When does heart disease begin (and what this tells us about prevention)? More on that momentarily. Before I get into this post I want to lay a few things out. Get the latest health news, diet & fitness information, medical research, health care trends and health issues that affect you and your family on ABCNews.com. This post is written mostly for doctors, but also for patients who really want to understand this topic, if for no other reason than to help them choose the right doctors. I don’t go out of my way to simplify the terminology and I assume the reader is familiar with the topics covered in the cholesterol series I wrote three or four years ago. If you encounter a term you don’t understand, Google is a pretty good place to find the definition. I will not use this post to in any way get into prescriptive strategies, which involve modifications of nutrition, hormones, and yes, lots of drugs across four or five classes (i. Even if I wanted to write out all of my prescriptive leanings I could not do it briefly. Please do not email your lab results or ask me to weigh in on your case. You know the disclaimer: I can’t practice medicine on a blog or over email. There was a day when the only thing I argued about was who the greatest boxer of all time was. ![]() If you’ve ever needed to upload an image or two, or deal with a scanned document, you know about all the headaches that come with conversion, and how finicky sites. Comments to this website are moderated by our editorial board. For approval, comments need to be relevant to the article and free of profanities and personal attacks. 1 The Greater East Asian War: How Japan Changed The World By Kase Hideaki Society for the Dissemination of Historical Facts © 2 Chapter 1 – Up to the Day Japan. BibMe Free Bibliography & Citation Maker - MLA, APA, Chicago, Harvard. 25 tips for backpacking around South East Asia, from tuk-tuks to temples, buckets to banana pancakes and everything in between. We provide excellent essay writing service 24/7. Enjoy proficient essay writing and custom writing services provided by professional academic writers. Joe Louis vs. 1. 94. Sugar Ray Robinson vs. Henry Armstrong.)Today, however, I find myself arguing about so many things—some of them actually important—from why symptomatic women should receive hormone replacement therapy after menopause (and, by extension, why the Women’s Health Initiative tells us so, if you know how to read it) to why monotherapy with T4 for hypothyroidism is a recipe for disaster for most patients. But there is nothing I find myself debating more than the misconceptions most doctors have about heart disease. This is especially troubling since heart disease kills more Americans than any other disease. The English version offers selected articles from.To put this in perspective, a woman in the United States is 7 to 8 times more likely to die from heart disease than she is from breast cancer. Here are the typical arguments put forth, almost always by doctors, which invariably result in my need/desire to counter: Heart disease is caused by too much “bad” cholesterol (LDL- C). LDL- C is the only target of therapy you need to worry about. ![]() Calcium scores and CT angiograms (CTA) are great ways to further risk- stratify (the corollary: when these tests are negative, there is no need to treat the patient). Atherosclerosis is a “pipe narrowing” disease (ok, nobody uses these words, but they imply this by saying it’s a luminal narrowing disease). There is no role for preventatively treating young people, except in very rare cases like familial hypercholesterolemia. Briefly, here are my counters: Atherosclerosis is caused by an inflammatory response to sterols in artery walls. Sterol delivery is lipoprotein- mediated, and therefore much better predicted by the number of lipoprotein particles (LDL- P) than by the cholesterol they carry (LDL- C) . And don’t ever bring up LDL- C again. Calcium scores and CT angiograms of exceptional quality (the operative word being exceptional—most are not) are helpful in a few settings, but this assertion is patently false, and I will leave this discussion for another blog post as the topic is too rich in nuance for a few lines. We’ll discuss this today. By necessity, we’ll be forced to confront this today, also. Before diving into this topic it’s really important for me to acknowledge the person who has taught me almost everything I know about this disease, beginning back in 2. ![]() I first became aware that I basically had no idea what atherosclerosis was. For the past 5 years Dr. Tom Dayspring’s generosity has been remarkable and I’m humbled to be his most sponge- like student. Tom has not only given me an on- the- side lipidology fellowship, but he has also introduced me to the finest lipidologists and cardiologists in the country who have, in turn, been incredibly generous with their time and knowledge. I’m not the only one to benefit from Tom’s wisdom and generosity. I had dinner with Tom’s son and his wife once and I described Tom to them as a national treasure. That’s really how I feel about him. He is a nationally- recognized educator and his writing and presentations are devoured by fanatics like me across the globe. With Tom’s permission, I’ve deconstructed a video he put together into a series of figures which I’ll use to begin this discussion of how atherosclerosis actually takes place. The physics of luminal narrowing. Traditionally, the atherosclerotic process was believed to involve plaque accumulation that prompted the gradual narrowing of the lumen, with the eventual development of stenosis. Stenosis then caused impaired control of flow (stable angina) and plaque rupture and thrombosis (unstable angina and MI). Consequently, prevailing opinion held that coronary angiography would be able to gauge the atherosclerotic process at all stages of disease. However, in 1. 98. Glagov and colleagues proposed an alternative model of atherosclerosis development. After performing histological analyses of coronary artery sections, Glagov et al. At this point, the lumen area began to narrow. These findings have since been confirmed by intravascular ultrasound (IVUS). Due to the complex remodeling that occurs in the earlier stages of atherosclerosis, coronary angiography, which only visualizes the lumen, tends to underestimate the degree of atherosclerosis. In other words, atherosclerosis is well under way long before angiography is able to identify it. I was reminded of the words of my Pathology professor back in the first year of medical school, “The only doctors who actually understand atherosclerosis are pathologists.” I would add lipidologists to that list, but I saw his point. Most people, doctors included, think atherosclerosis is a luminal- narrowing condition—a so- called “pipe narrowing” condition. 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. To reiterate: atherosclerosis development begins with plaque accumulation in the vessel wall, which is accompanied by expansion of the outer vessel wall without a change in the size of the lumen. Only in advanced disease, and after significant plaque accumulation, does the lumen narrow. Michael Rothberg wrote a fantastic article on the misconception of the “clogged pipe” model of atherosclerosis. He opens with the following story: A recent advertisement on the back cover of a special health issue of the New York Times Magazine section read “Ironic that a plumber came to us to help him remove a clog.” The ad referred to doctors in the cardiac catheterization laboratory as “one kind of pipe specialist,” and noted that the patient in the ad returned to work “just 2 days after having his own pipes cleaned out.” Although the image of coronary arteries as kitchen pipes clogged with fat is simple, familiar, and evocative, it is also wrong . Rothberg goes on to explain that for patients with stable disease, local interventions can only relieve symptoms; they do not prevent future myocardial infarctions. To be clear, at least 1. 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 root of the problem, in my view at least, is that we as doctors—and by extension, our patients and media—spend too much time looking at images like these (angiograms of coronary arteries complete with “clogged pipes”): And not enough time looking at images like these (the histological, i. But who can blame us, I mean, angiograms are cool! But, alas, it’s time to get serious about understanding this disease if we want to prevent/delay it. Atherosclerosis, for the cognoscenti. Ok, so now let’s get rigorous about the disease 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. 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 2. Each figure is preceded by a brief explanation of its content. The endothelium is a protective one cell layer lining the surface of the artery lumen. Endothelial cells perform many complex functions and are capable of modulating vascular tone, as well as inflammatory and thrombotic processes. Their function depends on many circulating and local factors. Low density lipoprotein (“LDL”) is a lipid (the bulk of which is cholesterol) transport particle. Please re- read this sentence. 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. If LDL particles are present in physiologic (i. The term LDL particle, LDL- P, and apo. B are used interchangeably (the latter, because LDL particles are defined by the wrapping of a lipoprotein called apolipoprotein B- 1. When LDL particle concentration is elevated, the lipoprotein penetrates into the subendothelial space. Once in the intimal layer, they are securely attached to intimal proteoglycan molecules. The first step in atherogenesis is surface phospholipid (PL) exposure to reactive oxygen species and oxidation of the PL. LDL particles that are not oxidized are not atherogenic. It is worth pausing here for a moment. This step is kind of the turning point in the story. It’s also a perfectly “normal” thing for the epithelium to do.
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