization services.
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From April 2010 to April 2011, 120 consecutive patients, undergoing TAVI, have been enrolled in the study. Patients were randomly assigned to DAPT group (aspirin and clopidogrel 75 mg/qd or ticlopidine 500 mg/bid) or ASA group (aspirin only). TAVI device was the Sapien XT-Novaflex Delivery System (Edwards Lifesciences, Inc.). All patients were followed up to 6 months. Device success was achieved in 100% of patients. No difference in the VARC combined 30 day safety endpoint, all cause and cardiovascular mortality was observed. At 30 days vascular complications were reduced in the ASA group (p<0.05). No differences in the clinical status were detected between the groups up to 6 months.
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The platelet aggregation, P-selectin expression and platelet/leukocyte conjugates as well as the clopidogrel response variability (evaluated by the VASP phosphorylation test and expressed as platelet reactivity index, PRI) were assessed in 74 ACS patients undergoing percutaneous coronary intervention (PCI) in relation to the PON-1 Q192R genotype and to serum HDL-cholesterol levels, and PON-1 (paraoxonase and arylesterase) activities. Patients were loaded with 600 mg of clopidogrel followed by 75 mg per day. HDL-cholesterol levels and PON-1 activities at baseline (before clopidogrel loading) were not altered at 5- and 30-day post-clopidogrel loading, whereas baseline platelet activation parameters were significantly attenuated. At 5 days, 17 patients were clopidogrel non-responders (PRI: 64.2 ± 11.1%). HDL-cholesterol was inversely associated with platelet activation parameters independently on platelet response variability to clopidogrel whereas a negative association between platelet activation parameters and paraoxonase activity was observed in patients adequately responding to clopidogrel but not in clopidogrel non-responders. Similarly, the platelet activation markers were significantly higher in PON-1 Q192Q genotype carriers compared with those having one or two R alleles only in patients adequately responding to clopidogrel.
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The thienopyridine antiplatelet agent clopidogrel is an effective drug for the prevention of vascular events. However, data has accumulated over time to suggest it is prone to significant interpatient variability. While there are several factors that contribute to this, one of the most important is variability in forming the active metabolite necessary for clopidogrel function. Several enzymes are involved in formation of this metabolite, and two, CYP2C19 and P-glycoprotein, appear to have alleles that both occur frequently in the population and have a clinically significant impact. Patients carrying these alleles can be identified, but it remains to be determined if this information is necessary or sufficient for risk stratification. Furthermore, if patients with high-risk alleles are identified, it is unclear how treatment should be adjusted.