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高血压患者 的抗栓治疗若干问题. 北京大学人民医院 孙宁玲. 高血压患者 需要抗栓治疗吗?. Endothelial Cell. VCAM-1 Monocyte Adhesion. NF B Activation. MCP-1 Monocyte Recruitment. A-II. IL-6. CRP. Smooth Muscle Cell. 高血压实质是血管性疾病. 高血压. 高血压导致. 动脉粥样硬化 斑块破裂后 血栓 形成. 动脉粥样硬化斑块使血管狭窄. 动脉粥样硬化斑块破裂. - PowerPoint PPT Presentation

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    IIb/IIIa

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    ADP = adenosine diphosphate, TXA2 = thromboxane A2, COX = cyclooxygenase.Schafer AI. Am J Med. 1996;101:199-209. TXA2ADPTXA2ADPADPCOXcAMP

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    PCIAMI IIb/IIIa PCI

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    20645.43.83.92.2P=0.04P=0.01+2.01.2P=0.072.21.4P=0.07n=3284

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    20646.97.9P=0.046+1.61.4P=0.392.11.3P7% >6%FraminghamCirculation,1998:1837

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    Age4040GenderMMSBP150 mmHg130 mmHgLDL-C 4.0 mmol/L 3.2 mmol/L HDL 1.0 mmol/L 1.0 mmol/L Smoking -+Diabetes--10-year CVD risk8%7%Patient 1CasePatient 2Risk calculated based on the Framingham Heart Study Risk Score10-year risk of suffering a heart attack or angina, or dying from heart disease

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    - 50 RR50-59 0.58 60-69 0.46 70-84 0.4950N Engl J Med 1989,321:129-35N=22071,ASA325qod vs. Placebo,5yrs

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    - 45*N Engl J Med 2005, 352:1295-1304*102.3%N=39876,ASA100mg qod vs. placebo,10yrs

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    45N Engl J Med 2005, 352:1295-1304N=39876,ASA100mg qod vs. placebo,10yrs

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    HOT RR(95%CI) P 0.85(0.73-0.99) 0.03 15% 0.64(0.49-0.85) 0.002 36%0 0.5 1HOTLancet,1998N= 18790,50-80yrs old HPT patients,ASA75mg/d vs.PlaceboDBPHTDBP115 mol/l01234567891011121301002003000123450100200300DBP >107mmHgAbsoluteBenefitAbsoluteRiskNNTNNHAbsoluteBenefitAbsoluteRiskNNTNNH01230100200SBP >180 mmHgAbsoluteBenefitAbsoluteRiskNNTNNH/1000(n)(n)(n)/1000/1000SBP >180 mmHg DBP >107mmHg

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    HOT 78532302 840P=NS12970723412122312 120600P 30%SCORESystemic Coronary Risk Evaluation< 4%4% - 5%5% - 8% > 8%

    TXA2

    ACS /TIA

    Reference:1. Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 16.5010Framingham 45106%6-10%26-10%

    We can see how their risk can easily increase with the addition of other risk factors.

    For patient 1:He now has severely elevated LDL-C

    For patient 2:He now has moderately elevated LDL-C and elevated BP2207150----PHS:The Physicians' Health Study is a randomized, double-blind, placebo-controlled trial designed to determine whether low-dose aspirin (325 mg every other day) decreases cardiovascular mortality and whether beta carotene reduces the incidence of cancer. The aspirin component was terminated earlier than scheduled, and the preliminary findings were published. We now present detailed analyses of the cardiovascular component for 22,071 participants, at an average follow-up time of 60.2 months. There was a 44 percent reduction in the risk of myocardial infarction (relative risk, 0.56; 95 percent confidence interval, 0.45 to 0.70; P less than 0.00001) in the aspirin group (254.8 per 100,000 per year as compared with 439.7 in the placebo group). A slightly increased risk of stroke among those taking aspirin was not statistically significant; this trend was observed primarily in the subgroup with hemorrhagic stroke (relative risk, 2.14; 95 percent confidence interval, 0.96 to 4.77; P = 0.06). No reduction in mortality from all cardiovascular causes was associated with aspirin (relative risk, 0.96; 95 percent confidence interval, 0.60 to 1.54). Further analyses showed that the reduction in the risk of myocardial infarction was apparent only among those who were 50 years of age and older. The benefit was present at all levels of cholesterol, but appeared greatest at low levels. The relative risk of ulcer in the aspirin group was 1.22 (169 in the aspirin group as compared with 138 in the placebo group; 95 percent confidence interval, 0.98 to 1.53; P = 0.08), and the relative risk of requiring a blood transfusion was 1.71. This trial of aspirin for the primary prevention of cardiovascular disease demonstrates a conclusive reduction in the risk of myocardial infarction, but the evidence concerning stroke and total cardiovascular deaths remains inconclusive because of the inadequate numbers of physicians with these end points.

    3987645----45 WHSWHS116%8% 2

    HOTHOT:BACKGROUND: Despite treatment, there is often a higher incidence of cardiovascular complications in patients with hypertension than in normotensive individuals. Inadequate reduction of their blood pressure is a likely cause, but the optimum target blood pressure is not known. The impact of acetylsalicylic acid (aspirin) has never been investigated in patients with hypertension. We aimed to assess the optimum target diastolic blood pressure and the potential benefit of a low dose of acetylsalicylic acid in the treatment of hypertension. METHODS: 18790 patients, from 26 countries, aged 50-80 years (mean 61.5 years) with hypertension and diastolic blood pressure between 100 mm Hg and 115 mm Hg (mean 105 mm Hg) were randomly assigned a target diastolic blood pressure. 6264 patients were allocated to the target pressure < or =90 mm Hg, 6264 to < or =85 mm Hg, and 6262 to < or =80 mm Hg. Felodipine was given as baseline therapy with the addition of other agents, according to a five-step regimen. In addition, 9399 patients were randomly assigned 75 mg/day acetylsalicylic acid (Bamycor, Astra) and 9391 patients were assigned placebo. FINDINGS: Diastolic blood pressure was reduced by 20.3 mm Hg, 22.3 mm Hg, and 24.3 mm Hg, in the < or =90 mm Hg, < or =85 mm Hg, and < or =80 mm Hg target groups, respectively. The lowest incidence of major cardiovascular events occurred at a mean achieved diastolic blood pressure of 82.6 mm Hg; the lowest risk of cardiovascular mortality occurred at 86.5 mm Hg. Further reduction below these blood pressures was safe. In patients with diabetes mellitus there was a 51% reduction in major cardiovascular events in target group < or =80 mm Hg compared with target group < or =90 mm Hg (p for trend=0.005). Acetylsalicylic acid reduced major cardiovascular events by 15% (p=0.03) and all myocardial infarction by 36% (p=0.002), with no effect on stroke. There were seven fatal bleeds in the acetylsalicylic acid group and eight in the placebo group, and 129 versus 70 non-fatal major bleeds in the two groups, respectively (p4,5%14>>4BMD:A six year randomised trial was conducted among 5139 apparently healthy male doctors to see whether 500 mg aspirin daily would reduce the incidence of and mortality from stroke, myocardial infarction, or other vascular conditions. Though total mortality was 10% lower in the treated than control group, this difference was not statistically significant and chiefly involved diseases other than stroke or myocardial infarction. Likewise, there was no significant difference in the incidence of non-fatal myocardial infarction or stroke--indeed, disabling strokes were somewhat commoner among those allocated aspirin. The lower confidence limit for the effect of aspirin on non-fatal stroke or myocardial infarction, however, was a substantial 25% reduction. Migraine and certain types of musculoskeletal pain were reported significantly less often in the treated than control group, but as the control group was not given a placebo the relevance of these findings was difficult to assess. There was no apparent reduction in the incidence of cataract in the treated group. The lack of any apparent reduction in disabling stroke or vascular death contrasts with the established value of antiplatelet treatment after occlusive vascular disease.TPT:BACKGROUND: We aimed to evaluate low intensity oral anticoagulation with warfarin and low-dose aspirin in the primary prevention of ischaemic heart disease (IHD). METHODS: 5499 men aged between 45 years and 69 years at high risk of IHD were recruited from 108 practices in the UK that belong to the Medical Research Council's General Practice Research Framework. Initially, warfarin or placebo was randomly allocated to 1427 men; 1013 of these men later moved to a factorial stage of the trial, retaining their warfarin or placebo warfarin allocation and adding randomly allocated active or placebo aspirin. Another 4072 men entered directly into the factorial stage making a total of 5085 men. The four factorial treatment groups were: active warfarin and active aspirin (WA, n = 1277), active warfarin and placebo aspirin (W, n = 1268), and placebo warfarin and active aspirin (A, n = 1268), and placebo warfarin and placebo aspirin (P, n = 1272). The primary end-point was all IHD defined as the sum of coronary death and fatal and non-fatal myocardial infarction (MI). FINDINGS: The mean International Normalised Ratio (INR) of those on active warfarin was 1.47. The mean warfarin dose was 4.1 mg a day (range 0.5 mg-12.5 mg). There were 410 IHD events (142 fatal, 268 non-fatal). The main effect of warfarin (i.e., WA and W vs A and P) was a reduction in all IHD of 21% (95% CI 4-35, p = 0.02) chiefly due to a 39% reduction (15-57, p = 0.003) in fatal events so that warfarin reduced the death rate from all causes by 17% (1-30, p = 0.04). The main effect of aspirin (i.e., WA and A vs W and P) was a reduction in all IHD of 20% (1-35, p = 0.04) almost entirely due to a 32% reduction (12-48, p = 0.004) in non-fatal events. Absolute reductions in all IHD due to warfarin or aspirin were 2.6 and 2.3 per 1000 person years, respectively. WA reduced all IHD by 34% (11-51, p = 0.006) compared with P. WA increased haemorrhagic and fatal strokes. Ruptured aortic or dissecting aneurysms occurred in 15 of those who were or had been on warfarin compared with three of those who had not (p = 0.01). INTERPRETATION: These results add to evidence that aspirin reduces non-fatal IHD. Warfarin reduced all IHD chiefly because of an effect on fatal events. Combined treatment with warfarin and aspirin is more effective in the reduction of IHD than either agent on its own.HOT:BACKGROUND: Despite treat