Renal function and aspirin resistance in patients with coronary artery disease

Blann, Andrew D.; Kuzniatsova, Nadzeya; Velu, S.; Lip, Gregory Y.H.

doi:10.1016/j.thromres.2012.06.026

Cited by 12 publications

(10 citation statements)

References 40 publications

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“…What is more, eGFR even showed an inverse correlation with platelet expression of CD62P. 31 Aksu et al observed higher incidence of HAPR in patients with severe chronic kidney disease (CKD), but not in mild or moderate CKD. HAPR might contribute to the increasing risk of cardiovascular complications in patients with declined renal function.…”

Section: Discussionmentioning

confidence: 98%

Predictors of high on-aspirin platelet reactivity in elderly patients with coronary artery disease

Zhang

Liu

McCaffrey

et al. 2017

CIA

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ObjectivesPrevious studies have illustrated the link between high on-aspirin platelet reactivity (HAPR) with increasing thrombotic risks. The aim of our study was to investigate relative risk factors of HAPR in elderly patients with coronary artery disease.MethodsElderly, hospitalized coronary artery disease patients on regular aspirin treatment were enrolled from January 2014 to September 2016. Medical records of each patient were collected, including demographic information, cardiovascular risk factors, concomitant drugs and routine biological parameters. Arachidonic acid (AA, 0.5 mg/mL) and adenosine diphosphate (ADP, 5 µmol/L) induced platelet aggregation were measured via light transmission assay (LTA) to evaluate antiplatelet responses, referred as LTA–AA and LTA–ADP.ResultsA total of 275 elderly patients were included, with mean age of 77.2±8.1 years, and males accounted for 81.8%. HAPR was defined as LTA–AA in the upper quartile of the enrolled population. HAPR patients tended to have lower renal function (P=0.052). Higher serum uric acid (SUA) level, as well as lower platelet count, hemoglobin and hematocrit were observed in HAPR patients, with a higher proportion of diuretics use (P<0.05). Multivariate analysis revealed that SUA (OR: 1.004, 95% CI: 1.000–1.007, P=0.048), platelet count (OR: 0.994, 95% CI: 0.989–1.000, P=0.045), hematocrit (OR: 0.921, 95% CI: 0.864–0.981, P=0.011) and concomitant P2Y12 receptor inhibitors use (OR: 1.965, 95% CI: 1.075–3.592, P=0.028) were correlated with HAPR. Spearman’s correlation analysis demonstrated an inverse association of LTA–AA with hematocrit (r=−0.234, P<0.001), hemoglobin (r=−0.209, P<0.001) and estimated glomerular filtration rate (r=−0.132, P=0.031).ConclusionSUA, platelet count, hematocrit and P2Y12 receptor inhibitors use were independently correlated with HAPR. These parameters might provide novel therapeutic targets for optimizing antiplatelet therapy.

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Section: Discussionmentioning

confidence: 98%

Predictors of high on-aspirin platelet reactivity in elderly patients with coronary artery disease

Zhang

Liu

McCaffrey

et al. 2017

CIA

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“…This phenomenon further highlights the unique feature of CD14++CD16+ monocytes in underlying disease processes. Interestingly, a recent work demonstrated a weak but statistical association between aspirin resistance and estimated GFR [50], implying a potential impact of platelet responsiveness on renal function. However, from the data available and our results, it’s still immature to establish a causal role between platelet responsiveness and renal function.…”

Section: Discussionmentioning

confidence: 98%

Variation in Dietary Salt Intake Induces Coordinated Dynamics of Monocyte Subsets and Monocyte-Platelet Aggregates in Humans: Implications in End Organ Inflammation

Zhou

Zhang

et al. 2013

PLoS ONE

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BackgroundMonocyte activation and tissue infiltration are quantitatively associated with high-salt intake induced target organ inflammation. We hypothesized that high-salt challenge would induce the expansion of CD14++CD16+ monocytes, one of the three monocyte subsets with a pro-inflammatory phenotype, that is associated with target organ inflammation in humans.Methodology/Principal FindingsA dietary intervention study was performed in 20 healthy volunteers, starting with a 3-day usual diet and followed with a 7-day high-salt diet (≥15 g NaCl/day), and a 7-day low-salt diet (≤5 g NaCl/day). The amounts of three monocyte subsets (“classical” CD14++CD16-, “intermediate” CD14++CD16+ and “non-classical” CD14+CD16++) and their associations with monocyte-platelet aggregates (MPAs) were measured by flow cytometry. Blood oxygen level-dependent magnetic resonance imaging (BOLD-MRI) was used to evaluate renal hypoxia. Switching to a high-salt diet resulted in CD14++ monocyte activation and a rapid expansion of CD14++CD16+ subset and MPAs, with a reciprocal decrease in the percentages of CD14++CD16- and CD14+CD16++ subsets. In vitro study using purified CD14++ monocytes revealed that elevation in extracellular [Na+] could lead to CD14++CD16+ expansion via a ROS dependent manner. In addition, high-salt intake was associated with progressive hypoxia in the renal medulla (increased R2* signal) and enhanced urinary monocyte chemoattractant protein-1 (MCP-1) excretion, indicating a temporal and spatial correlation between CD14++CD16+ subset and renal inflammation. The above changes could be completely reversed by a low-salt diet, whereas blood pressure levels remained unchanged during dietary intervention.Conclusions/SignificanceThe present work demonstrates that short-term increases in dietary salt intake could induce the expansion of CD14++CD16+ monocytes, as well as an elevation of MPAs, which might be the underlying cellular basis of high-salt induced end organ inflammation and potential thromboembolic risk. In addition, this process seems largely unrelated to changes in blood pressure levels. This finding provides novel links between dietary salt intake, innate immunity and end organ inflammation.

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“…Blann et al (87) have reported an association between resistance to the ASA effect of the platelets and GFR in patients who were taking 75 mg/day ASA. They noticed that ASA resistance was twice prevalent in patients with the greatest renal disease than those with the highest renal function.…”

Section: Glomerular Filtrationmentioning

confidence: 99%

Adverse Effects of Nonsteroidal Antiinflammatory Drugs: An Update of Gastrointestinal, Cardiovascular and Renal Complications

2014

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Non-steroidal anti-inflammatory drugs (NSAIDs) are used chronically to reduce pain and inflammation in patients with arthritic conditions, and also acutely as analgesics by many patients. Both therapeutic and adverse effects of NSAIDs are due to inhibition of cyclooxygenase (COX) enzyme. NSAIDs are classified as non-selective and COX-2-selective inhibitors (COXIBS) based on their extent of selectivity for COX inhibition. However, regardless of their COX selectivity, reports are still appearing on the GI side effect of NSAIDs particularly on the lower gastrointestinal (GI) tract and the harmful role of their controlled release formulations. In addition, previously unpublished data stored in the sponsor's files, question the GI sparing properties of rofecoxib, a COXIB that has been withdrawn due to cardiovascular (CV) side effects. Presently, the major side effects of NSAIDs are the GI complications, renal disturbances and CV events. There is a tendency to believe that all NSAIDs are associated with renal and CV side effects, a belief that is not supported by solid evidence. Indeed, lower but still therapeutics doses of some NSAIDs may be cardioprotective. In this review, we briefly discuss the GI toxicity of the NSAIDs and assess their renal and CV adverse effects in more detail.

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Renal function and aspirin resistance in patients with coronary artery disease

Cited by 12 publications

References 40 publications

Predictors of high on-aspirin platelet reactivity in elderly patients with coronary artery disease

Predictors of high on-aspirin platelet reactivity in elderly patients with coronary artery disease

Variation in Dietary Salt Intake Induces Coordinated Dynamics of Monocyte Subsets and Monocyte-Platelet Aggregates in Humans: Implications in End Organ Inflammation

Adverse Effects of Nonsteroidal Antiinflammatory Drugs: An Update of Gastrointestinal, Cardiovascular and Renal Complications

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