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Each figure is preceded by a brief explanation of its content.

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And yet, despite this overwhelming evidence, the plumbing model, complete with blockages that can be fixed, continues to be used to explain stable coronary disease to patients, who understandably assume that angioplasty or stents will prevent heart attacks—which they patently do not.The following figures were constructed from a video Tom Dayspring produced in one of his stellar lectures on the development of atherosclerosis.I’ve broken the video down into 20 or so steps which show the transition from a completely normal endothelium (i.e., at birth) through myocardial infarction.reported that early atherosclerosis was characterized by plaque accumulation in the vessel wall and enlargement of the external elastic membrane (EEM) a change in lumen size.As atherosclerosis progressed, they found that plaque continued to accumulate in the vessel wall until the lesion occupied approximately 40% of the area within the EEM. These findings have since been confirmed by intravascular ultrasound (IVUS).Low density lipoprotein (“LDL”) is a lipid (the bulk of which is cholesterol) transport particle. It is not “bad cholesterol,” a term that has no meaning.

LDL—the particle—allows lipids (cholesterol, but also triglyceride, phospholipid) to be delivered through the aqueous medium of the blood, since lipids are hydrophobic (i.e., repel water) and a “carrier” is needed to transport them in blood (which is mostly water).

It’s true that eventually the lumen of a diseased vessel does narrow, but this is sort of like saying the defining feature of a subprime collateralized debt obligation (CDO) is the inevitable default on its underlying assets.

By the time that happens, eleven other pathologic things have already happened and you’ve missed the opportunity for the most impactful intervention to prevent the cascade of events from occurring at all.

Ok, so now let’s get rigorous about the pathology that kills more Americans than any other disease.

To understand this, as Frederic Bastiat wrote long ago, we must resort to “long and arid dissertations.” Buckle up.

However, in 1987, Glagov and colleagues proposed an alternative model of atherosclerosis development.