CLINICAL STUDY: ANTIPLATELET THERAPY
A prospective, blinded determination of the natural history of aspirin resistance among stable patients with cardiovascular disease
Patricia A. Gum, MD*,
Kandice Kottke-Marchant, MD, PhD*,
Patricia A. Welsh*,
Jennifer White, MS* and
Eric J. Topol, MD, FACC*,*
* Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA
Manuscript received May 6, 2002;
revised manuscript received October 3, 2002,
accepted November 11, 2002.
* Reprint requests and correspondence: Dr. Eric J. Topol, Department of Cardiovascular Medicine, Desk F25, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA.
topole{at}ccf.org
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Abstract
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OBJECTIVES: This study was designed to determine if aspirin resistance is associated with clinical events.
BACKGROUND: Aspirin resistance, defined by platelet function testing and presumed clinical unresponsiveness to aspirin, has been previously reported by our group and others. However, little information exists linking the laboratory documentation of aspirin resistance and long-term clinical events.
METHODS: We prospectively enrolled 326 stable cardiovascular patients from 1997 to 1999 on aspirin (325 mg/day for  7 days) and no other antiplatelet agents. We tested for aspirin sensitivity by optical platelet aggregation using adenosine diphosphate (ADP) and arachidonic acid (AA). The primary outcome was the composite of death, myocardial infarction (MI), or cerebrovascular accident (CVA). Mean follow-up was 679 ± 185 days. Aspirin resistance was defined as a mean aggregation of 70% with 10 µM ADP and 20% with 0.5 mg/ml AA.
RESULTS: Of the patients studied, 17 (5.2%) were aspirin resistant and 309 (94.8%) were not aspirin resistant. During follow-up, aspirin resistance was associated with an increased risk of death, MI, or CVA compared with patients who were aspirin sensitive (24% vs. 10%, hazard ratio [HR] 3.12, 95% confidence interval [CI] 1.10 to 8.90, p = 0.03). Stratified multivariate analyses identified platelet count, age, heart failure, and aspirin resistance to be independently associated with major adverse long-term outcomes (HR for aspirin resistance 4.14, 95% CI 1.42 to 12.06, p = 0.009).
CONCLUSIONS: This study demonstrates the natural history of aspirin resistance in a stable population, documenting a greater than threefold increase in the risk of major adverse events associated with aspirin resistance.
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Abbreviations and Acronyms
| | AA | | arachidonic acid | | ADP | | adenosine diphosphate | | CI | | confidence interval | | CVA | | cerebrovascular accident | | HR | | hazard ratio | | MI | | myocardial infarction |
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Aspirin is the cornerstone of antiplatelet therapy in cardiovascular medicine today. It exerts its antiplatelet effect by acetylation of the platelet cyclooxygenase, resulting in an irreversible inhibition of platelet-dependent thromboxane formation (1). In their most recent meta-analysis of more than 200,000 patients from 287 randomized trials, the Antithrombotic Trialists’ Collaboration has documented the powerful effect of aspirin in reducing ischemic vascular events by 22% compared with control in a wide array of atherothrombotic conditions (2). However, aspirin has been shown to have variable antiplatelet activity in individual patients. Previous studies have estimated that 5% to 45% of the population do not achieve an adequate antiplatelet effect from aspirin (3–7). Little prospective data are available for extended long-term follow-up of stable patients concerning the clinical consequences of aspirin resistance.
In a cohort of 326 stable cardiovascular patients, we previously demonstrated approximately 1 in 20 has laboratory evidence of aspirin resistance as measured by optical platelet aggregation (3). We used this prospectively collected population of patients to determine the long-term clinical significance of aspirin resistance.
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Methods
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Study group.
We prospectively enrolled 326 stable cardiovascular patients between January 1997 and September 1999. The patients were recruited from consecutive patients presenting to the outpatient clinic or for elective cardiac catheterization. All patients had prior history of cardiovascular disease as defined by previous documented coronary stenosis on cardiac catheterization of 60%, previous history of myocardial infarction (MI) or stroke, or previous invasive cardiovascular revascularization procedure. The study was reviewed and approved by the Institutional Review Board. All participants gave informed consent before enrollment. We evaluated these patients for laboratory evidence of aspirin resistance. Patients who were 21 years old and taking 325 mg of aspirin for 7 days immediately before were eligible for enrollment. Compliance on aspirin was determined by patient interview both at study enrollment and follow-up. Exclusion criteria included: ingestion of ticlopidine, dipyridamole, or other nonsteroidal anti-inflammatory drugs; use of other drugs containing aspirin; administration of heparin or low-molecular-weight heparin within 24 h before enrollment; major surgical procedure within one week before enrollment; malignant paraproteinemias; family or personal history of bleeding disorders; platelet count <150 x 103/µl or >450 x 103/µl; hemoglobin <8g/dl, history of myeloproliferative disorders; or history of heparin-induced thrombocytopenia.
Blood samples.
Four samples of whole blood were collected in 3.8% sodium citrate for platelet aggregation testing. One tube of blood anticoagulated with ethylenediaminetetraacetic acid was collected for baseline hemoglobin and platelet count. The last dose of aspirin was administered within 1 to 24 h before blood sampling. Room-temperature blood samples were processed within 1 h of blood collection. Whole-blood specimens were centrifuged for 10 min at 200 g to obtain platelet-rich plasma. Platelet-poor plasma was obtained on the remaining specimen by re-centrifugation at 2,000 g for 15 min. A platelet count was measured on the platelet-rich plasma and was adjusted to between 200 x 103/µl and 300 x 103/µl with platelet-poor plasma. The baseline optical density was set with platelet-poor plasma. Aggregation was performed using adenosine 5'-diphosphate (ADP) (BioData, Horsham, Pennsylvania) at 10 µM and arachidonic acid (AA) at 0.5 mg/ml with a BioData PAPS-4 platelet aggregometer (BioData).
For optical platelet aggregation, optical density changes were detected photoelectrically as platelets began to aggregate. Adenosine diphosphate promotes the release of endogenous ADP and thromboxane A2 when added to platelet-rich plasma, causing irreversible aggregation. The test is abnormal in patients using aspirin or having aspirin-like release defects, storage pool disease, afibrinogenemia, or Glanzmann’s thrombasthenia. Arachidonic acid is used to evaluate the degree of inhibition of platelet aggregation by aspirin. The addition of AA to platelet-rich plasma enhances platelet aggregation by producing thromboxane A2. The test is abnormal in patients using aspirin, having aspirin-like release defects, and Glanzmann’s thrombasthenia. Aspirin resistance was defined as a mean aggregation of 70% with 10 µM ADP and a mean aggregation of 20% with 0.5 mg/ml AA. Laboratory norms were established by screening 40 in-house normal samples.
Study end points.
The primary end point was the composite of death, MI, or cerebrovascular accident (CVA). Secondary end points were the individual events of death, MI, and CVA. Death was defined as all-cause mortality due to MI, ischemic CVA, and other vascular and nonvascular causes. Myocardial infarction was defined as the presence of at least two of these criteria: prolonged angina >30 min; total creatinine kinase elevation >2 times the upper limit of normal as confirmed by creatine kinase-MB fraction isoenzyme elevation; electrocardiogram evidence of infarction, defined as ST-segment elevation of at least 0.1 mV (measured 0.2 s after the J-point) in two contiguous leads; or new significant Q-wave of >0.04 s duration or having a depth greater than one-fourth of the corresponding R-wave amplitude, or both. Cerebrovascular accident was defined as an acute neurologic vascular event with focal signs for more than 24 h.
Follow-up.
Follow- up was performed by telephone interview and query of the Social Security Death Index on all patients enrolled regardless of aspirin resistance status between November 2000 and June 2001. Persons performing follow-up interviews were blind to aspirin sensitivity status. For those patients having reached at least one of the primary end points, a medical chart review was initiated to determine whether the event met the definitions described. Follow-up was complete on 96.9% of all patients enrolled. Of those determined to be aspirin resistant, follow-up was complete on 94.1%, and of those determined to not be aspirin resistant, follow-up was complete on 97.1%. Follow-up via telephone and chart review was complete on 293 patients and data concerning death were retrieved solely via the Social Security Death Index on 23 patients.
Statistical analysis.
Categorical variables are presented as frequencies and percentages. For the categorical variables, patient demographics between groups were compared using chi-square tests or, if expected cell frequencies were small, exact tests. Continuous variables are presented as means ± SD. The p values associated with continuous variables were generated by Wilcoxon two-sample tests (because the factors were not normally distributed). Kaplan-Meier product limits were computed for freedom from death, MI, CVA, and the primary end point of composite death, MI, or CVA with respect to aspirin resistance status. Log-rank tests were used for screening univariable group results with respect to outcomes. Cox proportional modeling techniques were used to describe the risks for the composite end point of death, MI, or CVA. Variables entered into the model include: age, gender, race, history of tobacco use, diabetes, hypertension, hyperlipidemia, revascularization, MI, hemoglobin, platelet count, creatinine, and aspirin sensitivity.
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Results
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Patient characteristics.
Of the 326 patients enrolled, follow-up was available on 315 (97%). Mean follow-up was 679 days. Baseline characteristics comparing the two groups, aspirin resistant versus not aspirin resistant, are presented in Table 1. Of the 326 patients studied, 17 (5.2%) were aspirin resistant by optical aggregation. Patients who were aspirin resistant were more likely to be women and had a slightly lower hemoglobin count compared with patients who were not aspirin resistant. The two groups had similar rates of previous cardiovascular events, including history of prior revascularization procedures, MIs, or neurologic events. Classic atherosclerotic risk factors were similar between the two groups.
Additional medication use both at baseline and during follow-up was not significantly different between the two groups. Of the patients documented at baseline to be aspirin resistant, 12% discontinued aspirin for 1 month during follow-up compared with 8% of those documented to be aspirin sensitive (p = 0.6). Use of medications well proven to reduce clinical events by other previous studies, including beta-blockers, angiotensin-converting enzyme inhibitors, statins, and thienopyridine inhibitors, was similar between the two groups as well.
Clinical events.
Major events occurred in 34 (10%) of the 326 patients. Among the patients who were aspirin resistant, 4 of 17 (24%) experienced death, MI, or CVA, compared with 30 of 309 (10%) patients who were not aspirin resistant (p = 0.03). Hazard ratios (HRs) for both univariate and multivariate analyses are outlined in Table 2. Patients who were aspirin resistant were more likely to experience a major clinical event compared with patients who were not aspirin resistant. Although the association for aspirin resistance and adverse individual outcomes did not reach statistical significance, there was a consistent unfavorable trend associated with aspirin resistance for these end points as well (death 12% aspirin resistant vs. 5% not aspirin resistant, p = 0.13, MI 7% aspirin resistant vs. 4% not aspirin resistant, p = 0.54, and CVA 12% aspirin resistant vs. 1% not aspirin resistant, p = 0.09). Figure 1 depicts the Kaplan-Meier time-to-event curves for event-free survival based on aspirin sensitivity with log-rank test results. After adjustment for other clinical factors, aspirin resistance remained an independent predictor of long-term adverse events (HR 4.14, 95% confidence interval [CI] 1.42 to 12.06), p = 0.009). Other factors identified as correlates of poor outcome were history of congestive heart failure, elevated platelet count, and increasing age.
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Figure 1 Time-to-event curves, log rank chi-square = 5.05, p = 0.03. CVA = cerebrovascular accident; MI = myocardial infarction.
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Although the primary purpose of this study sought to evaluate clinical risk associated with a predefined set point of platelet aggregation despite aspirin therapy, we further evaluated events on a continuous basis. Figure 2 depicts all events (death, MI, or CVA) in relation to the mean percent platelet aggregation with ADP. Although the results do not reach statistical significance, a distinct gradation of increased risk for clinical events with increased platelet aggregation despite aspirin therapy can be seen.
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Figure 2 Events (death, myocardial infarction, or cerebrovascular accident) by mean percent platelet aggregation with adenosine diphosphate (ADP).
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Discussion
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In this blinded, prospective study, we demonstrated aspirin resistance as documented by optical platelet aggregation testing to be negatively associated with long-term outcomes in a population of stable cardiovascular patients. Previous studies have demonstrated aspirin resistance by both clinical evidence of unresponsiveness to aspirin (8) and ex vivo platelet function testing (5,9–13). To date only three studies have evaluated the clinical consequence of aspirin resistance in select populations (14–16). Grotemeyer et al. (14) evaluated 180 acute stroke patients for evidence of aspirin’s effect on platelet reactivity. Patients with elevated platelet reactivity despite aspirin were more likely to experience vascular death, MI, or CVA. Mueller et al. (15) reported an association between failed inhibition of platelet reactivity by aspirin and risk of reocclusion after peripheral vascular angioplasty in patients with claudication. Most recently, Eikelboom et al. (16) reported an increased risk for MI, CVA, or cardiovascular death associated with aspirin resistance as documented by urinary concentrations of 11-dehydro thromboxane B2 in patients with cardiovascular disease or diabetes and one other risk factor for cardiovascular disease.
The current study extends these previous findings in several important respects. Our study was performed in a prospective, blinded fashion. Those performing the optical aggregation testing were blind to clinical histories, and follow-up was done in a blinded manner without regard to aspirin sensitivity. We prospectively set out to measure the incidence of aspirin resistance in a stable population and to determine its clinical significance. We utilized optical platelet aggregation, the current gold standard of platelet aggregation, to measure aspirin resistance. We established normal values via 40 in-house normal samples. With respect to clinical significance, we used "real-world" end points, including all-cause mortality, MI, and CVA, rather than vascular death or vessel reocclusion. Furthermore, this study evaluated the clinical significance of aspirin resistance in a stable cardiovascular population that had not experienced a recent acute event before enrollment. The natural history of aspirin resistance has not previously been evaluated in this population in a fully prospective manner.
Recent trials have demonstrated the superior clinical benefit of clopidogrel and the combination of clopidogrel with aspirin compared with aspirin alone (17–19). These studies make it apparent that alternative antiplatelet agents will likely play a significant role in the treatment of cardiovascular disease. It is plausible that the clinical benefit of clopidogrel and agents similar to it observed in these trials would be even more pronounced in patients who are aspirin resistant and therefore not benefiting from adequate antiplatelet inhibition. Thus, future treatment of aspirin resistance with additional antiplatelet agents such as clopidogrel may significantly improve the poor prognosis we found associated with this diagnosis.
The late divergence of the event curves that we observed is intriguing. It is not entirely clear why this occurred. That our patient population was composed of patients who were clinically stable upon enrollment and therefore less likely to have acute events during early follow-up may have influenced the timing of events. Alternatively, the small number of patients enrolled may have contributed to skewing the curves. This clinical finding needs to be further investigated with additional, larger trials.
There remain other significant areas in this field that need further investigation. The findings of our study should be confirmed with larger trials in various populations. Although possible explanations of aspirin resistance include the presence of PlA2 polymorphism, degree of cyclooxygenase-2 expression, and the role of erythrocytes, the definitive mechanism of aspirin resistance has not yet been elucidated. This will ultimately be important to allow prospective diagnosis of aspirin resistance, which will help guide the selection of antiplatelet therapy as well as potential pharmacogenomic therapy. Likewise, clinical studies evaluating the possible benefit from alternative antiplatelet agents in aspirin-resistant patients will be important. Finally, the possibility of thienopyridine resistance also warrants investigation.
Study limitations.
There are some inherent limitations to our study. Aspirin use was based on answers to questionnaires. Salicylate levels or pill counts were not performed. Aggregation studies were performed only at baseline, and it is possible that response to aspirin is variable. Although our study demonstrated an association between aspirin resistance and long-term clinical events, the overall number of events is small. Our estimate of the clinical consequences of aspirin resistance may therefore be under- or overestimated.
Conclusions.
Aspirin resistance is an important and real clinical diagnosis. Our study demonstrates it to be significantly associated with major adverse events during long-term follow-up. The availability of safe, alternative long-term antiplatelet agents makes screening for aspirin resistance in cardiovascular patients a potentially important and useful diagnostic test. Further investigation to confirm our findings, evaluate possible treatments, and elucidate the precise biologic mechanism of aspirin resistance should be performed.
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Footnotes
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Support for this study was received from Dade Behring.
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References
|
|---|
1. Schror K. Aspirin and platelets: the antiplatelet action of aspirin and its role in thrombosis treatment and prophylaxis. Semin Thromb Hemost. 1997;23:349–356[Medline]
2. Antithrombotic Trialists Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002;324:71–86[Abstract/Free Full Text]
3. Gum PA, Kottke-Marchant K, Poggio ED, et al. Profile and prevalence of aspirin resistance in patients with cardiovascular disease. Am J Cardiol. 2001;88:230–235[CrossRef][Medline]
4. Helgason CM, Tortorice KL, Winkler SR, et al. Aspirin response and failure in cerebral infarction. Stroke. 1993;24:345–350[Abstract/Free Full Text]
5. Pappas JM, Westengard JC, Bull BS. Population variability in the effect of aspirin on platelet function. Implications for clinical trials and therapy. Arch Pathol Lab Med. 1994;118:801–804[Medline]
6. Grotemeyer KH. Effects of acetylsalicylic acid in stroke patients. Evidence of nonresponders in a subpopulation of treated patients. Thromb Res. 1991;63:587–593[CrossRef][Medline]
7. Valles J, Santos MT, Aznar J, et al. Erythrocyte promotion of platelet reactivity decreases the effectiveness of aspirin as an antithrombotic therapeutic modality: the effect of low-dose aspirin is less than optimal in patients with vascular disease due to prothrombotic effects of erythrocytes on platelet reactivity. Circulation. 1998;97:350–355[Abstract/Free Full Text]
8. Chamorro A, Blanc R, Ascaso C, Saiz A, Vila N. Factors associated to aspirin failure for secondary stroke prevention. Med Clin (Barc). 1997;109:569–572[Medline]
9. Vermeer F, Vahanian A, Fels PW, et al. Argatroban and alteplase in patients with acute myocardial infarction: the ARGAMI study. J Thromb Thrombol. 2000;10:233–240[CrossRef][Medline]
10. Spranger M, Aspey BS, Harrison MJ. Sex difference in antithrombotic effect of aspirin. Stroke. 1989;20:34–37[Abstract/Free Full Text]
11. Buchanan MR, Brister SJ. Individual variation in the effects of ASA on platelet function: implications for the use of ASA clinically. Can J Cardiol. 1995;11:221–227[Medline]
12. Helgason CM, Bolin KM, Hoff JA, et al. Development of aspirin resistance in persons with previous ischemic stroke. Stroke. 1994;25:2331–2336[Abstract]
13. Cipollone F, Patrignani P, Greco A, et al. Differential suppression of thromboxane biosynthesis by indobufen and aspirin in patients with unstable angina. Circulation. 1997;96:1109–1116[Abstract/Free Full Text]
14. Grotemeyer KH, Scharafinski HW, Husstedt IW. Two-year follow-up of aspirin responder and aspirin non responder. A pilot-study including 180 post-stroke patients. Thromb Res. 1993;71:397–403[CrossRef][Medline]
15. Mueller MR, Salat A, Stangl P, et al. Variable platelet response to low-dose ASA and the risk of limb deterioration in patients submitted to peripheral arterial angioplasty. Thromb Haemost. 1997;78:1003–1007[Medline]
16. Eikelboom JW, Hirsch J, Weitz JI, Johnston M, Yi Q, Yusuf S. Aspirin-resistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Circulation. 2002;105:1650–1655[Abstract/Free Full Text]
17. Mehta SR, Yusuf S, Peters RJ, et al. Effects of pretreatment with clopidogrel and aspirin followed by long-term therapy in patients undergoing percutaneous coronary intervention: the PCI-CURE study. Lancet. 2001;358:527–533[CrossRef][Medline]
18. Mitka M. Results of CURE trial for acute coronary syndrome. JAMA. 2001;285:1828–1829[Free Full Text]
19. CAPRIE Steering Committee. A randomised, blinded trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). Lancet. 1996;348:1329–1339[CrossRef][Medline]
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|
|
|
|
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|
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|
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|
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|
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|
|
|
|
|
|
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|
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|
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[PDF]
|
|
|
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|
|
N. Zimmermann, M. Kurt, J. Winter, E. Gams, F. Wenzel, and T. Hohlfeld
Detection and duration of aspirin resistance after coronary artery bypass grafting.
J. Thorac. Cardiovasc. Surg.,
April 1, 2008;
135(4):
947 - 948.
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. J. Kereiakes and P. A. Gurbel
Peri-Procedural Platelet Function and Platelet Inhibition in Percutaneous Coronary Intervention
J. Am. Coll. Cardiol. Intv.,
April 1, 2008;
1(2):
111 - 121.
[Abstract]
[Full Text]
[PDF]
|
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C. Patrono and B. Rocca
Aspirin: Promise and Resistance in the New Millennium
Arterioscler. Thromb. Vasc. Biol.,
March 1, 2008;
28(3):
s25 - s32.
[Abstract]
[Full Text]
[PDF]
|
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|
|
|
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F. M. Gengo, M. Rainka, M. Robson, M. F. Gengo, A. Forrest, M. Hourihane, and V. Bates
Prevalence of Platelet Nonresponsiveness to Aspirin in Patients Treated for Secondary Stroke Prophylaxis and in Patients With Recurrent Ischemic Events
J. Clin. Pharmacol.,
March 1, 2008;
48(3):
335 - 343.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
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C. Manrique, G. Lastra, J. Palmer, M. Gardner, and J. R. Sowers
Review: Aspirin and Diabetes Mellitus: revisiting an old player
Therapeutic Advances in Cardiovascular Disease,
February 1, 2008;
2(1):
37 - 42.
[Abstract]
[PDF]
|
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Y.-W. Lee, Y.-H. Cho, Y.-H. Kim, J.-S. Na, H. B. Shin, C.-S. Ki, T.-Y. Choi, and Y. K. Lee
Aspirin Non-Responsiveness in Korean Subjects on Dual Anti-Platelet Treatment Determined by Two Different Platelet Function Assays
Ann. Clin. Lab. Sci.,
January 1, 2008;
38(2):
126 - 131.
[Abstract]
[Full Text]
[PDF]
|
|
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|
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R. F. Storey
Variability of response to antiplatelet therapy
Eur. Heart J. Suppl.,
January 1, 2008;
10(suppl_A):
A21 - A27.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
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|
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C. Gachet and B. Aleil
Testing antiplatelet therapy
Eur. Heart J. Suppl.,
January 1, 2008;
10(suppl_A):
A28 - A34.
[Abstract]
[Full Text]
[PDF]
|
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J. DiChiara, K. P. Bliden, U. S. Tantry, M. S. Hamed, M. J. Antonino, T. A. Suarez, O. Bailon, A. Singla, and P. A. Gurbel
The Effect of Aspirin Dosing on Platelet Function in Diabetic and Nondiabetic Patients: An Analysis From the Aspirin-Induced Platelet Effect (ASPECT) Study
Diabetes,
December 1, 2007;
56(12):
3014 - 3019.
[Abstract]
[Full Text]
[PDF]
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P. A. Gurbel, R. C. Becker, K. G. Mann, S. R. Steinhubl, and A. D. Michelson
Platelet Function Monitoring in Patients With Coronary Artery Disease
J. Am. Coll. Cardiol.,
November 6, 2007;
50(19):
1822 - 1834.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
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S. Wan, N. Shukla, G. D. Angelini, A. P.C. Yim, J. L. Johnson, and J. Y. Jeremy
Nitric oxide-donating aspirin (NCX 4016) inhibits neointimal thickening in a pig model of saphenous vein-carotid artery interposition grafting: A comparison with aspirin and morpholinosydnonimine (SIN-1).
J. Thorac. Cardiovasc. Surg.,
October 1, 2007;
134(4):
1033 - 1039.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. D. Snoep, M. M. C. Hovens, J. C. J. Eikenboom, J. G. van der Bom, and M. V. Huisman
Association of Laboratory-Defined Aspirin Resistance With a Higher Risk of Recurrent Cardiovascular Events: A Systematic Review and Meta-analysis
Arch Intern Med,
August 13, 2007;
167(15):
1593 - 1599.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. Van de Werf
Dual antiplatelet therapy in high-risk patients
Eur. Heart J. Suppl.,
August 1, 2007;
9(suppl_D):
D3 - D9.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Husted
New developments in oral antiplatelet therapy
Eur. Heart J. Suppl.,
August 1, 2007;
9(suppl_D):
D20 - D27.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Lordkipanidze, C. Pharand, E. Schampaert, J. Turgeon, D. A. Palisaitis, and J. G. Diodati
A comparison of six major platelet function tests to determine the prevalence of aspirin resistance in patients with stable coronary artery disease
Eur. Heart J.,
July 2, 2007;
28(14):
1702 - 1708.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. Faraday, L. R. Yanek, R. Mathias, J. E. Herrera-Galeano, D. Vaidya, T. F. Moy, M. D. Fallin, A. F. Wilson, P. F. Bray, L. C. Becker, et al.
Heritability of Platelet Responsiveness to Aspirin in Activation Pathways Directly and Indirectly Related to Cyclooxygenase-1
Circulation,
May 15, 2007;
115(19):
2490 - 2496.
[Abstract]
[Full Text]
[PDF]
|
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T. A. Meadows and D. L. Bhatt
Clinical Aspects of Platelet Inhibitors and Thrombus Formation
Circ. Res.,
May 11, 2007;
100(9):
1261 - 1275.
[Abstract]
[Full Text]
[PDF]
|
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A. O. Maree and D. J. Fitzgerald
Variable Platelet Response to Aspirin and Clopidogrel in Atherothrombotic Disease
Circulation,
April 24, 2007;
115(16):
2196 - 2207.
[Full Text]
[PDF]
|
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B. T. Ivandic, E. Giannitsis, P. Schlick, P. Staritz, H. A. Katus, and T. Hohlfeld
Determination of Aspirin Responsiveness by Use of Whole Blood Platelet Aggregometry
Clin. Chem.,
April 1, 2007;
53(4):
614 - 619.
[Abstract]
[Full Text]
[PDF]
|
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A. Undas, K. E. Brummel-Ziedins, and K. G. Mann
Antithrombotic properties of aspirin and resistance to aspirin: beyond strictly antiplatelet actions
Blood,
March 15, 2007;
109(6):
2285 - 2292.
[Abstract]
[Full Text]
[PDF]
|
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D. J. Fitzgerald and A. Maree
Aspirin and Clopidogrel Resistance
Hematology,
January 1, 2007;
2007(1):
114 - 120.
[Abstract]
[Full Text]
[PDF]
|
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M. Pfisterer, H. P. Brunner-La Rocca, P. T. Buser, P. Rickenbacher, P. Hunziker, C. Mueller, R. Jeger, F. Bader, S. Osswald, C. Kaiser, et al.
Late Clinical Events After Clopidogrel Discontinuation May Limit the Benefit of Drug-Eluting Stents: An Observational Study of Drug-Eluting Versus Bare-Metal Stents
J. Am. Coll. Cardiol.,
December 19, 2006;
48(12):
2584 - 2591.
[Abstract]
[Full Text]
[PDF]
|
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|
|
|
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A. D. Michelson, A. L. Frelinger, and M. I. Furman
Resistance to antiplatelet drugs
Eur. Heart J. Suppl.,
October 1, 2006;
8(suppl_G):
G53 - G58.
[Abstract]
[Full Text]
[PDF]
|
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S.-H. Hung, W. Zhang, R. A. Pixley, B. A. Jameson, Y. C. Huang, R. F. Colman, and R. W. Colman
New Insights from the Structure-Function Analysis of the Catalytic Region of Human Platelet Phosphodiesterase 3A: A ROLE FOR THE UNIQUE 44-AMINO ACID INSERT
J. Biol. Chem.,
September 29, 2006;
281(39):
29236 - 29244.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
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C. H. Hennekens, O. Sechenova, D. Hollar, and V. L. Serebruany
Dose of Aspirin in the Treatment and Prevention of Cardiovascular Disease: Current and Future Directions.
Journal of Cardiovascular Pharmacology and Therapeutics,
September 1, 2006;
11(3):
170 - 176.
[Abstract]
[PDF]
|
|
|
|
|
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D. Cox, A. O. Maree, M. Dooley, R. Conroy, M. F. Byrne, and D. J. Fitzgerald
Effect of Enteric Coating on Antiplatelet Activity of Low-Dose Aspirin in Healthy Volunteers
Stroke,
August 1, 2006;
37(8):
2153 - 2158.
[Abstract]
[Full Text]
[PDF]
|
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U. S. Tantry, K. P. Bliden, and P. A. Gurbel
Reply
J. Am. Coll. Cardiol.,
June 20, 2006;
47(12):
2566 - 2566.
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. H Cavallari, C. M Helgason, L. D Brace, M. A. Viana, and E. A Nutescu
Sex Difference in the Antiplatelet Effect of Aspirin in Patients with Stroke
Ann. Pharmacother.,
May 1, 2006;
40(5):
812 - 817.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. D. Michos, R. Ardehali, R. S. Blumenthal, R. A. Lange, and H. Ardehali
Aspirin and Clopidogrel Resistance
Mayo Clin. Proc.,
April 1, 2006;
81(4):
518 - 526.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. M. Becker, J. Segal, D. Vaidya, L. R. Yanek, J. E. Herrera-Galeano, P. F. Bray, T. F. Moy, L. C. Becker, and N. Faraday
Sex Differences in Platelet Reactivity and Response to Low-Dose Aspirin Therapy
JAMA,
March 22, 2006;
295(12):
1420 - 1427.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. H. Wang, D. L. Bhatt, and E. J. Topol
Aspirin and clopidogrel resistance: an emerging clinical entity
Eur. Heart J.,
March 2, 2006;
27(6):
647 - 654.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. I. Lev, R. T. Patel, K. J. Maresh, S. Guthikonda, J. Granada, T. DeLao, P. F. Bray, and N. S. Kleiman
Aspirin and Clopidogrel Drug Response in Patients Undergoing Percutaneous Coronary Intervention: The Role of Dual Drug Resistance
J. Am. Coll. Cardiol.,
January 3, 2006;
47(1):
27 - 33.
[Abstract]
[Full Text]
[PDF]
|
|
|
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|
|
|
R. S. Poston, C. White, J. Gu, J. Brown, J. Gammie, R. N. Pierson, A. Lee, I. Connerney, T. Avari, R. Christenson, et al.
Aprotinin Shows Both Hemostatic and Antithrombotic Effects During Off-Pump Coronary Artery Bypass Grafting
Ann. Thorac. Surg.,
January 1, 2006;
81(1):
104 - 111.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. I. Lev, R. T. Patel, K. J. Maresh, S. Guthikonda, J. Granada, T. DeLao, P. F. Bray, and N. S. Kleiman
Aspirin and Clopidogrel Drug Response in Patients Undergoing Percutaneous Coronary Intervention: The Role of Dual Drug Resistance
J. Am. Coll. Cardiol.,
December 13, 2005;
(2005)
j.jacc.2005.08.058v1.
[Abstract]
[Full Text]
[PDF]
|
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P. A. Gurbel, K. P. Bliden, W. Samara, J. A. Yoho, K. Hayes, M. Z. Fissha, and U. S. Tantry
Clopidogrel Effect on Platelet REactivity in Patients With Stent Thrombosis: Results of the CREST Study
J. Am. Coll. Cardiol.,
November 15, 2005;
46(10):
1827 - 1832.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
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U. S. Tantry, K. P. Bliden, and P. A. Gurbel
Overestimation of Platelet Aspirin Resistance Detection by Thrombelastograph Platelet Mapping and Validation by Conventional Aggregometry Using Arachidonic Acid Stimulation
J. Am. Coll. Cardiol.,
November 1, 2005;
46(9):
1705 - 1709.
[Abstract]
[Full Text]
[PDF]
|
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|
|
|
|
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A. O. Maree, R. J. Curtin, M. Dooley, R. M. Conroy, P. Crean, D. Cox, and D. J. Fitzgerald
Platelet Response to Low-Dose Enteric-Coated Aspirin in Patients With Stable Cardiovascular Disease
J. Am. Coll. Cardiol.,
October 4, 2005;
46(7):
1258 - 1263.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Fosslien
Cardiovascular Complications of Non-Steroidal Anti-Inflammatory Drugs
Ann. Clin. Lab. Sci.,
October 1, 2005;
35(4):
347 - 385.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. J. Mason, A. K. Jacobs, and J. E. Freedman
Aspirin Resistance and Atherothrombotic Disease
J. Am. Coll. Cardiol.,
September 20, 2005;
46(6):
986 - 993.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. J. Angiolillo, A. Fernandez-Ortiz, E. Bernardo, C. Ramirez, M. Sabate, P. Jimenez-Quevedo, R. Hernandez, R. Moreno, J. Escaned, F. Alfonso, et al.
Platelet Function Profiles in Patients With Type 2 Diabetes and Coronary Artery Disease on Combined Aspirin and Clopidogrel Treatment
Diabetes,
August 1, 2005;
54(8):
2430 - 2435.
[Abstract]
[Full Text]
[PDF]
|
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J. J. Saseen
ASHP Therapeutic Position Statement on the Daily Use of Aspirin for Preventing Cardiovascular Events
Am. J. Health Syst. Pharm.,
July 1, 2005;
62(13):
1398 - 1405.
[Full Text]
[PDF]
|
|
|
|
|
|
|
H Mani, B Luxembourg, C Klaffling, M Erbe, and E Lindhoff-Last
Use of native or platelet count adjusted platelet rich plasma for platelet aggregation measurements
J. Clin. Pathol.,
July 1, 2005;
58(7):
747 - 750.
[Abstract]
[Full Text]
[PDF]
|
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|
|
|
|
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P. Wenaweser, J. Dorffler-Melly, K. Imboden, S. Windecker, M. Togni, B. Meier, A. Haeberli, and O. M. Hess
Stent Thrombosis Is Associated With an Impaired Response to Antiplatelet Therapy
J. Am. Coll. Cardiol.,
June 7, 2005;
45(11):
1748 - 1752.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. R. Steinhubl, R. Charnigo, and D. J. Moliterno
Resistance to Antiplatelet Resistance: Is it Justified?
J. Am. Coll. Cardiol.,
June 7, 2005;
45(11):
1757 - 1758.
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Wenaweser, C. Rey, F. R. Eberli, M. Togni, D. Tuller, S. Locher, A. Remondino, C. Seiler, O. M. Hess, B. Meier, et al.
Stent thrombosis following bare-metal stent implantation: success of emergency percutaneous coronary intervention and predictors of adverse outcome
Eur. Heart J.,
June 2, 2005;
26(12):
1180 - 1187.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Papp, V. Havasi, J. Bene, K. Komlosi, L. Czopf, E. Magyar, C. Feher, G. Feher, B. Horvath, Z. Marton, et al.
Glycoprotein IIIA Gene (PlA) Polymorphism and Aspirin Resistance: Is There Any Correlation?
Ann. Pharmacother.,
June 1, 2005;
39(6):
1013 - 1018.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. R. Bates and W. C. Lau
Controversies in Antiplatelet Therapy for Patients With Cardiovascular Disease
Circulation,
May 3, 2005;
111(17):
e267 - e271.
[Full Text]
[PDF]
|
|
|
|
|
|
|
P. Harrison, H. Segal, K. Blasbery, C. Furtado, L. Silver, and P. M. Rothwell
Screening for Aspirin Responsiveness After Transient Ischemic Attack and Stroke: Comparison of 2 Point-of-Care Platelet Function Tests With Optical Aggregometry
Stroke,
May 1, 2005;
36(5):
1001 - 1005.
[Abstract]
[Full Text]
[PDF]
|
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|
|
|
|
|
J. Mikkelsson, M. Perola, and P. J. Karhunen
Genetics of Platelet Glycoprotein Receptors: Risk of Thrombotic Events and Pharmacogenetic Implications
Clinical and Applied Thrombosis/Hemostasis,
April 1, 2005;
11(2):
113 - 125.
[Abstract]
[PDF]
|
|
|
|
|
|
|
A. T.L. Ong, A. Hoye, J. Aoki, C. A.G. van Mieghem, G. A. Rodriguez Granillo, K. Sonnenschein, E. Regar, E. P. McFadden, G. Sianos, W. J. van der Giessen, et al.
Thirty-day incidence and six-month clinical outcome of thrombotic stent occlusion after bare-metal, sirolimus, or paclitaxel stent implantation
J. Am. Coll. Cardiol.,
March 15, 2005;
45(6):
947 - 953.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Sanderson, J. Emery, T. Baglin, and A.-L. Kinmonth
Narrative Review: Aspirin Resistance and Its Clinical Implications
Ann Intern Med,
March 1, 2005;
142(5):
370 - 380.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. L. Serebruany, S. R. Steinhubl, P. B. Berger, A. I. Malinin, D. L. Bhatt, and E. J. Topol
Variability in platelet responsiveness to clopidogrel among 544 individuals
J. Am. Coll. Cardiol.,
January 18, 2005;
45(2):
246 - 251.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A. D. Michelson
Platelet Function Testing in Cardiovascular Diseases
Circulation,
November 9, 2004;
110(19):
e489 - e493.
[Full Text]
[PDF]
|
|
|
|
|
|
|
D. J. Angiolillo, A. Fernandez-Ortiz, E. Bernardo, C. Ramirez, M. Sabate, C. Banuelos, R. Hernandez-Antolin, J. Escaned, R. Moreno, F. Alfonso, et al.
High clopidogrel loading dose during coronary stenting: effects on drug response and interindividual variability
Eur. Heart J.,
November 1, 2004;
25(21):
1903 - 1910.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Cattaneo
Aspirin and Clopidogrel: Efficacy, Safety, and the Issue of Drug Resistance
Arterioscler. Thromb. Vasc. Biol.,
November 1, 2004;
24(11):
1980 - 1987.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. P. Schulman
Antiplatelet Therapy in Non-ST-Segment Elevation Acute Coronary Syndromes
JAMA,
October 20, 2004;
292(15):
1875 - 1882.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. F. Toole, D. C. Sane, and K. Bettermann
Stroke Prevention: Optimizing the Response to a Common Threat
JAMA,
October 20, 2004;
292(15):
1885 - 1887.
[Full Text]
[PDF]
|
|
|
|
|
|
|
J.P. Collet, G. Montalescot, B. Blanchet, M.L. Tanguy, J.L. Golmard, R. Choussat, F. Beygui, L. Payot, N. Vignolles, J.P. Metzger, et al.
Impact of Prior Use or Recent Withdrawal of Oral Antiplatelet Agents on Acute Coronary Syndromes
Circulation,
October 19, 2004;
110(16):
2361 - 2367.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. S. Wiggins and S. Spinler
Antiplatelet and Antithrombin Therapy for Early Management of Acute Coronary Syndromes
Journal of Pharmacy Practice,
October 1, 2004;
17(5):
347 - 369.
[Abstract]
[PDF]
|
|
|
|
|
|
|
C. Patrono, B. Coller, G. A. FitzGerald, J. Hirsh, and G. Roth
Platelet-Active Drugs: The Relationships Among Dose, Effectiveness, and Side Effects: The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy
Chest,
September 1, 2004;
126(3_suppl):
234S - 264S.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. L. Ambrus, C. M. Ambrus, and S. Akhter
Aspirin "allergy" and resistance
J. Am. Coll. Cardiol.,
August 18, 2004;
44(4):
939 - 940.
[Full Text]
[PDF]
|
|
|
|
|
|
|
N. Cabeza, Z. Li, C. Schulz, E. Kremmer, S. Massberg, A. Bultmann, and M. Gawaz
Surface Expression of Collagen Receptor Fc Receptor-{gamma}/Glycoprotein VI Is Enhanced on Platelets in Type 2 Diabetes and Mediates Release of CD40 Ligand and Activation of Endothelial Cells
Diabetes,
August 1, 2004;
53(8):
2117 - 2121.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
S. Matetzky, B. Shenkman, V. Guetta, M. Shechter, R. Bienart, I. Goldenberg, I. Novikov, H. Pres, N. Savion, D. Varon, et al.
Clopidogrel Resistance Is Associated With Increased Risk of Recurrent Atherothrombotic Events in Patients With Acute Myocardial Infarction
Circulation,
June 29, 2004;
109(25):
3171 - 3175.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. S. Varanasi and S. R. Steinhubl
Antiplatelet Effect of Aspirin in Patients With Cerebrovascular Disease
Stroke,
June 1, 2004;
35(6):
e144 - e145.
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Jilma
Therapeutic failure or resistance to aspirin
J. Am. Coll. Cardiol.,
April 7, 2004;
43(7):
1332 - 1332.
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. J. Topol
Reply
J. Am. Coll. Cardiol.,
April 7, 2004;
43(7):
1332 - 1333.
[Full Text]
[PDF]
|
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Top
Abstract
Methods