摘要:

SUMMARYDuring the last two decades, significant advances have been made in the understanding of atherosclerotic disease. The pathogenesis of atherosclerosis appears to depend on a precise sequence of critical events based on the interaction of blood elements and lipids with the arterial wall. The major critical events and their sequence appears to be as follows: hemodynamic stress and endothelial injury; arterial wall‐platelet interaction; smooth muscle cell proliferation; lipid entry and accumulation; significant arterial narrowing with fibrosis and development of thrombi; and complications in the form of calcification, ulceration, aneurysm, acute thrombotic occlusion and embolization. This sequence of critical events starts at a young age and in all geographic racial groups. Their evolution into advanced symptomatic lesions takes many years and varies in incidence and extent among different geographic and ethnic groups. It appears that in promoting and accelerating this process into the advanced stage of the disease, the presence at a young age of the so‐called risk factors of atherosclerotic disease is most important.The recent advances in the understanding of the atherosclerotic process will be highlighted in this chapter with particular attention being focused on the role of platelets and thrombosis in the development of the disease and the possible role of platelet inhibitor drugs on the prevention of coronary atherosclerotic dise

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01602.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01603.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01604.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01605.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01606.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01607.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

摘要:

SUMMARYIn the Anturan Reinfarction Italian Study (ARIS) some specific and quantitative hemostatic parameters are being investigated at different times and in different series of patients balanced for sulfinpyrazone (S) and placebo (P) in order to ascertain if one or more of these parameters may be considered as forecasting elements. A series of 186 myocardial infarction (m. i.) patients was randomly allocated to S and P 15–25 days after the m.i. episode, and tests performed at treatment allocation and after 1, 6 and 12 months. In comparison with 44 healthy volunteers, the results have provided striking confirmation of “hyperactive” platelets in the early phase of m.i.: the bleeding time (BT) was shorter, β‐thromboglobulin (β‐TG) increased, PF4release increased, heparin thrombin clotting time (HTCT) shorter, and platelet sensitivity to threshold concentrations of ADP and collagen increased. Significant changes in BT, P F4release and HTCT persisted at successive testing times. Platelet aggregation by low collagen concentrations was inhibited in the S subsample patients.In a different series of young male patients who had had a m.i. 6 months previously, it has been shown that the P treatment subsample presented shortened platelet production time (PPT), increased levels of plasma ‐TG and PF4and increased factor VIII:RAg compared with a matched control group. The S treatment subsample presented normalized PPT accompanied by reduction of VIlhRAg but not of β‐TG or PF4. plasma levels. It will be possible to evaluate the prognostic significance of these results only when the above pattern in the parameters can be correlated with the major and minor clinical events observed in patient follow‐up, that is, after ARIS closes.Prospective clinical trials with platelet anti‐aggregating agents were started when it was realized that for such drugs to be defined as anti‐thrombotic it was not sufficient to show that they had an effect on platelet functionin vitroorex vivo, and only the demonstration that they are efficacious in preventing specific clinical endpoints would justify defining

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01608.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01609.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01610.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY

ISSN:0036-553X    

DOI:10.1111/j.1600-0609.1981.tb01611.x

出版商:Blackwell Publishing Ltd    

年代:1981

数据来源: WILEY