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The Cochrane Database of Systematic... 2004CDP-choline is used in the treatment of disorders of a cerebrovascular nature. The many years of its presence in the clinical field have caused an evolution in dosage,... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
CDP-choline is used in the treatment of disorders of a cerebrovascular nature. The many years of its presence in the clinical field have caused an evolution in dosage, method of administration, and selection criteria of patients to which the treatments was given. Modalities of the clinical studies, including length of observation, severity of disturbance, and methodology of evaluation of the results were also heterogeneous. In spite of uncertainties about its efficacy due to these complexities, CDP-choline is a frequently prescribed drug for cognitive impairment in several European countries, especially when the clinical picture is predominantly one of cerebrovascular disease, hence the need for this review.
OBJECTIVES
The objective is to assess the efficacy of CDP-choline (cytidinediphosphocholine) in the treatment of cognitive, emotional, and behavioural deficits associated with chronic cerebral disorders in the elderly.
SEARCH STRATEGY
The trials were identified from a last updated search of the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group on 20 January 2004 using the terms CDP-choline, CDP, citicolone, cytidine diphosphate choline or diphosphocholine. This register contains records from all major health care databases and many ongoing trials databases and is updated regularly.
SELECTION CRITERIA
All relevant unconfounded, double-blind, placebo-controlled, randomized trials of CDP-choline for cognitive impairment due to chronic cerebral disorders are considered for inclusion in the review.
DATA COLLECTION AND ANALYSIS
Two reviewers independently reviewed the included studies, extracted the data, and pooled it when appropriate and possible. The pooled odd ratios (95% CI) or the average differences (95% CI) were estimated. No intention-to-treat data were available from the studies included.
MAIN RESULTS
Seven of the included studies observed the subjects for a period between 20 to 30 days, one study was of 6 weeks duration, 4 studies used cycles extending over 2 and 3 months and one study observed continuous administration over 3 months. The studies were heterogeneous in dose, inclusion criteria for subjects, and outcome measures. Results are reported for the domains of attention, memory testing, behavioural rating scales, global clinical impression and tolerability. There is no significant evidence of a beneficial effect of CDP-choline on attention. There are significant beneficial effects of CDP-choline on memory function and behaviour. The drug is well tolerated.
REVIEWERS' CONCLUSIONS
There is some evidence that CDP Choline has a positive effect on memory and behaviour in at least the short/medium term. The evidence of benefit from global impression is stronger, but is still limited by the duration of the studies. Further research with CDP-choline should focus on longer term studies in subjects who have been diagnosed with currently accepted standardised criteria, especially vascular dementia.
Topics: Aged; Cerebrovascular Disorders; Chronic Disease; Cognition Disorders; Cytidine Diphosphate Choline; Dementia; Humans; Mental Disorders; Nootropic Agents; Randomized Controlled Trials as Topic
PubMed: 15106147
DOI: 10.1002/14651858.CD000269.pub2 -
Sports Medicine (Auckland, N.Z.) Jun 2022The 5' adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a cellular energy sensor that is activated by increases in the cellular AMP/adenosine... (Meta-Analysis)
Meta-Analysis
BACKGROUND
The 5' adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a cellular energy sensor that is activated by increases in the cellular AMP/adenosine diphosphate:adenosine triphosphate (ADP:ATP) ratios and plays a key role in metabolic adaptations to endurance training. The degree of AMPK activation during exercise can be influenced by many factors that impact on cellular energetics, including exercise intensity, exercise duration, muscle glycogen, fitness level, and nutrient availability. However, the relative importance of these factors for inducing AMPK activation remains unclear, and robust relationships between exercise-related variables and indices of AMPK activation have not been established.
OBJECTIVES
The purpose of this analysis was to (1) investigate correlations between factors influencing AMPK activation and the magnitude of change in AMPK activity during cycling exercise, (2) investigate correlations between commonly reported measures of AMPK activation (AMPK-α2 activity, phosphorylated (p)-AMPK, and p-acetyl coenzyme A carboxylase (p-ACC), and (3) formulate linear regression models to determine the most important factors for AMPK activation during exercise.
METHODS
Data were pooled from 89 studies, including 982 participants (93.8% male, maximal oxygen consumption [[Formula: see text]] 51.9 ± 7.8 mL kg min). Pearson's correlation analysis was performed to determine relationships between effect sizes for each of the primary outcome markers (AMPK-α2 activity, p-AMPK, p-ACC) and factors purported to influence AMPK signaling (muscle glycogen, carbohydrate ingestion, exercise duration and intensity, fitness level, and muscle metabolites). General linear mixed-effect models were used to examine which factors influenced AMPK activation.
RESULTS
Significant correlations (r = 0.19-0.55, p < .05) with AMPK activity were found between end-exercise muscle glycogen, exercise intensity, and muscle metabolites phosphocreatine, creatine, and free ADP. All markers of AMPK activation were significantly correlated, with the strongest relationship between AMPK-α2 activity and p-AMPK (r = 0.56, p < 0.001). The most important predictors of AMPK activation were the muscle metabolites and exercise intensity.
CONCLUSION
Muscle glycogen, fitness level, exercise intensity, and exercise duration each influence AMPK activity during exercise when all other factors are held constant. However, disrupting cellular energy charge is the most influential factor for AMPK activation during endurance exercise.
Topics: AMP-Activated Protein Kinases; Acetyl-CoA Carboxylase; Adenosine Diphosphate; Adenosine Monophosphate; Female; Glycogen; Humans; Male; Muscle, Skeletal
PubMed: 34878641
DOI: 10.1007/s40279-021-01610-x -
Clinical Nutrition ESPEN Jun 2018The WHO 2016 report indicates that worldwide obesity is rising, with over 600 million people in the obese range (BMI>30). The recommended daily calorie intake for adults...
The WHO 2016 report indicates that worldwide obesity is rising, with over 600 million people in the obese range (BMI>30). The recommended daily calorie intake for adults is 2000 kcal and 2500 kcal for women and men respectively. The average American consumes 3770 kcal/day and the average person in the UK consumes 3400 kcal/day. With such increased caloric intake, there is an increased load on metabolic pathways, in particular glucose metabolism. Such metabolism requires micronutrients as enzyme co-factors. The recommended daily allowance (RDA) for thiamine is 1.3 mg/day and 0.5 mg thiamine is required to process 1000 kilocalories (kcal). Therefore, despite the appearance of being overfed, there is now increasing evidence that the obese population may nutritionally depleted of essential micronutrients. Thiamine deficiency has been reported to be in the region of 16-47% among patients undergoing bariatric surgery for obesity. Thiamine, in turn, requires magnesium to be in its active form thiamine diphosphate, (TDP). TDP also requires magnesium to achieve activation of TDP dependent enzymes, including transketolase (TK), pyruvate dehydrogenase (PDH) and alpha-keto glutaric acid dehydrogenase (AKGDH), during metabolism of glucose. Thiamine and magnesium therefore play a critical role in glucose metabolism and their deficiency may result in the accumulation of anaerobic metabolites including lactate due to a mismatch between caloric burden and function of thiamine dependent enzymes. It may therefore be postulated that thiamine and magnesium deficiency are under-recognized in obesity and may be important in the progress of obesity and obesity related chronic disease states. The aim of the present systematic review was to examine the role of thiamine dependent enzymes in obesity and obesity related chronic disease states.
Topics: Body Mass Index; Chronic Disease; Energy Intake; Glucose; Humans; Magnesium; Magnesium Deficiency; Nutritional Status; Obesity; Prevalence; Prognosis; Recommended Dietary Allowances; Risk Factors; Thiamine; Thiamine Deficiency
PubMed: 29779823
DOI: 10.1016/j.clnesp.2018.02.007 -
Restorative Neurology and Neuroscience 2013Surgical repair alone does not lead to satisfactory recovery after nerve laceration injury, yet no adjuvant clinical treatments are available. The goal of this review is... (Review)
Review
Surgical repair alone does not lead to satisfactory recovery after nerve laceration injury, yet no adjuvant clinical treatments are available. The goal of this review is to systematically survey all adjuvant treatments after surgery investigated in rat and mouse models. Both PubMed and Embase were explored with a systematic bibliographic search algorithm. Inclusion criteria consisted of treatments applied to rats or mice after complete transection and microsurgical repair of lower-limb motor or mixed nerves. Effect size statistics enabled numerical comparison between outcomes of treated and untreated animals and ranked the best treatments. 1,553 articles were found according to our search strategies, and 22 of them corresponded to our pre-defined inclusion criteria. After data extraction and analysis, the top 3 adjuvant strategies in terms of combined average effect size were citicoline, neurotrophin-4, and nitric oxide synthesis inhibitor, with values of 5.52, 5.14 and 4.08, respectively. Definitive treatment comparison was difficult due to the lack of uniformity in outcome evaluation in the experiments performed. Animal studies, comparing treatments administered within the same experimental protocol, are needed to truly assess efficiency and to provide solid recommendations for future clinical investigation.
Topics: Animals; Cytidine Diphosphate Choline; Disease Models, Animal; Humans; Lacerations; Nerve Growth Factors; Nitric Oxide Synthase; Peripheral Nerves; Rodentia; Treatment Outcome
PubMed: 23478341
DOI: 10.3233/RNN-120253 -
AIDS Education and Prevention :... Oct 2023Prevalence of human immunodeficiency virus (HIV) is higher in transgender populations. Pre-exposure prophylaxis (PrEP) intervention is successful in reducing HIV...
Prevalence of human immunodeficiency virus (HIV) is higher in transgender populations. Pre-exposure prophylaxis (PrEP) intervention is successful in reducing HIV acquisition. We aimed to investigate the adherence to oral PrEP by HIV-negative transgender women (TW). We followed the and the PRISMA Statement. We searched in WoS, OVID, Scopus, MEDLINE, and the Cochrane Central Register of Controlled Trials databases. Participation and adherence to the intervention were low for TW compared to cisgender men who have sex with men (cMSM), and it was measured mostly by self-report (72.7%) or tenofovir-diphosphate/emtricitabine triphosphate dried blood spot (45.5%). Awareness should increase and the effect of oral PrEP on gender-affirming hormone therapy should be explained to TW at the beginning of the trials. One limitation is that our sample size was dominated by two Thai studies with TW sex workers. Future studies should evaluate adherence to new PrEP modalities.
Topics: Male; Humans; Female; HIV Infections; Tenofovir; Homosexuality, Male; Pre-Exposure Prophylaxis; Transgender Persons; Sexual and Gender Minorities; Anti-HIV Agents; Medication Adherence
PubMed: 37843906
DOI: 10.1521/aeap.2023.35.5.362 -
Clinical Cardiology Apr 2013There is considerable debate about whether concomitant use of proton pump inhibitors (PPIs) should be recommended for patients who are prescribed clopidogrel after acute... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
There is considerable debate about whether concomitant use of proton pump inhibitors (PPIs) should be recommended for patients who are prescribed clopidogrel after acute coronary syndrome. Most pharmacokinetic and pharmacodynamic studies in vivo were conducted using small sample sizes and were single centered, resulting in conflicting data.
HYPOTHESIS
PPIs may attenuate the antiplatelet effect of clopidogrel in vivo and lead to an increased risk of cardiovascular events.
METHODS
PubMed, the Cochrane Library, Embase, Web of Science, and China Biology Medicine Disc were searched. Randomized controlled trials that compared pharmacodynamic impacts of a PPI on the efficacy of clopidogrel in vivo were included. Two independent reviewers evaluated study quality and extracted data for meta-analysis.
RESULTS
We identified 8 eligible studies. Compared to clopidogrel treatment alone, patients who received both a PPI and clopidogrel had less of a decrease in the platelet reactivity index (weighted mean difference [WMD]: 8.18; 95% confidence interval [CI]: 6.81-9.56; P<0.00001), less adenosine 5'-diphosphate-induced platelet aggregation inhibition (WMD: 7.28; 95% CI: 2.44-12.11; P=0.003), higher P2Y12 reaction units (WMD: 40.58; 95% CI: 19.31-61.86; P=0.0002), and higher risks of clopidogrel resistance (odds ratio [OR]: 2.49; 95% CI: 1.49-4.14; P=0.0005). There were no significant differences, however, for the incidences of major adverse cardiovascular events between the 2 groups (OR: 1.07; 95% CI: 0.44-2.59; P=0.88), and treatment with a PPI and clopidogrel significantly reduced the risk of adverse gastrointestinal events (OR: 0.16; 95% CI: 0.04-0.62; P=0.008).
CONCLUSIONS
Concomitant use of a PPI with clopidogrel attenuated the antiplatelet effect of clopidogrel, but may be clinically unimportant because there were no clinical differences in the risk for major adverse cardiovascular events.
Topics: Adenosine Diphosphate; Blood Platelets; Cardiovascular Diseases; Clopidogrel; Drug Interactions; Drug Resistance; Gastrointestinal Diseases; Humans; Platelet Aggregation; Platelet Aggregation Inhibitors; Proton Pump Inhibitors; Receptors, Purinergic P2Y12; Ticlopidine
PubMed: 23450832
DOI: 10.1002/clc.22094 -
The Cochrane Database of Systematic... Aug 2020Stroke is one of the leading causes of long-lasting disability and mortality and its global burden has increased in the past two decades. Several therapies have been... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Stroke is one of the leading causes of long-lasting disability and mortality and its global burden has increased in the past two decades. Several therapies have been proposed for the recovery from, and treatment of, ischemic stroke. One of them is citicoline. This review assessed the benefits and harms of citicoline for treating patients with acute ischemic stroke.
OBJECTIVES
To assess the clinical benefits and harms of citicoline compared with placebo or any other control for treating people with acute ischemic stroke.
SEARCH METHODS
We searched in the Cochrane Stroke Group Trials Register, CENTRAL, MEDLINE Ovid, Embase Ovid, LILACS until 29 January 2020. We searched the World Health Organization Clinical Trials Search Portal and ClinicalTrials.gov. Additionally, we also reviewed reference lists of the retrieved publications and review articles, and searched the websites of the US Food and Drug Administration (FDA) and European Medicines Agency (EMA).
SELECTION CRITERIA
We included randomized controlled trials (RCTs) in any setting including participants with acute ischemic stroke. Trials were eligible for inclusion if they compared citicoline versus placebo or no intervention.
DATA COLLECTION AND ANALYSIS
We selected RCTs, assessed the risk of bias in seven domains, and extracted data by duplicate. Our primary outcomes of interest were all-cause mortality and the degree of disability or dependence in daily activities at 90 days. We estimated risk ratios (RRs) for dichotomous outcomes. We measured statistical heterogeneity using the I² statistic. We conducted our analyses using the fixed-effect and random-effects model meta-analyses. We assessed the overall quality of evidence for six pre-specified outcomes using the GRADE approach.
MAIN RESULTS
We identified 10 RCTs including 4281 participants. In all these trials, citicoline was given either orally, intravenously, or a combination of both compared with placebo or standard care therapy. Citicoline doses ranged between 500 mg and 2000 mg per day. We assessed all the included trials as having high risk of bias. Drug companies sponsored six trials. A pooled analysis of eight trials indicates there may be little or no difference in all-cause mortality comparing citicoline with placebo (17.3% versus 18.5%; RR 0.94, 95% CI 0.83 to 1.07; I² = 0%; low-quality evidence due to risk of bias). Four trials found no difference in the proportion of patients with disability or dependence in daily activities according to the Rankin scale comparing citicoline with placebo (21.72% versus 19.23%; RR 1.11, 95% CI 0.97 to 1.26; I² = 1%; low-quality evidence due to risk of bias). Meta-analysis of three trials indicates there may be little or no difference in serious cardiovascular adverse events comparing citicoline with placebo (8.83% versus 7.77%; RR 1.04, 95% CI 0.84 to 1.29; I² = 0%; low-quality evidence due to risk of bias). Overall, either serious or non-serious adverse events - central nervous system, gastrointestinal, musculoskeletal, etc. - were poorly reported and harms may have been underestimated. Four trials assessing functional recovery with the Barthel Index at a cut-off point of 95 points or more did not find differences comparing citicoline with placebo (32.78% versus 30.70%; RR 1.03, 95% CI 0.94 to 1.13; I² = 24%; low-quality evidence due to risk of bias). There were no differences in neurological function (National Institutes of Health Stroke Scale at a cut-off point of ≤ 1 points) comparing citicoline with placebo according to five trials (24.31% versus 22.44%; RR 1.08, 95% CI 0.96 to 1.21; I² = 27%, low-quality evidence due to risk of bias). A pre-planned Trial Sequential Analysis suggested that no more trials may be needed for the primary outcomes but no trial provided information on quality of life.
AUTHORS' CONCLUSIONS
This review assessed the clinical benefits and harms of citicoline compared with placebo or any other standard treatment for people with acute ischemic stroke. The findings of the review suggest there may be little to no difference between citicoline and its controls regarding all-cause mortality, disability or dependence in daily activities, severe adverse events, functional recovery and the assessment of the neurological function, based on low-certainty evidence. None of the included trials assessed quality of life and the safety profile of citicoline remains unknown. The available evidence is of low quality due to either limitations in the design or execution of the trials.
Topics: Activities of Daily Living; Acute Disease; Aged; Aged, 80 and over; Bias; Brain Ischemia; Cause of Death; Cytidine Diphosphate Choline; Humans; Middle Aged; Nootropic Agents; Randomized Controlled Trials as Topic; Recovery of Function; Stroke
PubMed: 32860632
DOI: 10.1002/14651858.CD013066.pub2 -
Journal of Neurochemistry Oct 2012The neuroprotective actions of citicoline have been documented for experimental stroke therapy. We used a systematic review and meta-analysis to assess this evidence.... (Meta-Analysis)
Meta-Analysis Review
Citicoline in pre-clinical animal models of stroke: a meta-analysis shows the optimal neuroprotective profile and the missing steps for jumping into a stroke clinical trial.
The neuroprotective actions of citicoline have been documented for experimental stroke therapy. We used a systematic review and meta-analysis to assess this evidence. From 64 identified studies using citicoline in stroke animal models, only those describing ischemic occlusive stroke and reporting data on infarct volume and/or neurological outcome were included (14 studies, 522 animals). Overall, the quality of the studies was modest (5, 4-6), while the absence of studies involving animals with co-morbidities, females, old animals or strain differences indicated that studies did not fulfill the STAIR recommendations. Weighted mean difference meta-analysis showed citicoline to reduce infarct volume by 27.8% [(19.9%, 35.6%); p < 0.001]. In the stratified analysis, citicoline effect on reducing infarct volume was higher in proximal occlusive models of middle cerebral artery (MCA) compared with distal occlusion. Moreover, the efficacy was superior using multiple doses than single dose and when a co-treatment was administered compared with citicoline monotherapy, the only independent factor identified in the meta-regression. Citicoline improved neurological deficit by 20.2% [(6.8%, 33.7%); p = 0.015], but only four studies including 176 animals reported these data. In conclusion, this meta-analysis provides evidence of citicoline efficacy in stroke animal models and shows the optimal neuroprotective profile and the missing experimental requirements before jumping into clinical trials.
Topics: Animals; Clinical Trials as Topic; Cytidine Diphosphate Choline; Disease Models, Animal; Humans; Neuroprotective Agents; Nootropic Agents; Stroke
PubMed: 22845688
DOI: 10.1111/j.1471-4159.2012.07891.x -
The Cochrane Database of Systematic... Apr 2007Delirium is a common mental disorder with serious adverse outcomes in hospitalised patients. It is associated with increases in mortality, physical morbidity, length of... (Review)
Review
BACKGROUND
Delirium is a common mental disorder with serious adverse outcomes in hospitalised patients. It is associated with increases in mortality, physical morbidity, length of hospital stay, institutionalisation and costs to healthcare providers. A range of risk factors has been implicated in its aetiology, including aspects of the routine care and environment in hospitals. Prevention of delirium is clearly desirable from patients' and carers' perspectives, and to reduce hospital costs. Yet it is currently unclear whether interventions for prevention of delirium are effective, whether they can be successfully delivered in all environments, and whether different interventions are necessary for different groups of patients.
OBJECTIVES
Our primary objective was to determine the effectiveness of interventions designed to prevent delirium in hospitalised patients. We also aimed to highlight the quality and quantity of research evidence to prevent delirium in these settings.
SEARCH STRATEGY
We searched the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group on 28th September, 2005. As the searches in MEDLINE, EMBASE, CINAHL and PsycINFO for the Specialized Register would not necessarily have picked up all delirium prevention trials, these databases were searched again on 28th October, 2005. We also examined reference lists of retrieved articles, reviews and books. Experts in this field were contacted and the Internet searched for further references and to locate unpublished trials.
SELECTION CRITERIA
Randomised controlled trials evaluating any interventions to prevent delirium in hospitalised patients.
DATA COLLECTION AND ANALYSIS
Data collection and quality assessment were performed by three reviewers independently and agreement reached by consensus.
MAIN RESULTS
Six studies with a total of 833 participants were identified for inclusion. All were conducted in surgical settings, five in orthopaedic surgery and one in patients undergoing resection for gastric or colon cancer. Only one study of 126 hip fracture patients comparing proactive geriatric consultation with usual care was sufficiently powered to detect a difference in the primary outcome, incident delirium. Total cumulative delirium incidence during admission was reduced in the intervention group (OR 0.48 [95% CI 0.23, 0.98]; RR 0.64 [95% CI 0.37, 0.98]), suggesting a 'number needed to treat' of 5.6 patients to prevent one case. The intervention was particularly effective in preventing severe delirium. In logistic regression analyses adjusting for pre fracture dementia and Activities of Daily Living impairment, there was no reduction in effect size, OR 0.6, but this no longer remained significant [95% CI 0.3,1.3]. There was no effect on the duration of delirium episodes, length of hospital stay, and cognitive status or institutionalisation at discharge. There was also no significant difference in cumulative delirium incidence between treatment and control groups in a sub-group of 50 patients with dementia (RR 0.9 [95% CI 0.59, 1.36]). In another trial of low dose haloperidol prophylaxis, there was no difference in delirium incidence but the severity and duration of a delirium episode, and length of hospital stay were all reduced. We identified no completed studies in hospitalised medical, care of the elderly, general surgery, cancer or intensive care patients. In outcomes, no studies examined for death, use of psychotropic medication, activities of daily living, psychological morbidity, quality of life, carers or staff psychological morbidity, cost of intervention and cost to health care services. Outcomes were only reported up to discharge, with no studies reporting medium or longer-term effects.
AUTHORS' CONCLUSIONS
Research evidence on effectiveness of interventions to prevent delirium is sparse. Based on a single study, a programme of proactive geriatric consultation may reduce delirium incidence and severity in patients undergoing surgery for hip fracture. Prophylactic low dose haloperidol may reduce severity and duration of delirium episodes and shorten length of hospital admission in hip surgery. Further studies of delirium prevention are needed.
Topics: Anesthesia, Epidural; Anesthetics, Inhalation; Cytidine Diphosphate Choline; Delirium; Donepezil; Halothane; Hospitalization; Humans; Indans; Nootropic Agents; Piperidines
PubMed: 17443600
DOI: 10.1002/14651858.CD005563.pub2 -
The American Journal of Cardiology Jun 2014Several prospective studies have shown that high on-clopidogrel platelet reactivity (HPR) in patients undergoing percutaneous coronary intervention (PCI) is a risk... (Meta-Analysis)
Meta-Analysis Review
Several prospective studies have shown that high on-clopidogrel platelet reactivity (HPR) in patients undergoing percutaneous coronary intervention (PCI) is a risk factor for ischemic events. All studies were insufficiently powered to detect differences in stroke between patients with HPR and those without. Therefore, we performed a systematic review and meta-analysis of available publications aimed at determining whether patients undergoing PCI with HPR are also at increased risk of stroke. We searched for prospective studies enrolling patients undergoing PCI and treated with aspirin and clopidogrel that reported on clinical relevance of HPR to adenosine diphosphate. Study end point was the rate of stroke. We also investigated whether there was an interaction on the relative risk of stroke between HPR, clinical presentation, duration of follow-up, or laboratory methods. Fourteen studies including 11,959 patients were deemed eligible. On pooled analysis, the risk of stroke was higher in patients with HPR compared with patients with no HPR (1.2% vs 0.7%, relative risk on fixed effect 1.84, 95% confidence interval 1.21 to 2.80). There was no heterogeneity among the studies (I(2) = 0%, p = 0.5). Clinical presentation (p = 0.39 for interaction), duration of follow-up (p = 0.87 for interaction), and laboratory method for detection of HPR (p = 0.99 for interaction) did not affect the relative increase in the risk of stroke in patients with HPR compared with patients with no HPR. In conclusion, in patients with coronary artery disease undergoing PCI, the presence of HPR to adenosine diphosphate is a risk factor for stroke.
Topics: Adenosine Diphosphate; Blood Platelets; Clopidogrel; Dose-Response Relationship, Drug; Global Health; Humans; Incidence; Myocardial Ischemia; Percutaneous Coronary Intervention; Platelet Aggregation; Platelet Aggregation Inhibitors; Platelet Function Tests; Postoperative Period; Risk Factors; Stroke; Ticlopidine
PubMed: 24837257
DOI: 10.1016/j.amjcard.2014.03.009