Increased Platelet Aggregability During Exercise in Patients With Previous Myocardial Infarction. Lack of Inhibition by Aspirin

Hurlen, Mette; Seljeflot, Ingebjørg; Arnesen, Harald

doi:10.1016/s0049-3848(00)00277-2

Cited by 61 publications

(29 citation statements)

References 38 publications

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“…This would explain the incomplete TxB 2 suppression in the face of robust ASA-induced platelet antagonism, as demonstrated ex vivo. Other potential causes of ASA resistance include increased formation of isoprostanes (nonenzymatic products of lipid peroxidation reflective of oxidant stress) and elevated norepinephrine levels [22][23][24]. Augmented production of both has been reported in IPAH [25,26].…”

Section: Discussionmentioning

confidence: 99%

A study of aspirin and clopidogrel in idiopathic pulmonary arterial hypertension

Robbins

Kawut

Yung

et al. 2006

European Respiratory Journal

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Idiopathic pulmonary arterial hypertension (IPAH) is characterised by in situ thrombosis and increased thromboxane (Tx) A 2 synthesis; however, there are no studies of antiplatelet therapy in IPAH. The aim of the current study was to determine the biochemical effects of aspirin (ASA) and clopidogrel on platelet function and eicosanoid metabolism in patients with IPAH.A randomised, double-blind, placebo-controlled crossover study of ASA 81 mg once daily and clopidogrel 75 mg once daily was performed. Plasma P-selectin levels and aggregometry were measured after exposure to adenosine diphosphate, arachidonic acid and collagen. Serum levels of TxB 2 and urinary metabolites of TxA 2 and prostaglandin I 2 (Tx-M and PGI-M, respectively) were assessed.A total of 19 IPAH patients were enrolled, of whom nine were being treated with continuous intravenous epoprostenol. ASA and clopidogrel significantly reduced platelet aggregation to arachidonic acid and adenosine diphosphate, respectively. ASA significantly decreased serum TxB 2 , urinary Tx-M levels and the Tx-M/PGI-M ratio, whereas clopidogrel had no effect on eicosanoid levels. Neither drug significantly lowered plasma P-selectin levels. Epoprostenol use did not affect the results.In conclusion, aspirin and clopidogrel inhibited platelet aggregation, and aspirin reduced thromboxane metabolite production without affecting prostaglandin I 2 metabolite synthesis. Further clinical trials of aspirin in patients with idiopathic pulmonary arterial hypertension should be performed.

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Section: Discussionmentioning

confidence: 99%

A study of aspirin and clopidogrel in idiopathic pulmonary arterial hypertension

Robbins

Kawut

Yung

et al. 2006

European Respiratory Journal

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“…Therefore, sympathetic overactivity in patients with aspirin resistance may cause platelet activation and may contribute to aspirin resistance in the patients with CAD. Similarly, Hurlen, et al 38) found that the antiplatelet action of aspirin is decreased during exercise although this effect is normal during rest in patients who previously experienced a myocardial infarction. They concluded that aspirin is not sufficiently effective when platelets are activated by catecholamines.…”

Section: Discussionmentioning

confidence: 90%

Heart Rate Variability in Patients With Stable Coronary Artery Disease and Aspirin Resistance

Durmaz¹,

Keleş²,

Özdemir³

et al. 2008

Int. Heart J.

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SUMMARYAspirin resistance as defined by failure to effectively inhibit thromboxane synthesis is associated with a higher risk of recurrent myocardial ischemia and cardiovascular death. Heart rate variability (HRV) analysis has been extensively used to identify patients at risk for increased cardiac mortality. The aim of this study was to evaluate the association between HRV and aspirin resistance in patients with stable coronary artery disease (CAD).Sixty-nine (69) consecutive patients with stable CAD were included in this study. Of the 69 patients, 18 (26%) were aspirin nonresponders. When the aspirin responders were compared with the nonresponders, there was no significant difference between the groups with respect to most clinical parameters, major cardiovascular risk factors, medical treatments, and aspirin dosages. However, the patients with aspirin resistance had a higher previous myocardial infarction history and lower left ventricular ejection fraction. Moreover, mean platelet volume, CT/EPI, CT/ADP values, LF and LF/HF ratio were higher while HF, SDNN, SDANN, and RMSSD were lower in the nonresponder group than the responders. Regarding HRV parameters, CT/ADP time was negatively correlated with SDNN (r = -0.5, P = 0.02) and HF (r = -0.4, P = 0.03), and positively correlated with LF (r = 0.6, P = 0.01) and LF/HF (r = 0.7, P = 0.001). Similarly, CT/EPI time was negatively correlated with SDNN (r = -0.4, P = 0.03), and positively correlated with LF (r = 0.5, P = 0.02) and the LF/HF ratio (r = 0.5, P = 0.02). Regression analysis revealed that the only parameters affecting SDNN and LF/HF ratio were left ventricle ejection fraction and aspirin resistance.The heart rate variability decreased and sympathetic activity increased in the patients with aspirin resistance and stable CAD. This may contribute to a higher risk of recurrent myocardial ischemia and cardiovascular death in patients with aspirin resistance. (Int Heart J 2008; 49: 413-422)

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“…There are many studies showing variability in the baseline response to aspirin using a variety of ex vivo, laboratory based, assays of platelet function including bleeding time [31], platelet aggregability [32], flow cytometric analyses of markers of platelet activation [33], classical platelet aggregometry [34,35] and point-of-care assays [36].…”

Section: Aspirin Monotherapymentioning

confidence: 99%

http://oatext.com/Dual-antiplatelet-therapy-after-coronary-artery-bypass-grafting-Do-we-have-a-consensus.php

Jaaly¹,

Zakkar²,

Pufulete³

et al. 2015

J Integr Cardiol

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Coronary artery bypass grafting (CABG) remains the gold standard treatment in patients with complex multivessel coronary artery disease (CAD). Reversed long saphenous vein is the most commonly used conduit despite the known early thrombotic failure and low long-term patency rate. Post-operative antiplatelet therapy is an established treatment to improve graft patency and also a secondary treatment of the underlying native CAD.Aspirin has traditionally been the first line therapy; however, aspirin resistance especially in the early period after CABG, has been reported over the years and as a result, the use of dual antiplatelet therapy (DAPT) has become more common. However, there is limited evidence about the effect of DAPT and duration of use after CABG on graft patency, clinical outcomes (such as bleeding and myocardial infarction), and survival. The optimal dose of aspirin when given in DAPT is unclear and the duration of DAPT in association with quality of life is unknown.Furthermore, a better understanding of the pathology of vein graft disease and how available drugs influence it, could lead to the development of customised therapy for cohorts of patients undergoing CABG with potential benefits to early and long term outcomes. Here we review the available evidence on the routine use of DAPT after CABG. Coronary artery bypass grafting (CABG)Ischaemic heart disease (IHD) is the main leading cause of death in the world, with 7.4 million deaths in 2012 [1,2]. Coronary artery bypass grafting (CABG) is the gold standard intervention in patients with complex multivessel disease [3]. In the UK, there are about 25,000 CABG operations performed annually [4] and the majority of these operations is carried out on patients over 70 years of age [5]. Demand for CABG is likely to increase considerably in the future as a result of rapidly ageing populations [6] and increased expectations of patients and surgeons to expand their indications for surgery.During the early years of coronary surgery, saphenous vein grafts (SVGs) were the only conduits used [7]. Over the years different arterial conduits were introduced with variable degree of success [8][9][10]. Contemporary data on international use of grafts are available from the SYNTAX trial that included 1541 patients who underwent CABG at 85 sites in 18 countries between 2005 and 2007 [11]. The SYNTAX trial confirmed that the long saphenous vein (LSV) graft, is the most used conduit for multivessel revascularisation, despite its known low early and late patency rates.The underlying mechanism behind vein graft disease is multifactorial and can include conduit trauma/graft thrombosis (within 1 month, early failure), activation of intimal hyperplasia associated with harvest and implantation into the arterial high-pressure system (1 to 12 months, intermediate failure), superimposed atherosclerosis (beyond 12 months, late failure) [12][13][14][15]. A prospective cohort study of 1,388 patients carried out between 1969 to 1994, in which patency was assessed using coronary...

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Increased Platelet Aggregability During Exercise in Patients With Previous Myocardial Infarction. Lack of Inhibition by Aspirin

Cited by 61 publications

References 38 publications

A study of aspirin and clopidogrel in idiopathic pulmonary arterial hypertension

A study of aspirin and clopidogrel in idiopathic pulmonary arterial hypertension

Heart Rate Variability in Patients With Stable Coronary Artery Disease and Aspirin Resistance

http://oatext.com/Dual-antiplatelet-therapy-after-coronary-artery-bypass-grafting-Do-we-have-a-consensus.php

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