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SEATTLE — Blood tests on 507 patients seen in emergency departments for chest pain found resistance to aspirin in 20% of those with a history of heart failure and 12% of patients without heart failure, Dr. Lori B. Daniels reported in a poster presentation at the annual meeting of the Heart Failure Society of America.
“Physicians should be aware of the high rate of aspirin nonresponsiveness in patients with heart failure, since they may be susceptible to thrombotic events” even if treated with aspirin, and may need other antithrombotic therapy, said Dr. Daniels of the University of California, San Diego, and her associates.
Aspirin prevents MI, stroke, or other vascular events by causing platelet dysfunction so that platelets do not aggregate. It irreversibly inhibits platelet cyclooxygenase, a key enzyme in prostaglandin synthesis, so that platelets lose the capacity to synthesize thromboxane A2, an inducer of platelet aggregation with vasoconstrictive properties.
Between 8% and 18% of patients treated with aspirin, however, develop recurrent vascular events within 2 years, a phenomenon described as aspirin resistance “or perhaps more accurately as aspirin nonresponsiveness,” the investigators wrote.
They took blood samples from patients with suspected acute coronary syndromes seen at five medical centers. All were on outpatient aspirin therapy or were given an aspirin when they arrived at the emergency department. The 25% of patients with a history of heart failure were older than those without heart failure (62 vs. 58 years) and were more likely to be taking aspirin as an outpatient (81% vs. 60%), but the two groups did not differ by sex or body mass index.
Blood samples were tested using the Ultegra Rapid Platelet Function Assay on a VerifyNow testing device. The Ultegra assay is a turbidimetric-based optical detection system that measures platelet-induced aggregation as an increase in light transmittance. Aspirin nonresponsiveness was defined as an “aspirin reaction unit” value of at least 550. Results showed a mean of 479 aspirin reaction units in patients with a history of heart failure, compared with 458 units in patients without heart failure.
None of the investigators are associated with Accumetrix, the company that makes the VerifyNow device.
Heart failure patients were more likely to have a history of hypertension, coronary artery disease, MI, diabetes, chronic renal insufficiency, and tobacco use than were non-heart failure patients. Those with heart failure had averaged 4 years of aspirin use, compared with 2 years in patients without prior heart failure, she said.
The high rate of aspirin nonres-ponsiveness in heart failure patients may make them susceptible to thrombotic events. DR. DANIELS
SEATTLE — Blood tests on 507 patients seen in emergency departments for chest pain found resistance to aspirin in 20% of those with a history of heart failure and 12% of patients without heart failure, Dr. Lori B. Daniels reported in a poster presentation at the annual meeting of the Heart Failure Society of America.
“Physicians should be aware of the high rate of aspirin nonresponsiveness in patients with heart failure, since they may be susceptible to thrombotic events” even if treated with aspirin, and may need other antithrombotic therapy, said Dr. Daniels of the University of California, San Diego, and her associates.
Aspirin prevents MI, stroke, or other vascular events by causing platelet dysfunction so that platelets do not aggregate. It irreversibly inhibits platelet cyclooxygenase, a key enzyme in prostaglandin synthesis, so that platelets lose the capacity to synthesize thromboxane A2, an inducer of platelet aggregation with vasoconstrictive properties.
Between 8% and 18% of patients treated with aspirin, however, develop recurrent vascular events within 2 years, a phenomenon described as aspirin resistance “or perhaps more accurately as aspirin nonresponsiveness,” the investigators wrote.
They took blood samples from patients with suspected acute coronary syndromes seen at five medical centers. All were on outpatient aspirin therapy or were given an aspirin when they arrived at the emergency department. The 25% of patients with a history of heart failure were older than those without heart failure (62 vs. 58 years) and were more likely to be taking aspirin as an outpatient (81% vs. 60%), but the two groups did not differ by sex or body mass index.
Blood samples were tested using the Ultegra Rapid Platelet Function Assay on a VerifyNow testing device. The Ultegra assay is a turbidimetric-based optical detection system that measures platelet-induced aggregation as an increase in light transmittance. Aspirin nonresponsiveness was defined as an “aspirin reaction unit” value of at least 550. Results showed a mean of 479 aspirin reaction units in patients with a history of heart failure, compared with 458 units in patients without heart failure.
None of the investigators are associated with Accumetrix, the company that makes the VerifyNow device.
Heart failure patients were more likely to have a history of hypertension, coronary artery disease, MI, diabetes, chronic renal insufficiency, and tobacco use than were non-heart failure patients. Those with heart failure had averaged 4 years of aspirin use, compared with 2 years in patients without prior heart failure, she said.
The high rate of aspirin nonres-ponsiveness in heart failure patients may make them susceptible to thrombotic events. DR. DANIELS
SEATTLE — Blood tests on 507 patients seen in emergency departments for chest pain found resistance to aspirin in 20% of those with a history of heart failure and 12% of patients without heart failure, Dr. Lori B. Daniels reported in a poster presentation at the annual meeting of the Heart Failure Society of America.
“Physicians should be aware of the high rate of aspirin nonresponsiveness in patients with heart failure, since they may be susceptible to thrombotic events” even if treated with aspirin, and may need other antithrombotic therapy, said Dr. Daniels of the University of California, San Diego, and her associates.
Aspirin prevents MI, stroke, or other vascular events by causing platelet dysfunction so that platelets do not aggregate. It irreversibly inhibits platelet cyclooxygenase, a key enzyme in prostaglandin synthesis, so that platelets lose the capacity to synthesize thromboxane A2, an inducer of platelet aggregation with vasoconstrictive properties.
Between 8% and 18% of patients treated with aspirin, however, develop recurrent vascular events within 2 years, a phenomenon described as aspirin resistance “or perhaps more accurately as aspirin nonresponsiveness,” the investigators wrote.
They took blood samples from patients with suspected acute coronary syndromes seen at five medical centers. All were on outpatient aspirin therapy or were given an aspirin when they arrived at the emergency department. The 25% of patients with a history of heart failure were older than those without heart failure (62 vs. 58 years) and were more likely to be taking aspirin as an outpatient (81% vs. 60%), but the two groups did not differ by sex or body mass index.
Blood samples were tested using the Ultegra Rapid Platelet Function Assay on a VerifyNow testing device. The Ultegra assay is a turbidimetric-based optical detection system that measures platelet-induced aggregation as an increase in light transmittance. Aspirin nonresponsiveness was defined as an “aspirin reaction unit” value of at least 550. Results showed a mean of 479 aspirin reaction units in patients with a history of heart failure, compared with 458 units in patients without heart failure.
None of the investigators are associated with Accumetrix, the company that makes the VerifyNow device.
Heart failure patients were more likely to have a history of hypertension, coronary artery disease, MI, diabetes, chronic renal insufficiency, and tobacco use than were non-heart failure patients. Those with heart failure had averaged 4 years of aspirin use, compared with 2 years in patients without prior heart failure, she said.
The high rate of aspirin nonres-ponsiveness in heart failure patients may make them susceptible to thrombotic events. DR. DANIELS