Diabetes and Platelet Response to Low-Dose Aspirin

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Abstract

Context: Previous studies have suggested less cardioprotective benefit of aspirin in adults with diabetes, raising concerns about "aspirin resistance" and potentially reduced effectiveness for prevention of cardiovascular disease (CVD). Objective: To examine differences in platelet response to aspirin by diabetes status. Design, Setting, Participants: We examined platelet response before and after aspirin (81 mg/day for 14 days) in 2113 adults (175 with diabetes, 1,938 without diabetes), in the Genetic Study of Aspirin Responsiveness cohort, who had family history of early-onset CVD. Main Outcome Measures: In vivo platelet activation (urinary thromboxane B2), in vitro platelet aggregation to agonists (arachidonic acid, adenosine diphosphate, collagen), and platelet function analyzer-100 closure time. Results: Although adults with diabetes had higher in vivo platelet activation before aspirin, the reduction in in vivo platelet activation after aspirin was similar in those with vs without diabetes. Likewise, the reduction in multiple in vitro platelet measures was similar after aspirin by diabetes status. In regression analyses adjusted for age, sex, race, BMI, smoking, platelet counts, and fibrinogen levels, in vivo platelet activation remained higher in adults with vs without diabetes after aspirin (P = 0.04), but this difference was attenuated after additional adjustment for preaspirin levels (P = 0.10). No differences by diabetes status were noted for any of the in vitro platelet measures after aspirin in fully adjusted models that also accounted for preaspirin levels. Conclusions: In vitro platelet response to aspirin does not differ by diabetes status, suggesting no intrinsic differences in platelet response to aspirin. Instead, factors extrinsic to platelet function should be investigated to give further insights into aspirin use for primary prevention in diabetes.

Original languageEnglish (US)
Pages (from-to)4599-4608
Number of pages10
JournalThe Journal of clinical endocrinology and metabolism
Volume103
Issue number12
DOIs
StatePublished - Dec 1 2018

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Medical problems
Platelets
Aspirin
Blood Platelets
Platelet Activation
Chemical activation
Cardiovascular Diseases
Thromboxane B2
Primary Prevention
Type 1 Diabetes Mellitus
Platelet Count
Platelet Aggregation
Arachidonic Acid
Adenosine Diphosphate
Fibrinogen
Collagen
Smoking
Regression Analysis
Outcome Assessment (Health Care)
Agglomeration

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

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title = "Diabetes and Platelet Response to Low-Dose Aspirin",
abstract = "Context: Previous studies have suggested less cardioprotective benefit of aspirin in adults with diabetes, raising concerns about {"}aspirin resistance{"} and potentially reduced effectiveness for prevention of cardiovascular disease (CVD). Objective: To examine differences in platelet response to aspirin by diabetes status. Design, Setting, Participants: We examined platelet response before and after aspirin (81 mg/day for 14 days) in 2113 adults (175 with diabetes, 1,938 without diabetes), in the Genetic Study of Aspirin Responsiveness cohort, who had family history of early-onset CVD. Main Outcome Measures: In vivo platelet activation (urinary thromboxane B2), in vitro platelet aggregation to agonists (arachidonic acid, adenosine diphosphate, collagen), and platelet function analyzer-100 closure time. Results: Although adults with diabetes had higher in vivo platelet activation before aspirin, the reduction in in vivo platelet activation after aspirin was similar in those with vs without diabetes. Likewise, the reduction in multiple in vitro platelet measures was similar after aspirin by diabetes status. In regression analyses adjusted for age, sex, race, BMI, smoking, platelet counts, and fibrinogen levels, in vivo platelet activation remained higher in adults with vs without diabetes after aspirin (P = 0.04), but this difference was attenuated after additional adjustment for preaspirin levels (P = 0.10). No differences by diabetes status were noted for any of the in vitro platelet measures after aspirin in fully adjusted models that also accounted for preaspirin levels. Conclusions: In vitro platelet response to aspirin does not differ by diabetes status, suggesting no intrinsic differences in platelet response to aspirin. Instead, factors extrinsic to platelet function should be investigated to give further insights into aspirin use for primary prevention in diabetes.",
author = "Al-Sofiani, {Mohammed E.} and Lisa Yanek and Nauder Faraday and Kral, {Brian G} and Rasika Mathias and Lewis Becker and Becker, {Diane M} and Dhananjay Vaidya and Kalyani, {Rita R.}",
year = "2018",
month = "12",
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doi = "10.1210/jc.2018-01254",
language = "English (US)",
volume = "103",
pages = "4599--4608",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
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TY - JOUR

T1 - Diabetes and Platelet Response to Low-Dose Aspirin

AU - Al-Sofiani, Mohammed E.

AU - Yanek, Lisa

AU - Faraday, Nauder

AU - Kral, Brian G

AU - Mathias, Rasika

AU - Becker, Lewis

AU - Becker, Diane M

AU - Vaidya, Dhananjay

AU - Kalyani, Rita R.

PY - 2018/12/1

Y1 - 2018/12/1

N2 - Context: Previous studies have suggested less cardioprotective benefit of aspirin in adults with diabetes, raising concerns about "aspirin resistance" and potentially reduced effectiveness for prevention of cardiovascular disease (CVD). Objective: To examine differences in platelet response to aspirin by diabetes status. Design, Setting, Participants: We examined platelet response before and after aspirin (81 mg/day for 14 days) in 2113 adults (175 with diabetes, 1,938 without diabetes), in the Genetic Study of Aspirin Responsiveness cohort, who had family history of early-onset CVD. Main Outcome Measures: In vivo platelet activation (urinary thromboxane B2), in vitro platelet aggregation to agonists (arachidonic acid, adenosine diphosphate, collagen), and platelet function analyzer-100 closure time. Results: Although adults with diabetes had higher in vivo platelet activation before aspirin, the reduction in in vivo platelet activation after aspirin was similar in those with vs without diabetes. Likewise, the reduction in multiple in vitro platelet measures was similar after aspirin by diabetes status. In regression analyses adjusted for age, sex, race, BMI, smoking, platelet counts, and fibrinogen levels, in vivo platelet activation remained higher in adults with vs without diabetes after aspirin (P = 0.04), but this difference was attenuated after additional adjustment for preaspirin levels (P = 0.10). No differences by diabetes status were noted for any of the in vitro platelet measures after aspirin in fully adjusted models that also accounted for preaspirin levels. Conclusions: In vitro platelet response to aspirin does not differ by diabetes status, suggesting no intrinsic differences in platelet response to aspirin. Instead, factors extrinsic to platelet function should be investigated to give further insights into aspirin use for primary prevention in diabetes.

AB - Context: Previous studies have suggested less cardioprotective benefit of aspirin in adults with diabetes, raising concerns about "aspirin resistance" and potentially reduced effectiveness for prevention of cardiovascular disease (CVD). Objective: To examine differences in platelet response to aspirin by diabetes status. Design, Setting, Participants: We examined platelet response before and after aspirin (81 mg/day for 14 days) in 2113 adults (175 with diabetes, 1,938 without diabetes), in the Genetic Study of Aspirin Responsiveness cohort, who had family history of early-onset CVD. Main Outcome Measures: In vivo platelet activation (urinary thromboxane B2), in vitro platelet aggregation to agonists (arachidonic acid, adenosine diphosphate, collagen), and platelet function analyzer-100 closure time. Results: Although adults with diabetes had higher in vivo platelet activation before aspirin, the reduction in in vivo platelet activation after aspirin was similar in those with vs without diabetes. Likewise, the reduction in multiple in vitro platelet measures was similar after aspirin by diabetes status. In regression analyses adjusted for age, sex, race, BMI, smoking, platelet counts, and fibrinogen levels, in vivo platelet activation remained higher in adults with vs without diabetes after aspirin (P = 0.04), but this difference was attenuated after additional adjustment for preaspirin levels (P = 0.10). No differences by diabetes status were noted for any of the in vitro platelet measures after aspirin in fully adjusted models that also accounted for preaspirin levels. Conclusions: In vitro platelet response to aspirin does not differ by diabetes status, suggesting no intrinsic differences in platelet response to aspirin. Instead, factors extrinsic to platelet function should be investigated to give further insights into aspirin use for primary prevention in diabetes.

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U2 - 10.1210/jc.2018-01254

DO - 10.1210/jc.2018-01254

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JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

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