Coronary artery bypass graft surgery up‐regulates genes involved in platelet aggregation

Reilly, Sarah-Jayne; Li, N.; Líška, Ján; Ekström, Mattias; Tornvall, Per

doi:10.1111/j.1538-7836.2012.04660.x

Cited by 11 publications

(11 citation statements)

References 44 publications

(43 reference statements)

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“…Most early strokes purportedly arise from particulate and gaseous embolism during surgery,(5) and/or are precipitated by intraoperative hemodynamic perturbations. (6) In contrast, a crucial factor in the development of delayed strokes is likely the prothrombotic postoperative state(7) promoted by significant and protracted humoral and cellular inflammatory responses,(8) and platelet activation(9,10) during and after cardiac surgery.…”

Section: Introductionmentioning

confidence: 99%

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Karhausen

Smeltz

Akushevich

et al. 2017

Anesthesia &Amp; Analgesia

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Background Declining platelet counts may reveal platelet activation and aggregation in a postoperative prothrombotic state. Therefore, we hypothesized that nadir platelet counts after on-pump coronary artery bypass grafting (CABG) surgery are associated with stroke. Methods We evaluated 6,130 adult CABG surgery patients. Postoperative platelet counts were evaluated as continuous and categorical (mild vs. moderate to severe) predictors of stroke. Extended Cox proportional hazard regression analysis with a time-varying covariate for daily minimum postoperative platelet count assessed the association of day-to-day variations in postoperative platelet count with time to stroke. Competing risks proportional hazard regression models examined associations between day-to-day variations in postoperative platelet counts with timing of stroke (early: 0–1 days; delayed: ≥2 days). Results Median [interquartile range] postoperative nadir platelet counts were 123.0 [98.0, 155.0] × 109/L. The incidences of postoperative stroke were 1.09%, 1.50%, and 3.02% for platelet counts, >150×109/L, 100–150×109/L, and <100×109/L, respectively. The risk for stroke increased by 12% on a given postoperative day for every 30 × 109/L decrease in platelet counts (adjusted hazard ratio [HR], 1.12; 95% confidence interval [CI], 1.01–1.24; P=0.0255). On a given day, patients with moderate to severe thrombocytopenia were twice as likely to develop stroke (adjusted HR, 1.99; 95% CI, 1.18–3.34; P=0.0093) as patients with nadir platelet counts >150×109/L. Importantly, such thrombocytopenia, defined as a time-varying covariate, was significantly associated with delayed (≥2days after surgery; adjusted HR, 2.87; 95% CI, 1.49–5.55; P=0.0016), but not early postoperative stroke. Conclusion Our findings suggest an independent association between moderate to severe postoperative thrombocytopenia and postoperative stroke, and timing of stroke after CABG surgery.

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Section: Introductionmentioning

confidence: 99%

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Karhausen

Smeltz

Akushevich

et al. 2017

Anesthesia &Amp; Analgesia

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“…Body mass index and circulating levels of C‐reactive protein and interleukin‐6 are also associated with changes in platelet gene expression , and there are many other published lines of evidence consistent with the supposition that human diseases are associated with changes in the genetic code of platelets . While an in‐depth discussion of these established and emerging findings is beyond the scope of the current brief review, the reader is encouraged to keep an eye on this rapidly evolving area of investigation.…”

Section: Megakaryocyte Investment Of the Genetic Code Into Plateletsmentioning

confidence: 81%

“…These findings also support the hypothesis that in SLE patients, circulating IFNa production by plasmacytoid dendritic cells may alter the genetic code of megakaryocytes within the bone marrow niche, leading to the production of platelets enriched for IFN-regulated proteins. Body mass index and circulating levels of C-reactive protein and interleukin-6 are also associated with changes in platelet gene expression [40,41], and there are many other published lines of evidence consistent with the supposition that human diseases are associated with changes in the genetic code of platelets [30,[42][43][44][45]. While an indepth discussion of these established and emerging findings is beyond the scope of the current brief review, the reader is encouraged to keep an eye on this rapidly evolving area of investigation.…”

Section: Megakaryocyte Investment Of the Genetic Code Into Plateletsmentioning

confidence: 83%

Regulation of the genetic code in megakaryocytes and platelets

Rondina

Weyrich

2015

Journal of Thrombosis and Haemostasis

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Summary Platelets are generated from nucleated precursors referred to as megakaryocytes. The formation of platelets is one of the most elegant and unique developmental processes in eukaryotes. Because they enter the circulation without nuclei, platelets are often considered simple, non-complex cells that have limited functions beyond halting blood flow. However, emerging evidence over the past decade demonstrates that platelets are more sophisticated than previously considered. Platelets carry a rich repertoire of messenger RNAs (mRNAs), microRNAs (miRNAs), and proteins that contribute to primary (adhesion, aggregation, secretion) and alternative (immune regulation, RNA transfer, translation) functions. It is also becoming increasing clear that the “genetic code” of platelets changes with race, genetic disorders, or disease. Changes in the “genetic code” can occur at multiple points including megakaryocyte development, platelet formation, or in circulating platelets. This review focuses on regulation of the “genetic code” in megakaryocytes and platelets and its potential contribution to health and disease.

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“…Compared with group A, the patients of group B had a significant increase in amino-terminal pro-brain natriuretic peptide (NT-pro-BNP), an early marker of ventricular stress (*p50.005), and an insignificant tendency to elevated myonecrosis (mean AE SEM), creatine kinase (CK), CK-MB, and highsensitivity troponin T (hs-TnT). activated [30], and an increase in the amount of COX1 mRNA has been detected in patients after CABG associated with inflammation and hypercoagulability [31]. In addition, residual COX1 activity and epinephrine elevated in patients with AMI increase platelet TX synthesis in patients with AMI [15].…”

Section: Discussionmentioning

confidence: 99%

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A₂-dependent platelet reactivity

Santos¹,

Madrid

Moscardó³

et al. 2013

Platelets

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The optimal dose of aspirin for patients presenting with acute myocardial infarction (AMI) while receiving chronic aspirin therapy has not been clearly established. We evaluated whether continued treatment with 100 mg of aspirin or a loading dose (200-500 mg) influences thromboxane A2 (TX) suppression or platelet reactivity. Sixty-four consecutive patients with AMI and 98 healthy subjects (82 aspirin-free and 16 receiving 100 mg daily for a week) were evaluated. Treatment was at the discretion of the attending physician. Collagen (1 µg/ml)-induced TX synthesis, (14)C-serotonin-release, platelet aggregation, and the PFA-100 assay were evaluated. The platelet TX synthesis of patients receiving a loading dose of aspirin was sixfold lower than that of patients receiving 100 mg of aspirin (p<0.005). This was associated with marked reductions in (14)C-serotonin-release and arachidonic-acid-induced aggregation and an increase in the PFA-100 closure time (p<0.01). Categorization of patients according to their TX synthesis (<95% or ≥ 95% inhibition vs. healthy aspirin-free subjects) revealed that 8% of the patients treated with loading doses had a poor response (<95% inhibition) vs. 53% of those treated with 100 mg (p<0.001). Patients with lower TX inhibition had higher serum NT-Pro-BNP (p<0.005), a marker of poor left ventricular systolic function. Administration of a loading dose of aspirin to patients with AMI during existing chronic aspirin treatment induced greater reductions in platelet TX synthesis and TX-dependent platelet reactivity than the continued treatment alone.

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Coronary artery bypass graft surgery up‐regulates genes involved in platelet aggregation

Abstract: To cite this article: Reilly S-J, Li N, Liska J, Ekströ m M, Tornvall P. Coronary artery bypass graft surgery up-regulates genes involved in platelet aggregation. J Thromb Haemost 2012; 10: 557-63.

Cited by 11 publications

References 44 publications

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Regulation of the genetic code in megakaryocytes and platelets

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A₂-dependent platelet reactivity

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Coronary artery bypass graft surgery up‐regulates genes involved in platelet aggregation

Abstract: To cite this article: Reilly S-J, Li N, Liska J, Ekströ m M, Tornvall P. Coronary artery bypass graft surgery up-regulates genes involved in platelet aggregation. J Thromb Haemost 2012; 10: 557-63.

Cited by 11 publications

References 44 publications

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Platelet Counts and Postoperative Stroke After Coronary Artery Bypass Grafting Surgery

Regulation of the genetic code in megakaryocytes and platelets

The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A2-dependent platelet reactivity

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Product

Resources

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The administration of a loading dose of aspirin to patients presenting with acute myocardial infarction while receiving chronic aspirin treatment reduces thromboxane A₂-dependent platelet reactivity