참고문헌 (36)

1. 10.1161/circ.86.3.1516192 

   

2. Lewis Jr., H. Daniel, Davis, James W., Archibald, Donald G., Steinke, William E., Smitherman, Thomas C., Doherty III, James E., Schnaper, Harold W., LeWinter, Martin M., Linares, Esteban, Pouget, J. Maurice, Sabharwal, Subhash C., Chesler, Elliot, DeMots, Henry. Protective Effects of Aspirin against Acute Myocardial Infarction and Death in Men with Unstable Angina : Results of a Veterans Administration Cooperative Study. The New England journal of medicine, vol.309, no.7, 396-403.

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3. Cairns, John A., Gent, Michael, Singer, Joel, Finnie, Keith J., Froggatt, Gordon M., Holder, Douglas A., Jablonsky, George, Kostuk, William J., Melendez, Libardo J., Myers, Martin G., Sackett, David L., Sealey, Brian J., Tanser, Paul H.. Aspirin, Sulfinpyrazone, or Both in Unstable Angina : Results of a Canadian Multicenter Trial. The New England journal of medicine, vol.313, no.22, 1369-1375.

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4. 10.1161/circ.82.1.2194694 

   

5. Iuliano, Luigi, Violi, Francesco, Pedersen, Jens Z., Praticò, Domenico, Rotilio, Giuseppe, Balsano, Francesco. Free radical-mediated platelet activation by hemoglobin released from red blood cells. Archives of biochemistry and biophysics, vol.299, no.2, 220-224.

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6. Reply Balsano and coworkers present a hypothetical claim in their letter: 

7. "Whereas an increased lipid peroxidation mediated by iron stores 

8. may accelerate atherosclerosis progression this could not be the 

9. mechanism eventually involved in the occurrence of myocardial 

10. infarction which in fact is due to a thrombotic complication of 

11. atherosclerotic coronary artery disease." In our understanding the 

12. current consensus concerning the pathophysiology of myocardial 

13. infarction is that both atherosclerotic and thrombotic phenomena 

14. may contribute to the acute event but not both of them in all cases.' 

15. Fatal acute myocardial infarctions (AMIs) have been described in 

16. patients with no signs of either atherosclerosis or thrombosis in the 

17. autopsy. In these cases AMI has been thought to have been due to 

18. "coronary spasm" or serious arrhythmia. Also AMI may occur 

19. without any coronary thrombosis.' As coronary atherosclerosis is 

20. present in the majority of patients with AMI in our view pathophys 

21. iological mechanisms contributing to atherogenesis are also impor 

22. tant in the etiology of AMI. On the basis of the evidence concerning 

23. the role of lipid peroxidation 2 in atherogenesis these include factors 

24. promoting the oxidation of lipids such as redox-active iron. The finding by Balsano and coworkers concerning the role of 

25. iron-derived oxygen free radicals in the activation of platelets is an 

26. important additional contribution to the comprehensive under 

27. standing of the mechanisms through which iron overload and high 

28. exposure to redox-active iron promote the development of athero 

29. sclerosis and coronary heart disease. Activated platelets play an 

30. important role (besides in thrombogenesis) in atherogenesis.3'4 

31. However their observation does not in any way exclude the 

32. possibility of other mechanisms. 

33. 10.1056/NEJM199201233260406 Fuster V Badimon L Badimon JJ Cheseboro JH. The pathogenesis of coronary artery disease and the acute coronary syndromes. N EngI JMed. 1992;326:242-250. 

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34. Salonen, J.T., Korpela, H., Salonen, R., Nyyssonen, K., Yla-Herttuala, S., Yamamoto, R., Butler, S., Palinski, W., Witztum, J.L.. Autoantibody against oxidised LDL and progression of carotid atherosclerosis. The Lancet, vol.339, no.8798, 883-887.

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35. Epstein, Franklin H., Steinberg, Daniel, Parthasarathy, Sampath, Carew, Thomas E., Khoo, John C., Witztum, Joseph L.. Beyond Cholesterol. The New England journal of medicine, vol.320, no.14, 915-924.

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36. 10.1056/NEJM198602203140806 Ross R. The pathogenesis of atherosclerosis: an update. N EngI J Med. 1986;314:488-500. 

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