Thursday, 28 February 2019

The New Way of Thinking About Coronary Artery Disease

The New Way of Thinking About Coronary Artery Disease

Be wary of cardiologists thinking in the "traditional way"
By Richard N. Fogoros, MD | Medically reviewed by a board-certified physician
Updated August 08, 2018

The way we think about Coronary Artery Disease (CAD) and its treatment is in the midst of a major shift, and today, some cardiologists have completely moved to the "new way" of thinking, while others are still stuck in the "traditional way." The differences between these two schools of thought largely explain much of the debate currently taking place among cardiovascular specialists about who to test for CAD, how to test based on symptoms, who needs to be treated for CAD, and how to treat them. Unfortunately, doctors still mired in the traditional way of thinking are missing the boat -- and as a result, are subjecting many of their patients to both undertreatment and overtreatment.

The Traditional Way of Thinking About CAD
Traditionally, CAD means there are one or more blockages in the coronary arteries. These blockages can restrict blood flow, which can produce angina (chest discomfort), and, if severe, the blockages can suddenly become complete, causing the heart muscle supplied by that artery to die, which is called a "myocardial infarction" or heart attack. Since the chief problem is the blockage, the chief treatment is to relieve the blockage, which can be done with bypass surgery or stenting. The traditional view of CAD, then, focuses on blockages, which means that precise anatomic location and degree of blockages is critical in assessing CAD. Diagnostic tests that do not provide this information and treatments that do not relieve the blockages are not fully adequate. Cardiologists who think traditionally tend to insist on cardiac catheterizations as the only adequate diagnostic test and stenting as the only adequate therapy, though they will reluctantly allow that sometimes the cardiac surgeon needs to get involved for particularly extensive or difficult blockages.

The New Way of Thinking About CAD
We now know that CAD is about far more than just blockages. CAD is a chronic, progressive disease that tends to be far more widespread within the coronary arteries than is implied by the presence or absence of actual blockages. Plaques are often present in arteries that appear "normal" on cardiac catheterization. In fact, some patients, especially women, can have widespread CAD that produces a generalized narrowing of the coronary arteries without any actual blockages. Furthermore, heart attacks are produced when a plaque ruptures and causes a clot to form that suddenly blocks the artery -- and often this occurs at plaques that are not causing blockages prior to their rupture and would have been called "insignificant" on cardiac catheterization. The key to CAD is not whether specific blockages are present, but whether coronary artery plaques (which often do not cause significant blockages) are present.

What This Means for You
While actual blockages can and do cause angina and heart attacks and while treating specific blockages is often important, therapy aimed at treating blockages is often neither necessary nor sufficient to adequately treat CAD. Evidence is building that with intensive medical therapy -- largely based on statins but also including aggressive risk-factor modification -- CAD can be halted or even reversed, and plaques can be "stabilized" to reduce the odds that they will rupture. In these individuals, exercise, smoking cessation, weight loss, blood pressure control and (most experts believe) cholesterol control are especially important.

The key, then, is to decide whether an individual is likely to have active CAD, that is, whether plaques are likely to be present, and then direct therapy accordingly. To a large extent, deciding whether plaques are likely to be present can be accomplished noninvasively. Begin with a simple assessment of risk to decide whether your risk is low, intermediate or high. ( Here's how to assess your risk simply and easily.) People in the low-risk categories probably need no further intervention. People in the high-risk categories should be treated aggressively (with statins and risk-factor modification), as they are very likely to have plaques. People in the intermediate risk category should consider noninvasive testing with EBT scanning (calcium scans): if calcium deposits are present on the coronary arteries, then they have plaques and should be treated aggressively.

When to Look for Blockages
Blockages in the coronary arteries are still important. Most experts think that people in the high-risk category should have a stress thallium test. If this test is suggestive of a major blockage, cardiac catheterization should be considered. A stress test or cardiac catheterization should also be strongly considered in anybody (whatever their apparent level of risk) who has symptoms of angina. Relieving blockages by surgery or stenting can be extremely effective in treating angina and, in some circumstances, can improve survival.

Summary
Our thinking about CAD has changed significantly over the past decade or so. It is not simply a disease of blockages that ought to be treated with stents. Treatment aimed at halting or reversing chronic CAD and at stabilizing plaques to reduce the odds that they will rupture, is very important, whether "significant" blockages are present or not

Saturday, 23 February 2019

Lp(a) as an ascorbic-acid surrogate to repair arterial walls

https://en.wikipedia.org/wiki/Lipoprotein(a)#Function

Lipoprotein(a) (also called Lp(a) or LPA) is a lipoprotein subclass. Genetic studies and numerous epidemiologic studies have identified Lp(a) as a risk factor for atherosclerotic diseases such as coronary heart disease and stroke.[3][4][5][6][7]
Lipoprotein(a) was discovered in 1963 by Kåre Berg.[8] The human gene encoding apolipoprotein(a) was cloned in 1987.[9]

Contents

Nonetheless, individuals without Lp(a) or with very low Lp(a) levels seem to be healthy.[31] Thus, plasma Lp(a) is not vital, at least under normal environmental conditions. Since apo(a)/Lp(a) derived rather recently in mammalian evolution - only old world monkeys and humans have been shown to harbour Lp(a) - its function might not be vital, but just evolutionarily advantageous under certain environmental conditions, e.g. in case of exposure to certain infectious diseases.

Another possibility, suggested by Linus Pauling, is that Lp(a) is a primate adaptation to L-gulonolactone oxidase (GULO) deficiency, found only in certain lines of mammals. GULO is required for converting glucose to ascorbic acid (vitamin C), which is needed to repair arteries; following the loss of GULO, those primates who adopted diets less abundant in vitamin C may have used Lp(a) as an ascorbic-acid surrogate to repair arterial walls.[32]
Lp(a) carries cholesterol and binds atherogenic proinflammatory oxidized phospholipids as a preferential carrier of oxidized phospholipids in human plasma,[25] which attract inflammatory cells to vessel walls and leads to smooth muscle cell proliferation.[26] Moreover, Lp(a) also is hypothesized to be involved in wound healing and tissue repair, interacting with components of the vascular wall and extra cellular matrix.[27][28][29]