In Vivo Platelet Activation and Aspirin Responsiveness in Type 1 Diabetes

Zaccardi, Francesco; Rizzi, Alessandro; Petrucci, Giovanna; Ciaffardini, Flavia; Tanese, Luigi; Pagliaccia, Francesca; Cavalca, Viviana; Ciminello, Angela; Habib, Aı̈da; Squellerio, Isabella; Rizzo, Paola; Tremoli, Elena; Rocca, Bianca; Pitocco, Dario; Patrono, Carlo

doi:10.2337/db15-0936

Cited by 43 publications

(50 citation statements)

References 24 publications

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“…However, extraplatelet sources of TXA 2 production, such as the kidney [32] and COX-2-expressing inflammatory cells [33], may also contribute to TXM excretion. Similarly, the involvement of COX-2 in PGI 2 biosynthesis and PGIM excretion has been inferred by short-term intervention studies demonstrating a comparable reduction in urinary PGIM with structurally unrelated COX-2 inhibitors, such as nimesulide [20], celecoxib [14], rofecoxib [15] or naproxen [16], regardless of their variable COX isozyme selectivity, but not with aspirin 100 mg daily [16,19,27,31]. The contribution of endothelial COX-1 to physiological PGI 2 production [34] remains to be demonstrated in humans [35].…”

Section: From the Assessment Of Prostanoid Biosynthetic Capacity Ex Vmentioning

confidence: 94%

Cardiovascular effects of cyclooxygenase‐2 inhibitors: a mechanistic and clinical perspective

Patrono

2016

Brit J Clinical Pharma

Self Cite

129

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This article is part of a joint Themed section with the British Journal of Pharmacology on Targeting Inflammation to Reduce Cardiovascular Disease Risk: a Realistic Clinical Prospect? The rest of the Themed section will appear in a future issue of BJP and will be available at http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1476-5381 Prostaglandin (PG) H synthase 2 [also referred to colloquially as cyclooxygenase (COX) 2] represents a key enzyme in arachidonic acid metabolism in health and disease. It is both constitutively expressed in several human tissues (e.g. kidney and brain) and induced in various cell types (including monocytes/macrophages, vascular endothelial cells and colorectal cancer cells) in response to inflammatory cytokines, laminar shear stress and growth factors. Products of COX-2 activity (e.g. PGE2 and prostacyclin) are involved in diverse physiological and pathophysiological processes, including renal haemodynamics and the control of blood pressure, endothelial thromboresistance, pain and inflammation, and colorectal tumorigenesis. Therefore, it is not surprising that COX-2 inhibitors display multifaceted clinical effects, ranging from reduced pain and inflammation to increased blood pressure, an increased risk of atherothrombotic events and a decreased risk of colorectal cancer. The aim of the present article was to review the cardiovascular effects of COX-2 inhibitors [traditional nonsteroidal anti-inflammatory drugs (tNSAIDs) and coxibs alike], with a focus on the mechanisms contributing to the clinical readouts of COX-2 inhibition.

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Section: From the Assessment Of Prostanoid Biosynthetic Capacity Ex Vmentioning

confidence: 94%

Cardiovascular effects of cyclooxygenase‐2 inhibitors: a mechanistic and clinical perspective

Patrono

2016

Brit J Clinical Pharma

Self Cite

129

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“…Many alternate pathways for platelet activation exist that are independent of thromboxane A 2 and thus not sensitive to the effects of aspirin (104). "Aspirin resistance" has been described in patients with diabetes when measured by a variety of ex vivo and in vitro methods (platelet aggregometry, measurement of thromboxane B 2 ) (101), but other studies suggest no impairment in aspirin response among patients with diabetes (105). A recent trial suggested that more frequent dosing regimens of aspirin may reduce platelet reactivity in individuals with diabetes (106); however, these observations alone are insufficient to empirically recommend that higher doses of aspirin be used in this group at this time.…”

Section: Aspirin Dosingmentioning

confidence: 99%

9. Cardiovascular Disease and Risk Management: Standards of Medical Care in Diabetes—2018

2017

Diabetes Care

443

192

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The American Diabetes Association (ADA) “Standards of Medical Care in Diabetes” includes ADA’s current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, a multidisciplinary expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA’s clinical practice recommendations, please refer to the Standards of Care Introduction. Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC.

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“…Many alternate pathways for platelet activation exist that are independent of thromboxane A 2 and thus are not sensitive to the effects of aspirin (133). "Aspirin resistance" has been described in patients with diabetes when measured by a variety of ex vivo and in vitro methods (platelet aggregometry, measurement of thromboxane B 2 ) (134), but other studies suggest no impairment in aspirin response among patients with diabetes (135). A recent trial suggested that more frequent dosing regimens of aspirin may reduce platelet reactivity in individuals with diabetes (136); however, these observations alone are insufficient to empirically recommend that higher doses of aspirin be used in this group at this time.…”

Section: Aspirin Dosingmentioning

confidence: 99%

10. Cardiovascular Disease and Risk Management: Standards of Medical Care in Diabetes—2019

2018

Diabetes Care

684

108

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The American Diabetes Association (ADA) "Standards of Medical Care in Diabetes" includes ADA's current clinical practice recommendations and is intended to provide the components of diabetes care, general treatment goals and guidelines, and tools to evaluate quality of care. Members of the ADA Professional Practice Committee, a multidisciplinary expert committee, are responsible for updating the Standards of Care annually, or more frequently as warranted. For a detailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA's clinical practice recommendations, please refer to the Standards of Care Introduction. Readers who wish to comment on the Standards of Care are invited to do so at professional.diabetes.org/SOC. For prevention and management of diabetes complications in children and adolescents, please refer to Section 13 "Children and Adolescents." Atherosclerotic cardiovascular disease (ASCVD)ddefined as coronary heart disease, cerebrovascular disease, or peripheral arterial disease presumed to be of atherosclerotic origindis the leading cause of morbidity and mortality for individuals with diabetes and results in an estimated $37.3 billion in cardiovascular-related spending per year associated with diabetes (1). Common conditions coexisting with type 2 diabetes (e.g., hypertension and dyslipidemia) are clear risk factors for ASCVD, and diabetes itself confers independent risk. Numerous studies have shown the efficacy of controlling individual cardiovascular risk factors in preventing or slowing ASCVD in people with diabetes. Furthermore, large benefits are seen when multiple cardiovascular risk factors are addressed simultaneously. Under the current paradigm of aggressive risk factor modification in patients with diabetes, there is evidence that measures of 10-year coronary heart disease (CHD) risk among U.S. adults with diabetes have improved significantly over the past decade (2) and that ASCVD morbidity and mortality have decreased (3,4). Heart failure is another major cause of morbidity and mortality from cardiovascular disease. Recent studies have found that rates of incident heart failure hospitalization (adjusted for age and sex) were twofold higher in patients with diabetes compared with those without (5,6). People with diabetes may have heart failure with preserved ejection fraction (HFpEF) or with reduced ejection fraction (HFrEF). Hypertension is often a precursor of heart failure of either type, and ASCVD can coexist with either type (7), whereas prior myocardial infarction (MI) is often a major factor in HFrEF. Rates of heart failure hospitalization have been improved in recent trials including patients with type 2 diabetes, most of whom also had ASCVD, with sodiumglucose cotransporter 2 (SGLT2) inhibitors (8-10). For prevention and management of both ASCVD and heart failure, cardiovascular risk factors should be systematically assessed at least annually in all patients with diabetes. These risk factors include obesity/overweight, hypertension, d...

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In Vivo Platelet Activation and Aspirin Responsiveness in Type 1 Diabetes

Cited by 43 publications

References 24 publications

Cardiovascular effects of cyclooxygenase‐2 inhibitors: a mechanistic and clinical perspective

Cardiovascular effects of cyclooxygenase‐2 inhibitors: a mechanistic and clinical perspective

9. Cardiovascular Disease and Risk Management: Standards of Medical Care in Diabetes—2018

10. Cardiovascular Disease and Risk Management: Standards of Medical Care in Diabetes—2019

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