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Rapid Responses: Rapid Responses published:
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What about atrial fibrillation (AF) and oral anticoagulants (OA)
- Vittorio Pengo (28 April 2007)
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Too little too late?
- Richard J Prettyman (1 May 2007)
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Aspirin should not be misused or abused.
- Giuseppe Lippi, Giovanni Targher, Gian Cesare Guidi (1 May 2007)
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Assessment of the Effect of Low-Dose Aspirin on Platelet Inhibition
- Robert Hillman (8 May 2007)
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cognitive function and diabetes
- peter hilliard brunyate (16 May 2007)
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Vittorio Pengo, Clinical cardiologist at Padua University Padova (italy) 35128
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I read with interest the paper JH Gang and colleagues on the inability of aspirin (ASA)100 mg every other day to impede cognitive decline in elderly women. In my opinion, results of this and other primary prevention studies employing ASA are in line with the fact that a major pathogenic mechanism of mental impairment in the elderly, i.e. cardioembolism due to AF, is prevented by OA and not by antiplatelet drugs. In patients with AF small fibrin-rich thrombi, resembling those formed in the venous circulation, may in fact migrate from left appendage to the brain causing silent ischemia by occluding small brain penetrating arteries, which leads to cognitive impairment and dementia. In this large cohort study, patients with AF and those among them treated with OA may have been equally distrubuted in the two arms. In the same way new onset AF, an age-related rythm disturbance may have fallen equally in the two groups. Thus what the study may in part measure is the aspirin-independent mental decline occurring in patients with AF and silent brain embolism. Competing interests: None declared |
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Richard J Prettyman, Consultant Old Age Psychiatrist Bennion Centre, Leicester LE3 9DZ
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This study (1) represents an interesting contribution to the continuing debate about the usefulness (or lack thereof) of aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) in the prevention and treatment of cognitive decline in later life. The authors acknowledge the dose of aspirin used was insufficient to test a putative anti-inflammatory mechanism of action and would therefore only be likely to detect possible benefit resulting from platelet inhibition; an additional major consideration mentioned only briefly in their discussion is that of the timing of the relationship between either platelet aggregation or inflammatory mechanisms to the onset and progression of cognitive decline. Many of the observational studies of NSAIDs reporting associations between use of these drugs and reduced rates of cognitive decline (2,3,4,5) included subjects with long periods of exposure to these drugs in mid- adult life. This is increasingly recognised as the period during which neurodegenerative processes may become established (6). The potential of these agents for primary prevention of cognitive decline will remain unknown until we have seen the results of intervention studies involving younger adults. 1. Kang JH, Cook N, Manson J, Buring JE and Grodstein F. Low dose aspirin and cognitive function in the women's health study cognitive cohort. BMJ, Doi:10.1136/bmj.39166.597836.BE (published 27 April 2007) 2. Sturmer T Glynn RJ Field TS Taylor JO Hennekens CH. Aspirin use and cognitive function in the elderly. Am J Epidemiol 1996.143; 7: 683-691 3. Stewart WF Kawas C Corrada M Metter EJ. Risk of Alzheimer's disease and duration of NSAID use. Neurology 1997. 48;3:626-32 4.Bas A, Veld MD, Ruitenberg A, Hofman A, Launer LJ, Van Duijn CM, Stijenen T, Breteler MMB and Stricker BHC. Nonsteroidal anti-inflammatory drugs and the risk of Alzheimer's disease. NEJM 2001; 345; 21:1515-20 5. Jonker C, Comijs HC, Smit JH. Does aspirin or other NSAIDs reduce the risk of cognitive decline in elderly persons? Results from a population-based study. Neurobiol Aging 2003;24:583-8. 6. Braak E, Griffing K, Arai K, Bohl J, Bratzke H, Braak H. Neuropathology of Alzheimer's disease: what is new since A. Alzheimer? Eur Arch Psychiatry Clin Neurosci 1999;249(Suppl 3):14-22. Competing interests: None declared |
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Giuseppe Lippi, Associate Professor of Clinical Biochemistry Sezione di Chimica Clinica, Università degli Studi di Verona, 37134, Verona, Italy, Giovanni Targher, Gian Cesare Guidi
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We read with interest the recent article of Gang and colleagues who concluded that the long term use of low dose aspirin does not provide overall benefits for cognition among generally healthy women aged 65 or more (1). Regardless of its preventive and therapeutic efficacy in chronic inflammatory pathologies and cardiovascular disease, aspirin is widely used in the general population to reduce pain and inflammation with little awareness on safety, tolerability, risks and potential adverse complications. Aspirin it is not free from side effects, including kidney and gastric injury. The marked inhibition of the platelet function is also associated with important bleeding complications due to irreversible acetylation of the platelet cyclooxygenase (COX), especially the constitutive isoform COX-1 (2). There is evidence that aspirin is commonly abused, when administered to treat banal pathologies that would not require a drastic therapeutic intervention, minor migraine or tolerable muscle-skeletal pain among others (2). In such cases, the individual benefit/risk ratio should be carefully determined before administration and the brilliant conclusions of Gang and colleagues thoughtfully support our hypothesis. As recently highlighted by the Third Canadian Consensus Conference, that recommended to routinely reassess patients' risk before prescribing NSAIDs regardless of the individual lifestyle (3), aspirin must not be abused and, especially, should not be administered when no definitive proofs on benefits for a given pathology are demonstrated. Accordingly, major commitment should be placed in modifying the physicians' appropriate prescribing of easily accessible, over-the-counter drugs, including aspirin. References 1. Kang JH, Cook N, Manson J, Buring JE, Grodstein F. Low dose aspirin and cognitive function in the women's health study cognitive cohort. BMJ 2007; 0: bmj.39166.597836.BEv1 2. Lippi G, Franchini M, Guidi GC, Kean WF. Non-steroidal anti- inflammatory drugs in athletes. Br J Sports Med 2006;40:661-2. 3. Tannenbaum H, Bombardier C, Davis P, Russell AS; Third Canadian Consensus Conference Group. An evidence-based approach to prescribing nonsteroidal antiinflammatory drugs. Third Canadian Consensus Conference. J Rheumatol 2006;33:140-57. Competing interests: None declared |
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Robert Hillman, Chairman, Accumetrics, Inc. 3985 Sorrento Valley Blvd San Diego, CA 92121
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The recent editorial by Kang et al (1) further add to the uncertainty in recommending the appropriate dose of aspirin to women (2). The WHS used a low dose of aspirin, 100 mg every other day , that is lower than the typical "low dose" used for cardiovascular risk reduction in the United States, 81mg daily in order to improve the overall safety profile. To directly investigate if these two doses had different effects on overall platelet function, we assessed the effect on platelet inhibition of two different aspirin dosing regimens: 100 mg every other day and 81 mg daily. We enrolled 49 healthy female volunteers with same characteristics as those in WHS and used a sequential, crossover design to compare the two regimens. The participants received a 17-day course of each aspirin- dosing regimen separated by a 7-day washout period. The degree of platelet inhibition of each dosing regimen was measured using a validated point-of- care platelet function assay utilizing arachadonic acid to activate platelets (3). Participants platelet response attained a significantly greater level of platelet inhibition and less day- to-day variability while taking aspirin 81 mg daily compared to aspirin 100 mg every other day (31.3% vs. 12.7%, p < 0.0001). We found significantly less inhibition of platelet function with the dose used in the WHS than the usual U.S. dose, suggesting that results of the Women's Health Study may have underestimated the efficacy and toxicity of aspirin as it is commonly administered. These data support the use of at least aspirin 81 mg daily for primary prevention and raises the issue as to whether measurement of platelet function to determine if a patient is attaining adequate inhibition may improve therapy. These data need to be considered when extrapolating the efficacy and safety data from the WHS to U.S. women and comparing it to other studies. 1. Kang JH, Cook N, Manson J, Buring JE, and Grodstein F., Low dose aspirin and cognitive function in the women's health study cognitive cohort, BMJ 2007 2. Ridker, P.M., et al., A randomized trial of low-dose aspirin in the primary prevention of cardiovascular disease in women. N Engl J Med, 2005. 352(13): p. 1293-304. 3. Karha, J., et al., Lack of effect of enteric coating on aspirin-induced inhibition of platelet aggregation in healthy volunteers. Am Heart J, 2006. 151(5): p. 976 e7-11. Competing interests: None declared |
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peter hilliard brunyate, semi retired GP marshfield. SN14 8NE
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Reading your editorial on decline in cognitive function and the use of low dose aspirin it struck me that one seldom sees any correlation between cognitive decline and diabetes. Type 2 diabetes,in particular ,affects the most common age group for cognitive decline. It is also a disease which produces many of its major effects by small vessel arterial decline and ultimately blockage. Surely one would expect the cerebral circulation to suffer in the same way as the rest of the body. The presence or absence of such an effect would be an indicator as to the mechanism of cognitive failure. In primary care in the UK we have a very large database on diabetes and its effects. This is held in an anonymous form by the National Health Service [ NHS] as part of its Quality Management and Analysis System [QMAS] data. Can this not be used to investigate the possibilty of an effect ? If more questions need to be asked why not include them in the required dataset [ perhaps removing one or two others so as to relieve the burden on primary care]. Competing interests: None declared |
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