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Neovascularization of coronary tunica intima (DIT) is the cause of coronary atherosclerosis. Lipoproteins invade coronary intima via neovascularization from adventitial vasa vasorum, but not from the arterial lumen: a hypothesis

Vladimir M Subbotin

Theoretical Biology and Medical Modelling 2012, 9:11  doi:10.1186/1742-4682-9-11

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Epigraph

Vladimir Subbotin   (2012-12-31 17:48)  Vladimir Subbotin email

Accidentally, during production of the final Full text and PDF from the provisional text��s article, the epigraph of the manuscript was lost. Since the epigraph stresses the idea I truly believe, and has already been emphasized by great philosophers a long time ago, I think it would be useful for readers to find it in this temporary comment before final text is corrected. Here it is:

"- It has caused me the greatest trouble, and for ever causes me
the greatest trouble, to perceive that unspeakably more depends
upon what things are called, than on what they are"
Freidrich Nietzsche [1]

1. Nietzsche, F., The Gay Science (The Joyful Wisdom), Book Second, Chapter 58. Page 50. 2009, Digireads.com Publisher.

Competing interests

I am the author of the article

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Comments by author

Vladimir Subbotin   (2012-12-09 20:40)  Vladimir Subbotin email

Two important publications on morphology of human epicardial arteries were overlooked. Both studies examined hearts of young persons: by Milei et al., ��Coronary Intimal Thickening in Newborn Babies and ��1-Year-Old Infants�� [1] and by Angelini et al., ��Coronary arterial wall and atherosclerosis in youth (1-20 years): a histologic study in a northern Italian population�� [2]. These studies showed that coronary DIT occurs after birth and increases progressively with age: 12.5% of specimens from �� 30 days old, more than 30% between 1 month and 1 year [1], and more than 95% between 1 and 20 years [2]. Neither lipid accumulation nor neovascularization were detected. Both studies considered coronary DIT as pre-atherosclerosis lesion, and shared different than author��s vision on DIT and pathogenesis of coronary atherosclerosis [1, 2]. Both publications described the studied subjects as those who had died from causes unrelated to the cardiovascular pathology, which allows to suggest the described coronary morphology as average or norm.

Another oversight was that a neovascularization of deep layers of coronary DIT, coinciding with lipid deposition in early coronary atherosclerosis, was already reported. In 2007 Kolodgie et al. published the article ��Free cholesterol in atherosclerotic plaques: where does it come from? ��. In page 501 the legend for Figure 1 reads: ��(b) The neointima becomes thickened and when it exceeds >0.5mm the Vv (adventitial vasa vasorum ��VMS) begin to invade the media traversing into the deep intima close to acellular lipid pools.�� In the same page below the legend for Figure 2 reads: ���� note angiogenesis within deep intima near the medial (M) wall; ���� [3]. Although this analysis [3] did not suggest that intimal neovascularization could be the initial cause of lipid deposition in DIT and the disease, the significance of this publication [3] for theoretical considerations on initial mechanism of coronary atherosclerosis is evident.

Vladimir M Subbotin
602 Samuel Drive
Madison, WI 53717, USA
vladimir.m.subbotin@gmail.com

1. Milei J, Grana DR, Navari C, Azzato F, Guerri-Guttenberg RA, Ambrosio G: Coronary intimal thickening in newborn babies and ��1-year-old infants. Angiology 2010, 61:350-356.
2. Angelini A, Thiene G, Frescura C, Baroldi G: Coronary arterial wall and atherosclerosis in youth (1-20 years): a histologic study in a northern Italian population. Int J Cardiol 1990, 28:361-370.
3. Kolodgie FD, Burke AP, Nakazawa G, Cheng Q, Xu X, Virmani R: Free cholesterol in atherosclerotic plaques: where does it come from? Curr Opin Lipidol 2007, 18:500-507.

Competing interests

None.

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