Endothelial injury and acquired aspirin resistance as promoters of regional thrombin formation and early vein graft failure after coronary artery bypass grafting

Poston, Robert; Gu, Jun; Brown, James M.; Gammie, James S.; White, Charles S.; Nie, Lei; Pierson, Richard N.; Griffith, Bartley P.

doi:10.1016/j.jtcvs.2005.08.058

Cited by 101 publications

(94 citation statements)

References 34 publications

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“…In addition, these investigations demonstrate a clear correlation between the extent of coronary artery disease and ASA hyporesponsiveness (Table 4, Figure 4). This correlation between ASA hyporesponsiveness and CAD severity is consistent with previous reports demonstrating persistent formation of TX in ASA-treated patients with CAD requiring surgical revascularization 39 and in patients with known severe CAD 40 . Mechanistically, a higher inflammatory milieu in patients with extensive CAD might promote platelet activation and thus contribute to ASA hyporesponsiveness.…”

Section: No Of Patientssupporting

confidence: 92%

Prevalência de alta reatividade plaquetária em pacientes tratados com aspirina encaminhados para angiografia coronária

Manica¹,

Sarmento‐Leite²,

Manfroi³

et al. 2013

Arq. Bras. Cardiol.

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Section: No Of Patientssupporting

confidence: 92%

Prevalência de alta reatividade plaquetária em pacientes tratados com aspirina encaminhados para angiografia coronária

Manica¹,

Sarmento‐Leite²,

Manfroi³

et al. 2013

Arq. Bras. Cardiol.

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“…208,216 By comparison, the current review found 57 distinct monotherapy studies overall 46 were also included in the seven previous reviews [207][208][209]211,[215][216][217] which provided any information on exclusion criteria (see Table 75). Conversely, of the studies included by at least one other review, the current review excluded 16 at the full-text stage 38, [235][236][237][238][239][240][241][242][243][244][245][246][247][248][249] and seven at the title and abstract stage, 250-256 as they did not meet the inclusion criteria. Three studies were included in other reviews which were not identified by the search strategy; one was subsequently excluded as it was a cross-sectional study, 256 while the correct citation was not identifiable for the other two studies.…”

Section: Systematic Reviewsmentioning

confidence: 99%

The prognostic utility of tests of platelet function for the detection of ‘aspirin resistance’ in patients with established cardiovascular or cerebrovascular disease: a systematic review and economic evaluation

Dretzke

Riley

Lordkipanidzé

et al. 2015

Health Technology Assessment

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BackgroundThe use of aspirin is well established for secondary prevention of cardiovascular disease. However, a proportion of patients suffer repeat cardiovascular events despite being prescribed aspirin treatment. It is uncertain whether or not this is due to an inherent inability of aspirin to sufficiently modify platelet activity. This report aims to investigate whether or not insufficient platelet function inhibition by aspirin (‘aspirin resistance‘), as defined using platelet function tests (PFTs), is linked to the occurrence of adverse clinical outcomes, and further, whether or not patients at risk of future adverse clinical events can be identified through PFTs.ObjectivesTo review systematically the clinical effectiveness and cost-effectiveness evidence regarding the association between PFT designation of ‘aspirin resistance’ and the risk of adverse clinical outcome(s) in patients prescribed aspirin therapy. To undertake exploratory model-based cost-effectiveness analysis on the use of PFTs.Data sourcesBibliographic databases (e.g. MEDLINE from inception and EMBASE from 1980), conference proceedings and ongoing trial registries up to April 2012.MethodsStandard systematic review methods were used for identifying clinical and cost studies. A risk-of-bias assessment tool was adapted from checklists for prognostic and diagnostic studies. (Un)adjusted odds and hazard ratios for the association between ‘aspirin resistance’, for different PFTs, and clinical outcomes are presented; however, heterogeneity between studies precluded pooling of results. A speculative economic model of a PFT and change of therapy strategy was developed.ResultsOne hundred and eight relevant studies using a variety of PFTs, 58 in patients on aspirin monotherapy, were analysed in detail. Results indicated that some PFTs may have some prognostic utility, i.e. a trend for more clinical events to be associated with groups classified as ‘aspirin resistant’. Methodological and clinical heterogeneity prevented a quantitative summary of prognostic effect. Study-level effect sizes were generally small and absolute outcome risk was not substantially different between ‘aspirin resistant’ and ‘aspirin sensitive’ designations.No studies on the cost-effectiveness of PFTs for ‘aspirin resistance’ were identified. Based on assumptions of PFTs being able to accurately identify patients at high risk of clinical events and such patients benefiting from treatment modification, the economic model found that a test–treat strategy was likely to be cost-effective. However, neither assumption is currently evidence based.LimitationsPoor or incomplete reporting of studies suggests a potentially large volume of inaccessible data. Analyses were confined to studies on patients prescribed aspirin as sole antiplatelet therapy at the time of PFT. Clinical and methodological heterogeneity across studies precluded meta-analysis. Given the lack of robust data the economic modelling was speculative.ConclusionsAlthough evidence indicates that some PFTs may have some prognostic value, methodological and clinical heterogeneity between studies and different approaches to analyses create confusion and inconsistency in prognostic results, and prevented a quantitative summary of their prognostic effect. Protocol-driven and adequately powered primary studies are needed, using standardised methods of measurements to evaluate the prognostic ability of each test in the same population(s), and ideally presenting individual patient data. For any PFT to inform individual risk prediction, it will likely need to be considered in combination with other prognostic factors, within a prognostic model.Study registrationThis study is registered as PROSPERO 2012:CRD42012002151.FundingThe National Institute for Health Research Health Technology Assessment programme.

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“…During intraoperative handling and temporary storage of the vessel segments in the course of bypass operations, the antigen expression level in the intima increases dramatically (52). Our laboratory has shown recently that surgical manipulation of venous bypass vessels often results in extensive endothelial lesions (73).…”

mentioning

confidence: 99%

Pericytes in the macrovascular intima: possible physiological and pathogenetic impact

Juchem¹,

Weiss

Gansera

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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The frequently observed de-endothelialization of venous coronary bypass grafts prepared using standard methods exposes subendothelial prothrombotic cells to blood components, thus endangering patients by inducing acute thromboembolic infarction or long-term proliferative stenosis. Our aim was to gain deeper histological and physiological insight into these relations. An intricate network of subendothelial cells, characterized by histological features specific for true pericytes, was detected even in healthy vessels and forms, coupled to the luminal endothelium, a second leaflet of the macrovascular intima. These cells, and particularly those in the venous intima, express enormous concentrations of tissue factor and can recruit additional amounts of up to the 25-fold concentration within 1 h during preincubation with serum (intimal pericytes of venous origin activate 30.71 ± 4.07 pmol coagulation factor x·min−1·10−6 cells; n = 15). Moreover, decoupled from the endothelium, they proliferate rapidly (generation time, 15 ± 2.1 h, n = 8). Central regions of atherosclerotic plaques, as well as of those of restenosed areas of coronary vein grafts, consist almost completely of these cells. In stark contrast with the prothrombogenicity of the intimal pericytes, intact luminal endothelium recruits high concentrations of thrombomodulin (CD 141) specifically within its intercellular junctions, activates Protein C rapidly (42 ± 5.1 pmol/min·106 venous endothelial cells at thrombin saturation; n = 15), can thus actively prevent coagulatory processes, and never expresses histologically detectable and functionally active tissue factor. Given this strongly prothrombotic potential of the intimal pericytes and their overshooting growth behavior in endothelium-denuded vascular regions, they may play important roles in the development of atherosclerosis, thrombosis, and saphenous vein graft disease.

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Endothelial injury and acquired aspirin resistance as promoters of regional thrombin formation and early vein graft failure after coronary artery bypass grafting

Cited by 101 publications

References 34 publications

Prevalência de alta reatividade plaquetária em pacientes tratados com aspirina encaminhados para angiografia coronária

Prevalência de alta reatividade plaquetária em pacientes tratados com aspirina encaminhados para angiografia coronária

The prognostic utility of tests of platelet function for the detection of ‘aspirin resistance’ in patients with established cardiovascular or cerebrovascular disease: a systematic review and economic evaluation

Pericytes in the macrovascular intima: possible physiological and pathogenetic impact

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