Aspirin-Resistant Thromboxane Biosynthesis and the Risk of Myocardial Infarction, Stroke, or Cardiovascular Death in Patients at High Risk for Cardiovascular Events
Background — We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in a high-risk population. Methods and Results — Baseline urine samples were obtained from 5529 Canadian patients enrolled in the Heart Outcome...
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| Published in | Circulation (New York, N.Y.) Vol. 105; no. 14; pp. 1650 - 1655 |
|---|---|
| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hagerstown, MD
Lippincott Williams & Wilkins
09.04.2002
American Heart Association, Inc |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Background
—
We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in a high-risk population.
Methods and Results
—
Baseline urine samples were obtained from 5529 Canadian patients enrolled in the Heart Outcomes Prevention Evaluation (HOPE) Study. Using a nested case-control design, we measured urinary 11-dehydro thromboxane B
2
levels, a marker of in vivo thromboxane generation, in 488 cases treated with aspirin who had myocardial infarction, stroke, or cardiovascular death during 5 years of follow-up and in 488 sex- and age-matched control subjects also receiving aspirin who did not have an event. After adjustment for baseline differences, the odds for the composite outcome of myocardial infarction, stroke, or cardiovascular death increased with each increasing quartile of 11-dehydro thromboxane B
2
, with patients in the upper quartile having a 1.8-times-higher risk than those in the lower quartile (OR, 1.8; 95% CI, 1.2 to 2.7;
P
=0.009). Those in the upper quartile had a 2-times-higher risk of myocardial infarction (OR, 2.0; 95% CI, 1.2 to 3.4;
P
=0.006) and a 3.5-times-higher risk of cardiovascular death (OR, 3.5; 95% CI, 1.7 to 7.4;
P
<0.001) than those in the lower quartile.
Conclusions
—
In aspirin-treated patients, urinary concentrations of 11-dehydro thromboxane B
2
predict the future risk of myocardial infarction or cardiovascular death. These findings raise the possibility that elevated urinary 11-dehydro thromboxane B
2
levels identify patients who are relatively resistant to aspirin and who may benefit from additional antiplatelet therapies or treatments that more effectively block in vivo thromboxane production or activity. |
|---|---|
| AbstractList | BACKGROUND: We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in a high-risk population. METHODS AND RESULTS: Baseline urine samples were obtained from 5529 Canadian patients enrolled in the Heart Outcomes Prevention Evaluation (HOPE) Study. Using a nested case-control design, we measured urinary 11-dehydro thromboxane B2 levels, a marker of in vivo thromboxane generation, in 488 cases treated with aspirin who had myocardial infarction, stroke, or cardiovascular death during 5 years of follow-up and in 488 sex- and age-matched control subjects also receiving aspirin who did not have an event. After adjustment for baseline differences, the odds for the composite outcome of myocardial infarction, stroke, or cardiovascular death increased with each increasing quartile of 11-dehydro thromboxane B2, with patients in the upper quartile having a 1.8-times-higher risk than those in the lower quartile (OR, 1.8; 95% CI, 1.2 to 2.7; P=0.009). Those in the upper quartile had a 2-times-higher risk of myocardial infarction (OR, 2.0; 95% CI, 1.2 to 3.4; P=0.006) and a 3.5-times-higher risk of cardiovascular death (OR, 3.5; 95% CI, 1.7 to 7.4; P<0.001) than those in the lower quartile. CONCLUSIONS: In aspirin-treated patients, urinary concentrations of 11-dehydro thromboxane B2 predict the future risk of myocardial infarction or cardiovascular death. These findings raise the possibility that elevated urinary 11-dehydro thromboxane B2 levels identify patients who are relatively resistant to aspirin and who may benefit from additional antiplatelet therapies or treatments that more effectively block in vivo thromboxane production or activity. We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in a high-risk population. Baseline urine samples were obtained from 5529 Canadian patients enrolled in the Heart Outcomes Prevention Evaluation (HOPE) Study. Using a nested case-control design, we measured urinary 11-dehydro thromboxane B2 levels, a marker of in vivo thromboxane generation, in 488 cases treated with aspirin who had myocardial infarction, stroke, or cardiovascular death during 5 years of follow-up and in 488 sex- and age-matched control subjects also receiving aspirin who did not have an event. After adjustment for baseline differences, the odds for the composite outcome of myocardial infarction, stroke, or cardiovascular death increased with each increasing quartile of 11-dehydro thromboxane B2, with patients in the upper quartile having a 1.8-times-higher risk than those in the lower quartile (OR, 1.8; 95% CI, 1.2 to 2.7; P=0.009). Those in the upper quartile had a 2-times-higher risk of myocardial infarction (OR, 2.0; 95% CI, 1.2 to 3.4; P=0.006) and a 3.5-times-higher risk of cardiovascular death (OR, 3.5; 95% CI, 1.7 to 7.4; P<0.001) than those in the lower quartile. In aspirin-treated patients, urinary concentrations of 11-dehydro thromboxane B2 predict the future risk of myocardial infarction or cardiovascular death. These findings raise the possibility that elevated urinary 11-dehydro thromboxane B2 levels identify patients who are relatively resistant to aspirin and who may benefit from additional antiplatelet therapies or treatments that more effectively block in vivo thromboxane production or activity. We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in a high-risk population.BACKGROUNDWe studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in a high-risk population.Baseline urine samples were obtained from 5529 Canadian patients enrolled in the Heart Outcomes Prevention Evaluation (HOPE) Study. Using a nested case-control design, we measured urinary 11-dehydro thromboxane B2 levels, a marker of in vivo thromboxane generation, in 488 cases treated with aspirin who had myocardial infarction, stroke, or cardiovascular death during 5 years of follow-up and in 488 sex- and age-matched control subjects also receiving aspirin who did not have an event. After adjustment for baseline differences, the odds for the composite outcome of myocardial infarction, stroke, or cardiovascular death increased with each increasing quartile of 11-dehydro thromboxane B2, with patients in the upper quartile having a 1.8-times-higher risk than those in the lower quartile (OR, 1.8; 95% CI, 1.2 to 2.7; P=0.009). Those in the upper quartile had a 2-times-higher risk of myocardial infarction (OR, 2.0; 95% CI, 1.2 to 3.4; P=0.006) and a 3.5-times-higher risk of cardiovascular death (OR, 3.5; 95% CI, 1.7 to 7.4; P<0.001) than those in the lower quartile.METHODS AND RESULTSBaseline urine samples were obtained from 5529 Canadian patients enrolled in the Heart Outcomes Prevention Evaluation (HOPE) Study. Using a nested case-control design, we measured urinary 11-dehydro thromboxane B2 levels, a marker of in vivo thromboxane generation, in 488 cases treated with aspirin who had myocardial infarction, stroke, or cardiovascular death during 5 years of follow-up and in 488 sex- and age-matched control subjects also receiving aspirin who did not have an event. After adjustment for baseline differences, the odds for the composite outcome of myocardial infarction, stroke, or cardiovascular death increased with each increasing quartile of 11-dehydro thromboxane B2, with patients in the upper quartile having a 1.8-times-higher risk than those in the lower quartile (OR, 1.8; 95% CI, 1.2 to 2.7; P=0.009). Those in the upper quartile had a 2-times-higher risk of myocardial infarction (OR, 2.0; 95% CI, 1.2 to 3.4; P=0.006) and a 3.5-times-higher risk of cardiovascular death (OR, 3.5; 95% CI, 1.7 to 7.4; P<0.001) than those in the lower quartile.In aspirin-treated patients, urinary concentrations of 11-dehydro thromboxane B2 predict the future risk of myocardial infarction or cardiovascular death. These findings raise the possibility that elevated urinary 11-dehydro thromboxane B2 levels identify patients who are relatively resistant to aspirin and who may benefit from additional antiplatelet therapies or treatments that more effectively block in vivo thromboxane production or activity.CONCLUSIONSIn aspirin-treated patients, urinary concentrations of 11-dehydro thromboxane B2 predict the future risk of myocardial infarction or cardiovascular death. These findings raise the possibility that elevated urinary 11-dehydro thromboxane B2 levels identify patients who are relatively resistant to aspirin and who may benefit from additional antiplatelet therapies or treatments that more effectively block in vivo thromboxane production or activity. Background — We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in a high-risk population. Methods and Results — Baseline urine samples were obtained from 5529 Canadian patients enrolled in the Heart Outcomes Prevention Evaluation (HOPE) Study. Using a nested case-control design, we measured urinary 11-dehydro thromboxane B 2 levels, a marker of in vivo thromboxane generation, in 488 cases treated with aspirin who had myocardial infarction, stroke, or cardiovascular death during 5 years of follow-up and in 488 sex- and age-matched control subjects also receiving aspirin who did not have an event. After adjustment for baseline differences, the odds for the composite outcome of myocardial infarction, stroke, or cardiovascular death increased with each increasing quartile of 11-dehydro thromboxane B 2 , with patients in the upper quartile having a 1.8-times-higher risk than those in the lower quartile (OR, 1.8; 95% CI, 1.2 to 2.7; P =0.009). Those in the upper quartile had a 2-times-higher risk of myocardial infarction (OR, 2.0; 95% CI, 1.2 to 3.4; P =0.006) and a 3.5-times-higher risk of cardiovascular death (OR, 3.5; 95% CI, 1.7 to 7.4; P <0.001) than those in the lower quartile. Conclusions — In aspirin-treated patients, urinary concentrations of 11-dehydro thromboxane B 2 predict the future risk of myocardial infarction or cardiovascular death. These findings raise the possibility that elevated urinary 11-dehydro thromboxane B 2 levels identify patients who are relatively resistant to aspirin and who may benefit from additional antiplatelet therapies or treatments that more effectively block in vivo thromboxane production or activity. |
| Author | Hirsh, Jack Johnston, Marilyn Weitz, Jeffrey I. Eikelboom, John W. Yusuf, Salim Yi, Qilong |
| Author_xml | – sequence: 1 givenname: John W. surname: Eikelboom fullname: Eikelboom, John W. organization: From the Department of Medicine, University of Western Australia, Thrombosis and Haemophilia Unit, Royal Perth Hospital, Perth, Australia (J.W.E.); Hamilton Civic Hospitals Research Centre, Hamilton, Canada (J.H., J.I.W.); the Department of Medicine, McMaster University, Hamilton, Canada (J.H., J.I.W., S.Y.); Hemostasis Reference Laboratory, Hamilton Civic Hospitals, Hamilton, Canada (M.J.); the Biostatistics Department, Princess Margaret Hospital, Toronto, Canada (Q.Y.); and Population Health – sequence: 2 givenname: Jack surname: Hirsh fullname: Hirsh, Jack organization: From the Department of Medicine, University of Western Australia, Thrombosis and Haemophilia Unit, Royal Perth Hospital, Perth, Australia (J.W.E.); Hamilton Civic Hospitals Research Centre, Hamilton, Canada (J.H., J.I.W.); the Department of Medicine, McMaster University, Hamilton, Canada (J.H., J.I.W., S.Y.); Hemostasis Reference Laboratory, Hamilton Civic Hospitals, Hamilton, Canada (M.J.); the Biostatistics Department, Princess Margaret Hospital, Toronto, Canada (Q.Y.); and Population Health – sequence: 3 givenname: Jeffrey I. surname: Weitz fullname: Weitz, Jeffrey I. organization: From the Department of Medicine, University of Western Australia, Thrombosis and Haemophilia Unit, Royal Perth Hospital, Perth, Australia (J.W.E.); Hamilton Civic Hospitals Research Centre, Hamilton, Canada (J.H., J.I.W.); the Department of Medicine, McMaster University, Hamilton, Canada (J.H., J.I.W., S.Y.); Hemostasis Reference Laboratory, Hamilton Civic Hospitals, Hamilton, Canada (M.J.); the Biostatistics Department, Princess Margaret Hospital, Toronto, Canada (Q.Y.); and Population Health – sequence: 4 givenname: Marilyn surname: Johnston fullname: Johnston, Marilyn organization: From the Department of Medicine, University of Western Australia, Thrombosis and Haemophilia Unit, Royal Perth Hospital, Perth, Australia (J.W.E.); Hamilton Civic Hospitals Research Centre, Hamilton, Canada (J.H., J.I.W.); the Department of Medicine, McMaster University, Hamilton, Canada (J.H., J.I.W., S.Y.); Hemostasis Reference Laboratory, Hamilton Civic Hospitals, Hamilton, Canada (M.J.); the Biostatistics Department, Princess Margaret Hospital, Toronto, Canada (Q.Y.); and Population Health – sequence: 5 givenname: Qilong surname: Yi fullname: Yi, Qilong organization: From the Department of Medicine, University of Western Australia, Thrombosis and Haemophilia Unit, Royal Perth Hospital, Perth, Australia (J.W.E.); Hamilton Civic Hospitals Research Centre, Hamilton, Canada (J.H., J.I.W.); the Department of Medicine, McMaster University, Hamilton, Canada (J.H., J.I.W., S.Y.); Hemostasis Reference Laboratory, Hamilton Civic Hospitals, Hamilton, Canada (M.J.); the Biostatistics Department, Princess Margaret Hospital, Toronto, Canada (Q.Y.); and Population Health – sequence: 6 givenname: Salim surname: Yusuf fullname: Yusuf, Salim organization: From the Department of Medicine, University of Western Australia, Thrombosis and Haemophilia Unit, Royal Perth Hospital, Perth, Australia (J.W.E.); Hamilton Civic Hospitals Research Centre, Hamilton, Canada (J.H., J.I.W.); the Department of Medicine, McMaster University, Hamilton, Canada (J.H., J.I.W., S.Y.); Hemostasis Reference Laboratory, Hamilton Civic Hospitals, Hamilton, Canada (M.J.); the Biostatistics Department, Princess Margaret Hospital, Toronto, Canada (Q.Y.); and Population Health |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13612962$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/11940542$$D View this record in MEDLINE/PubMed |
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| CODEN | CIRCAZ |
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| Cites_doi | 10.1055/s-0037-1615048 10.1016/S0140-6736(99)05388-X 10.1073/pnas.83.16.5861 10.1056/NEJMoa010746 10.1056/NEJM199405053301808 10.1074/jbc.271.20.12042 10.1136/jnnp.54.12.1044 10.1161/circ.97.4.350 10.1055/s-0038-1645038 10.1172/JCI109967 10.1161/str.23.10.1412573 10.1056/NEJM200001203420301 10.1136/bmj.308.6921.81 10.1161/circ.96.4.1109 10.1161/str.30.3.546 10.1378/chest.119.1_suppl.39S 10.1161/circ.101.10.1206 10.1161/str.25.12.7974569 10.1016/0049-3848(93)90164-J 10.1161/circ.102.8.840 10.1161/circ.104.8.921 10.1016/S0049-3848(98)00101-7 10.1161/str.24.3.8446967 10.1056/NEJM199901143400207 10.1161/circ.102.16.1924 10.1172/JCI111296 10.1056/NEJM200001203420302 10.1056/NEJM199110313251801 |
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| Keywords | Human Nervous system diseases Stroke Treatment resistance Prognosis Infarct Arachidonic acid derivatives Cardiovascular disease Acetylsalicylic acid Coronary heart disease Myocardial disease Antiplatelet agent Cerebral disorder Vascular disease Chemotherapy Treatment Central nervous system disease Myocardium Salicylates Thromboxane Cerebrovascular disease |
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| References | e_1_3_2_26_2 e_1_3_2_27_2 e_1_3_2_28_2 e_1_3_2_29_2 e_1_3_2_20_2 e_1_3_2_21_2 e_1_3_2_22_2 e_1_3_2_23_2 e_1_3_2_24_2 e_1_3_2_25_2 e_1_3_2_9_2 e_1_3_2_15_2 e_1_3_2_8_2 e_1_3_2_16_2 e_1_3_2_7_2 e_1_3_2_6_2 e_1_3_2_18_2 e_1_3_2_19_2 e_1_3_2_1_2 e_1_3_2_10_2 e_1_3_2_5_2 e_1_3_2_11_2 e_1_3_2_4_2 e_1_3_2_12_2 e_1_3_2_3_2 e_1_3_2_13_2 e_1_3_2_2_2 e_1_3_2_14_2 (e_1_3_2_17_2) 2000; 23 12473569 - Circulation. 2002 Dec 10;106(24):e200-1; author reply e200-1 11942339 - Circulation. 2002 Apr 9;105(14):e9094-5 12451018 - Circulation. 2002 Nov 26;106(22):e181-2; author reply e181-2 11940535 - Circulation. 2002 Apr 9;105(14):1620-2 |
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We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in... We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in a high-risk... BACKGROUND: We studied whether aspirin resistance, defined as failure of suppression of thromboxane generation, increases the risk of cardiovascular events in... |
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| SubjectTerms | Aged Angiotensin-Converting Enzyme Inhibitors - therapeutic use Aspirin - therapeutic use Biological and medical sciences Blood. Blood coagulation. Reticuloendothelial system Canada - epidemiology Cardiovascular Diseases - drug therapy Cardiovascular Diseases - epidemiology Cardiovascular Diseases - metabolism Case-Control Studies Cohort Studies Comorbidity Cyclooxygenase Inhibitors - therapeutic use Death, Sudden, Cardiac - epidemiology Death, Sudden, Cardiac - prevention & control Demography Female Follow-Up Studies Humans Male Medical sciences Myocardial Infarction - epidemiology Myocardial Infarction - prevention & control Odds Ratio Pharmacology. Drug treatments Randomized Controlled Trials as Topic Risk Assessment Risk Factors Secondary Prevention Stroke - epidemiology Stroke - prevention & control Thromboxane B2 - analogs & derivatives Thromboxane B2 - urine Thromboxanes - biosynthesis Thromboxanes - urine Vitamin E - therapeutic use |
| Title | Aspirin-Resistant Thromboxane Biosynthesis and the Risk of Myocardial Infarction, Stroke, or Cardiovascular Death in Patients at High Risk for Cardiovascular Events |
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