What causes heart disease part thirty one XXXIWhat is the final eventThe upside downThe final event in most heart attacks, and strokes, is the development of a large, and often fatal, blood clot. If this happens in an artery in the heart, a coronary artery, it cuts off blood supply to an area of heart muscle and can lead to a myocardial infarction MI myocardium heart muscle, infarction death of tissue due to lack of oxygen. Recently, I came across the book by Nebraska Sen. Ben Sasse, a firsttime elected office holder, titled The Vanishing American Adult Our ComingofAge Crisis and. Cast, crew, reviews, plot summary, comments, and related information. There is a related, but different mechanism of action, in most, strokes. In this case a blood clot that has formed in an artery in the neck carotid artery, breaks off and travels to the brain where it gets stuck, blocking an artery. This leads to a cerebral infarction. There are other forms of stroke, with other causes, but this is the most common. These are generally accepted models, and for the sake of brevity, it is also the model I am using here. Although I accept that it is not that simple. For example, you can have an MI with no blood clot found. Here, from a paper entitled Acute myocardial infarction with no obstructive coronary atherosclerosis mechanisms and management Myocardial infarction MI with no obstructive coronary atherosclerosis MINOCA is a syndrome with different causes. Its prevalence ranges between 5 and 2. Watch George Lopez: It`S Not Me, It`S You Online Metacritic. The official website of the City of New York. Find information about important alerts, 311 services, news, programs, events, government employment, the office of the. MIs. 1. A heart attack with no blood clot. In truth, I think this can be easily explained, within the obstructive model, but it would take too long for this blog. I will cover it at some point. Anyway, to get back on track. It is generally accepted that the final event in cardiovascular disease is the formation of a large blood clot. This is the thing that causes both fatal, and non fatal, strokes and heart attacks. Which is why atherosclerosis, as a disease, is often referred to as atherothrombosis. The idea being that atherosclerotic plaques gradually build up, over decades. In the final stage, the plaque ruptures triggering the formation of a large and deadly clot. The suggestion here, never ever explicitly stated, is that we have two different processes in operation. Plaque formation, then the blood clot. Or maybe you could look at this as one process, in two parts. Plaque growth, then plaque rupture causing thrombus formation. I showed my lipid clinic doctor your book the cholesterol con. He did not like it and challenged me with arguments such as how can the many be wrong and a. L. A. Times entertainment news from Hollywood including event coverage, celebrity gossip and deals. View photo galleries, read TV and movie reviews and more. However, it is perfectly possible for thrombi to form with no underlying plaque, so the two processes need not be associated with each other. People with Hughes syndrome, for example, can die of strokes and heart attacks quite suddenly, caused by blood clots, with no plaque to be seen. Hughes syndrome causes the blood to be highly likely to clot hypercoagulable. Which leaves the question hanging somewhat. Paper Heart Full Movie Part 1' title='Paper Heart Full Movie Part 1' />Do we have one process or two I believe that the main reason for using the term atherothrombosis, is because this allows mainstream thinking to draw everything together as different manifestations of the same underlying process. Raised cholesterol causes plaques, these rupture, then a clot develops which would not have formed had the plaque not been there. This allows clear wiggle room, but at some point you must decide, one process or two. This is not quantum physics. In my world, it is far simpler. There is only one process. Atherosclerotic plaque are simply blood clots, in various stages of growth andor repair. Plaque growth represents the formation of a new blood clot, at the same point, which is not cleared away properly. The final thrombotic event is just a big enough clot forming to do real damage. The first time I started to think about this seriously, was when I was reading a paper called A Definition of Advanced Types of Atherosclerotic Lesions and a Histological Classification of Atherosclerosis. A Report From the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Fairy Tail 2014 Episode 65 Dubbed more. The things I do for fun clearly, I am just a geek. Anyway, this paper rambled on and on, and on. Until, whilst propping my eyelids open, my interest suddenly sharpened as I came across the section on the definition of Type Va atherosclerotic plaques dont ask. For those who enjoy a bit of scientific jargon, here it comes. If you dont care for jargon, just look at the text I have put in bold at the end. Sequential histological studies of the lesions of large populations indicate that reparative connective tissue forms in and around regions of the intima in which large accumulations of extracellular lipid lipid cores disarrange or obliterate the normal cell and intercellular matrix structure. Sometimes the new fibrous tissue accounts for more of the thickness of the lesion than does the underlying lipid accumulation. The new tissue consists of substantial increases in collagen and smooth muscle cells rich in rough surfaced endoplasmic reticulum. In cases in which this tissue is particularly thick, some or much of it may be the remnant of thrombi that were incorporated and organized. Capillaries at the margins of the lipid core may be larger and more numerous than in type IV lesions, and they may also be present in the newly formed tissue. Lymphocytes, monocyte macrophages, and plasma cells are frequently associated with the capillaries, and microhemorrhages may be present around them. Type Va lesions may be multilayered several lipid cores, separated by thick layers of fibrous connective tissue, are stacked irregularly one above the other. The term multilayered fibroatheroma can be applied to this morphology. The lipid core that is deepest and closest to the media may have formed first. Mechanical forces may play a role in the modeling of such lesions. Additional lipid cores in locations and planes different from the first could be induced as asymmetric vascular narrowing and changes in lumen configuration modify hemodynamic and tensile forces, creating a redistribution of the regions of predisposition for lesion formation. The architecture of some multilayered fibroatheromas could also be explained by repeated disruptions of the lesion surface, hematomas, and thrombotic deposits. Organization fibrosis of hematomas and thrombi could be followed by renewed accumulation of macrophage foam cells and extracellular lipid between the newly formed fibrotic layer and the endothelial surface. In laymans terms what does it mean It means that a number of plaques look exactly as if they were created by the repeated formation of blood clots, one on top of another. A concept further reinforced, when the paper looked again at thrombosis. ThrombosisIt has been reported that advanced atherosclerotic lesions containing thrombi or the remnants of thrombi are frequent from the fourth decade of life on. In 1. 97. 5 Chandler and Pope compiled and reviewed studies that reported the frequency and nature of lesions with incorporated thrombi. In a recent study of a population aged 3. These thrombi ranged in size from minimal microscopic to grossly visible deposits, and some consisted of stratified layers of different ages. Immunohistochemistry revealed wavy bandlike deposits related to fibrin within the advanced lesions of an additional 2. Because of their structure, these were thought to represent the remnants of old thrombi. Similar data were reported by other authors. The fissures and hematomas that underlie thrombotic deposits in many cases may recur, and small thrombi may reform many times. Repeated incorporation of small recurrent hematomas and thrombi into a lesion over months or years contributes to gradual narrowing of the arterial lumen. Some thrombi continue to enlarge and occlude the lumen of a medium sized artery within hours or days. Perhaps the key sentence here, from my point of view, is the following Repeated incorporation of small recurrent hematomas and thrombi into a lesion over months or years contributes to gradual narrowing of the arterial lumen. Here, right here, is proof of the concept that plaques definitely do grow through repeated thrombus formation at the same point on the artery. Do all plaques do thisEntertainment News Los Angeles Times. Chris Barton. Imagine youre starting a sketch comedy show, one that will debut on network TV in prime time. Of course, such a bold, probably misguided, idea requires a big star, maybe one who became the centerpiece of Saturday Night Live and starred in a summer blockbuster. Fine, done. But such a series needs.