The Role of Aging in Atherosclerosis

1. Front Matter

   Pages i-x

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2. Introducing the Sequestration Hypothesis

   • Richard E. Tracy

   Pages 1-10

3. The Sampling Theory of Fibroplastic Arteriosclerosis

   • Richard E. Tracy

   Pages 11-17

4. Intrusion of Atheroma into the Most Fibrotically Thickened Intimal Sites

   • Richard E. Tracy

   Pages 19-27

5. Conditions for Intrusion Atheroma in Coronary Artery

   • Richard E. Tracy

   Pages 29-36

6. The Size of the SMC Realm Assessed with the Help of Sampling Theory

   • Richard E. Tracy

   Pages 37-49

7. Biased censoring of low SMC sites by atheroma in coronary artery

   • Richard E. Tracy

   Pages 51-66

8. Biased Censoring of Low SMC Sites by Atheroma in Thoracic Aorta

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   Pages 67-79

9. SMC Numbers at Varying Depths in Intima of Thoracic Aorta

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   Pages 81-95

10. Histologic Appearances of SMC Clusters and Realms

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    Pages 97-102

11. Direct Imaging of the Hypothetical Quantity, Sequestered Lipid

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    Pages 103-118

12. Local Sequestration of Lipid from Place to Place Within an Artery

    • Richard E. Tracy

    Pages 119-130

13. Fibroplasia in Microscopic Renal Arteries

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    Pages 131-140

14. Parameters of Fibroplasia in Renal Microvasculature

    • Richard E. Tracy

    Pages 141-148

15. The Course of Arterial Intimal Fibroplasia in Aging Arteries

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    Pages 149-158

16. The Course of Fibroplasia per SMC over Time in Aging Arteries

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    Pages 159-163

17. Fibroplasia Per SMC in the Media of Coronary Arteries

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    Pages 165-181

18. Influence of Arteriolar Hyalinization on Renovascular Fibroplasia

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    Pages 183-195

19. The Hy Effect on Ra in Widely Variable Circumstances

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    Pages 197-210

20. Hyalinized Renal Arterioles and the Maleness Coronary Risk Factor

    • Richard E. Tracy

    Pages 211-221

The cover of this book summarizes the central features of the sequestration hypothesis: Commonplace appearances seen in human coronary artery, fat stained in paraffin seetions by a new technique explained in Chapter Eleven, are arranged to suggest pathways of evolution toward atheroma. The hypothesis formulated and defended in the pages ofthis book is this: Fibroplasia progresses upward in column "a" from "la" to "3a" as a characteristic feature of aging. This starts sooner and progresses faster in men than in wornen. Numbers ofSMC's remain essentially constant so that fibroplasia per SMC steadily increases. The rise upward conveys an increasing propensity to sequester atherogenic lipids, causing transition rightward into column "b". Sequestered extracellular lipid then attracts fatty streak elements, especially foam cells and lyrnphocytes, to propel the arterial site rightward into column "c". Frame "lc" corresponds to the AHA Lesions Committee classification type IIb, the progression resistant fatty streak arising directly without prior lipid sequestration; this can progress to atheroma, but slowly after much delay, although extreme provocation can accelerate the process. Such progression is rightward toward atherorna with thin cap, not upward toward fibroplastic thickening. Frame "2c" corresponds to the AHA classification, type Ha, progression prone fatty streaks. These readily evolve into atheroma, again by horizontal progression.

• artery
• atherosclerosis
• diabetes
• histology
• hypertension
• treatment

• Department of Pathology, Louisiana State University Health Science Center, New Orleans, USA

  Richard E. Tracy

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