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Pastimes : Heart Attacks, Cancer and strokes. Preventative approaches -- Ignore unavailable to you. Want to Upgrade?

To: jrhana who wrote (216)	7/14/2008 2:36:28 PM
From: mistermj	Read Replies (2) \| Respond to of 39298

Regarding low dose ASA. There are also studies that suggest low dose metronomic (LDM)therapy with 81 mg ASA is more effective than large dose. ASA is a powerful angiogenesis inhibitor...and this is an emerging field for cancer and heart therapy. Again...its all related to the inflammation cascade. I don't pretend to understand the science...but what I understand about the counter intuitive results with low dose over high dose is it can be more effective against cancer because it doesn't kick in various tumor growth factor responses. In other words...using too high of a dose may in fact trigger responses that are able to overwhelm the effect of ASA...but if you just keep hitting it with a low dose ASA it can keep disease in check by inhibiting blood supply. In this case...less may be more. This also relates to cardiovascular therapy...in this case inhibiting the ability for plaque angiogenesis. This forum is way ahead of the curve in looking at these issues. The more you start looking at angiogenesis and inflammation...the more you start having Eureka moments seeing disease states tied together with the inflammation cascade. Like this for example: Atherosclerotic Plaque Progression and Vulnerability to Rupture Angiogenesis as a Source of Intraplaque Hemorrhage Renu Virmani; Frank D. Kolodgie; Allen P. Burke; Aloke V. Finn; Herman K. Gold; Thomas N. Tulenko; Steven P. Wrenn; Jagat Narula From the CVPath, International Registry of Pathology (R.V., F.D.K.), Gaithersburg, Md; Department of Pathology (A.P.B.), University of Maryland, Baltimore; Cardiac Unit (H.K.G., A.V.F.), Department of Internal Medicine, Massachusetts General Hospital, Boston; Department of Surgery (T.N.T.), Thomas Jefferson University, Philadelphia, Pa; Department of Chemical Engineering (S.P.W.), Drexel University, Philadelphia, Pa; and Department of Cardiology (J.N.), University of California, Irvine. Correspondence to Renu Virmani, MD, Medical Director, CVPath, International Registry of Pathology, 19 Firstfield Rd, Gaithersburg, MD 20878. E-mail rvirmani@cvpath.org Observational studies of necrotic core progression identify intraplaque hemorrhage as a critical factor in atherosclerotic plaque growth and destabilization. The rapid accumulation of erythrocyte membranes causes an abrupt change in plaque substrate characterized by increased free cholesterol within the lipid core and excessive macrophage infiltration. Neoangiogenesis is associated closely with plaque progression, and microvascular incompetence is a likely source of intraplaque hemorrhage. Intimal neovascularization is predominantly thought to arise from the adventitia, where there are a plethora of pre-existing vasa vasorum. In lesions that have early necrotic cores, the majority of vessels invading from the adventitia occur at specific sites of medial wall disruption. A breech in the medial wall likely facilitates the rapid in-growth of microvessels from the adventitia, and exposure to an atherosclerotic environment stimulates abnormal vascular development characterized by disorganized branching and immature endothelial tubes with "leaky" imperfect linings. This network of immature blood vessels is a viable source of intraplaque hemorrhage providing erythrocyte-derived phospholipids and free cholesterol. The rapid change in plaque substrate caused by the excessive accumulation of erythrocytes may promote the transition from a stable to an unstable lesion. This review discusses the potential role of intraplaque vasa vasorum in lesion instability as it relates to plaque rupture. Intraplaque hemorrhage is a major contributor to coronary lesion progression. The formation of immature blood vessels within a plaque promotes red blood cell leakage, an important source of free cholesterol. This review discusses the potential role of angiogenesis in lesion instability as it relates to plaque rupture. Key Words: angiogenesis • plaque rupture • sudden coronary death • free cholesterol • hemorrhage atvb.ahajournals.org