Heritability of Platelet Responsiveness to Aspirin in Activation Pathways Directly and Indirectly Related to Cyclooxygenase-1
Background— The inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial infarction, stroke, and cardiovascular death. Genetic variation is a proposed but unproved mechanism for insufficient ASA responsiveness. Methods an...
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| Published in | Circulation (New York, N.Y.) Vol. 115; no. 19; pp. 2490 - 2496 |
|---|---|
| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
15.05.2007
|
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background—
The inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial infarction, stroke, and cardiovascular death. Genetic variation is a proposed but unproved mechanism for insufficient ASA responsiveness.
Methods and Results—
We examined platelet ASA responsiveness in 1880 asymptomatic subjects (mean age, 44±13 years; 58% women) recruited from 309 white and 208 black families with premature coronary heart disease. Ex vivo platelet function was determined before and after ingestion of ASA (81 mg/d for 2 weeks) with the use of a panel of measures that assessed platelet activation in pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA. The proportion of phenotypic variance related to CHD risk factor covariates was determined by multivariable regression. Heritability of phenotypes was determined with the use of variance components models unadjusted and adjusted for covariates. ASA inhibited arachidonic acid–induced aggregation and thromboxane B
2
production by ≥99% (
P
<0.0001). Inhibition of urinary thromboxane excretion and platelet activation in pathways indirectly related to cyclooxygenase-1 was less pronounced and more variable (inhibition of 0% to 100%). Measured covariates contributed modestly to variability in ASA response phenotypes (
r
2
=0.001 to 0.133). Phenotypes indirectly related to cyclooxygenase-1 were strongly and consistently heritable across races (h
2
=0.266 to 0.762;
P
<0.01), but direct cyclooxygenase-1 phenotypes were not.
Conclusions—
Heritable factors contribute prominently to variability in residual platelet function after ASA exposure. These data suggest a genetic basis for the adequacy of platelet suppression by ASA and potentially for differences in the clinical efficacy of ASA. |
|---|---|
| AbstractList | The inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial infarction, stroke, and cardiovascular death. Genetic variation is a proposed but unproved mechanism for insufficient ASA responsiveness.
We examined platelet ASA responsiveness in 1880 asymptomatic subjects (mean age, 44+/-13 years; 58% women) recruited from 309 white and 208 black families with premature coronary heart disease. Ex vivo platelet function was determined before and after ingestion of ASA (81 mg/d for 2 weeks) with the use of a panel of measures that assessed platelet activation in pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA. The proportion of phenotypic variance related to CHD risk factor covariates was determined by multivariable regression. Heritability of phenotypes was determined with the use of variance components models unadjusted and adjusted for covariates. ASA inhibited arachidonic acid-induced aggregation and thromboxane B2 production by > or = 99% (P<0.0001). Inhibition of urinary thromboxane excretion and platelet activation in pathways indirectly related to cyclooxygenase-1 was less pronounced and more variable (inhibition of 0% to 100%). Measured covariates contributed modestly to variability in ASA response phenotypes (r2=0.001 to 0.133). Phenotypes indirectly related to cyclooxygenase-1 were strongly and consistently heritable across races (h2=0.266 to 0.762; P<0.01), but direct cyclooxygenase-1 phenotypes were not.
Heritable factors contribute prominently to variability in residual platelet function after ASA exposure. These data suggest a genetic basis for the adequacy of platelet suppression by ASA and potentially for differences in the clinical efficacy of ASA. The inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial infarction, stroke, and cardiovascular death. Genetic variation is a proposed but unproved mechanism for insufficient ASA responsiveness.BACKGROUNDThe inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial infarction, stroke, and cardiovascular death. Genetic variation is a proposed but unproved mechanism for insufficient ASA responsiveness.We examined platelet ASA responsiveness in 1880 asymptomatic subjects (mean age, 44+/-13 years; 58% women) recruited from 309 white and 208 black families with premature coronary heart disease. Ex vivo platelet function was determined before and after ingestion of ASA (81 mg/d for 2 weeks) with the use of a panel of measures that assessed platelet activation in pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA. The proportion of phenotypic variance related to CHD risk factor covariates was determined by multivariable regression. Heritability of phenotypes was determined with the use of variance components models unadjusted and adjusted for covariates. ASA inhibited arachidonic acid-induced aggregation and thromboxane B2 production by > or = 99% (P<0.0001). Inhibition of urinary thromboxane excretion and platelet activation in pathways indirectly related to cyclooxygenase-1 was less pronounced and more variable (inhibition of 0% to 100%). Measured covariates contributed modestly to variability in ASA response phenotypes (r2=0.001 to 0.133). Phenotypes indirectly related to cyclooxygenase-1 were strongly and consistently heritable across races (h2=0.266 to 0.762; P<0.01), but direct cyclooxygenase-1 phenotypes were not.METHODS AND RESULTSWe examined platelet ASA responsiveness in 1880 asymptomatic subjects (mean age, 44+/-13 years; 58% women) recruited from 309 white and 208 black families with premature coronary heart disease. Ex vivo platelet function was determined before and after ingestion of ASA (81 mg/d for 2 weeks) with the use of a panel of measures that assessed platelet activation in pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA. The proportion of phenotypic variance related to CHD risk factor covariates was determined by multivariable regression. Heritability of phenotypes was determined with the use of variance components models unadjusted and adjusted for covariates. ASA inhibited arachidonic acid-induced aggregation and thromboxane B2 production by > or = 99% (P<0.0001). Inhibition of urinary thromboxane excretion and platelet activation in pathways indirectly related to cyclooxygenase-1 was less pronounced and more variable (inhibition of 0% to 100%). Measured covariates contributed modestly to variability in ASA response phenotypes (r2=0.001 to 0.133). Phenotypes indirectly related to cyclooxygenase-1 were strongly and consistently heritable across races (h2=0.266 to 0.762; P<0.01), but direct cyclooxygenase-1 phenotypes were not.Heritable factors contribute prominently to variability in residual platelet function after ASA exposure. These data suggest a genetic basis for the adequacy of platelet suppression by ASA and potentially for differences in the clinical efficacy of ASA.CONCLUSIONSHeritable factors contribute prominently to variability in residual platelet function after ASA exposure. These data suggest a genetic basis for the adequacy of platelet suppression by ASA and potentially for differences in the clinical efficacy of ASA. Background— The inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial infarction, stroke, and cardiovascular death. Genetic variation is a proposed but unproved mechanism for insufficient ASA responsiveness. Methods and Results— We examined platelet ASA responsiveness in 1880 asymptomatic subjects (mean age, 44±13 years; 58% women) recruited from 309 white and 208 black families with premature coronary heart disease. Ex vivo platelet function was determined before and after ingestion of ASA (81 mg/d for 2 weeks) with the use of a panel of measures that assessed platelet activation in pathways directly and indirectly related to cyclooxygenase-1, the enzyme inhibited by ASA. The proportion of phenotypic variance related to CHD risk factor covariates was determined by multivariable regression. Heritability of phenotypes was determined with the use of variance components models unadjusted and adjusted for covariates. ASA inhibited arachidonic acid–induced aggregation and thromboxane B 2 production by ≥99% ( P <0.0001). Inhibition of urinary thromboxane excretion and platelet activation in pathways indirectly related to cyclooxygenase-1 was less pronounced and more variable (inhibition of 0% to 100%). Measured covariates contributed modestly to variability in ASA response phenotypes ( r 2 =0.001 to 0.133). Phenotypes indirectly related to cyclooxygenase-1 were strongly and consistently heritable across races (h 2 =0.266 to 0.762; P <0.01), but direct cyclooxygenase-1 phenotypes were not. Conclusions— Heritable factors contribute prominently to variability in residual platelet function after ASA exposure. These data suggest a genetic basis for the adequacy of platelet suppression by ASA and potentially for differences in the clinical efficacy of ASA. |
| Author | Faraday, Nauder Wilson, Alexander F. Moy, Taryn F. Bray, Paul F. Yanek, Lisa R. Mathias, Rasika Becker, Lewis C. Vaidya, Dhananjay Herrera-Galeano, J. Enrique Becker, Diane M. Fallin, M. Daniele |
| Author_xml | – sequence: 1 givenname: Nauder surname: Faraday fullname: Faraday, Nauder organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 2 givenname: Lisa R. surname: Yanek fullname: Yanek, Lisa R. organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 3 givenname: Rasika surname: Mathias fullname: Mathias, Rasika organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 4 givenname: J. Enrique surname: Herrera-Galeano fullname: Herrera-Galeano, J. Enrique organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 5 givenname: Dhananjay surname: Vaidya fullname: Vaidya, Dhananjay organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 6 givenname: Taryn F. surname: Moy fullname: Moy, Taryn F. organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 7 givenname: M. Daniele surname: Fallin fullname: Fallin, M. Daniele organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 8 givenname: Alexander F. surname: Wilson fullname: Wilson, Alexander F. organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 9 givenname: Paul F. surname: Bray fullname: Bray, Paul F. organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 10 givenname: Lewis C. surname: Becker fullname: Becker, Lewis C. organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns – sequence: 11 givenname: Diane M. surname: Becker fullname: Becker, Diane M. organization: From the Department of Anesthesiology/Critical Care Medicine, Division of Cardiac Surgical Intensive Care (N.F.), Department of Medicine, Division of General Internal Medicine (L.R.Y., J.E.H.-G., D.V., T.F.M., D.M.B.), and Department of Medicine, Division of Cardiology (L.C.B.), Johns Hopkins Medical Institutions, Baltimore, Md; Inherited Disease Research Branch, National Human Genome Research Institute/National Institutes of Health, Baltimore, Md (R.M., A.F.W.); Department of Epidemiology, Johns |
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| Keywords | Prostaglandin-endoperoxide synthase antiplatelet agents Enzyme Cyclooxygenase 1 Enzyme inhibitor Cardiovascular disease Acetylsalicylic acid Antiplatelet agent platelets Non steroidal antiinflammatory agent Platelet Analgesic genetics Antipyretic aspirin Oxidoreductases Salicylates |
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The inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial... The inability of aspirin (acetylsalicylic acid [ASA]) to adequately suppress platelet function is associated with future risk of myocardial infarction, stroke,... |
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| SubjectTerms | Adult African Americans - genetics Arachidonic Acid - antagonists & inhibitors Arachidonic Acid - pharmacology Aspirin - pharmacology Aspirin - therapeutic use beta-Thromboglobulin - metabolism Biological and medical sciences Blood and lymphatic vessels Blood coagulation. Blood cells Blood Platelets - drug effects Blood Platelets - enzymology Blood Platelets - physiology Blood vessels and receptors Cardiology. Vascular system Cardiovascular Diseases - epidemiology Cardiovascular Diseases - prevention & control Coronary Disease - blood Cyclooxygenase 1 - blood Cyclooxygenase 1 - physiology Cyclooxygenase Inhibitors - pharmacology Cyclooxygenase Inhibitors - therapeutic use Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous Drug Resistance - genetics Dyslipidemias - epidemiology European Continental Ancestry Group - genetics Female Fundamental and applied biological sciences. Psychology Genetic Heterogeneity Genetic Predisposition to Disease Genetic Variation Humans Hyperglycemia - epidemiology Hypertension - epidemiology Male Medical sciences Membrane Proteins - blood Membrane Proteins - physiology Middle Aged Molecular and cellular biology Phenotype Platelet Platelet Activation - drug effects Platelet Activation - genetics Platelet Aggregation - drug effects Platelet Aggregation - genetics Platelet Aggregation Inhibitors - pharmacology Platelet Aggregation Inhibitors - therapeutic use Prospective Studies Risk Factors Sex Characteristics Smoking - epidemiology Thrombophilia - drug therapy Thrombophilia - genetics Thrombosis - prevention & control Thromboxane B2 - analogs & derivatives Thromboxane B2 - metabolism Thromboxane B2 - urine Vertebrates: cardiovascular system |
| Title | Heritability of Platelet Responsiveness to Aspirin in Activation Pathways Directly and Indirectly Related to Cyclooxygenase-1 |
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