Preventing and Reversing Heart Disease For Dummies. James M. RippeЧитать онлайн книгу.
to gobble up more excess lipids. Other protective mechanisms such as platelets, T-cells, and growth factors for smooth muscle cells arrive and work hard to restore the damage from excess lipids. As these macrophages engulf the cholesterol, they transform into macrophage foam cells, which usually appear as yellow fatty streaks visible on the interior artery walls.
4. The fatty streaks continue to grow and form scar tissue.
When blood cholesterol levels are lower and plenty of HDL cholesterol (the good guys) is present to carry away LDL, then these fatty streaks can be halted or reversed. (For more on cholesterol and controlling it, see Chapter 9.) But when excess cholesterol and/or other risk factors such as the circulating platelets and other clotting factors and excess smooth muscles are present, the deposits typically continue growing. Through pathways not yet clear, risk factors can also help modify HDL lipoproteins so that they no longer act protectively but instead contribute to the atherosclerotic process.
As the process seals off the excess lipids, it actually creates cholesterol-rich pockets covered with scar tissue. These lesions narrow the arteries and typically deform artery walls as they grow larger.
Growing from fatty streaks to large plaques
Decades of time and the presence of various risk factors are required for the fatty streaks to develop into intermediate (moderate-sized, symptomless) and advanced (larger, symptom-producing) plaques. Figure 2-3 illustrates the typical but gradual development and progression of coronary heart disease.
Illustration by Kathryn Born
Figure 2-3: The process of coronary artery disease.
Growing to moderate, intermediate types of plaque
In the presence of normal mechanical forces, such as the impact of flowing blood against artery walls, and risk factors that can injure artery walls, many fatty streaks begin growing into larger deposits. More cholesterol and other lipid (fat) particles migrate into the artery walls. This happens particularly in areas where the intima of the artery has thickened, probably to adapt to mechanical forces exerted on the arteries.
More and more fatty substances aren’t taken into macrophages or the smooth muscle cells; instead, they begin pooling between them. Some cells die and release their lipids into this core. At that point, a thin layer of intimal tissue has begun forming a cap to contain this lipid pool. Other substances such as cytokines (various small proteins active in the immune system) and growth factors may also play a role in forming the cap and helping it continue to grow. The formation and growth of the cap mark the transition from intermediate lesions to what medspeak terms advanced (and typically more dangerous) lesions.
Becoming advanced atherosclerotic plaques
As plaques continue to grow, they reach a condition and size that may produce symptoms such as angina, unstable angina, or even heart attack or stroke. The various advanced types of atherosclerotic plaques are characterized by a well-defined lipid core that is contained by a cap composed of layers of smooth muscle cells and other substances.
At first this cap appears to be nearly normal intimal layers. But as the plaque grows larger, the composition of the cap’s layers changes, becoming more fibrous, or scarlike, as substances such as collagen and calcium enter the mix.
Some advanced plaques are stable, but others are vulnerable to cracking or rupture. When a crack or tear occurs, the lipid core is exposed to arterial blood from which sticky platelets may trigger the formation of a blood clot intended to repair the break. The clot, however, enlarges the size of the plaque. Some plaques grow larger by a cyclical process of cracking and clotting, which gradually narrows the artery. Fewer plaques may grow by a process of cap erosion rather than rupture.
Differentiating between stable and unstable plaques
As individual plaques grow to moderate size and begin exhibiting the rich lipid core and thin fibrous cap associated with the first level of advanced lesions, they appear to be more vulnerable to rupture and dangerous clot formation than larger, older, thicker plaques. Bigger doesn’t necessarily mean more vulnerable, either. The most vulnerable plaques, which can give rise to the deadliest heart attacks, typically block the vessel by only about 40 percent to 50 percent.
Medical scientists and physicians are particularly interested in ways to accurately identify these types of vulnerable plaques, because they seem to be responsible for the majority of sudden acute cardiovascular events, including heart attack, cardiac arrest, and stroke. Figure 2-4 illustrates the way in which such a process suddenly blocks an artery and causes an acute event.
Illustration by Kathryn Born
Figure 2-4: When the plaque narrowing a coronary artery cracks open or ruptures, a clot forms, which can block the artery entirely, causing a heart attack.
Current evidence suggests that stable plaques typically have thicker, more fibrous caps with few inflammatory cells and more calcification, which make the cap tougher. Stable plaques also appear to have fewer lipids within. Although stable plaques often are large, the edges or shoulders of the lesion usually are smooth and tapered.
Unstable plaques, by contrast, are smaller in size but are very rich in cholesterol and incorporate many more inflammatory cells, which release chemicals that degrade the fibrous cap. Unstable plaques often appear structurally weak. In addition, the thinner cap may be easily ruptured or torn by a number of forces, ranging from the normal flow of blood at high stress points in the arterial system to sudden pressures such as suddenly increased blood pressure from exertion.
Researchers continue to look for tests and techniques that accurately identify and assess unstable plaque. Such tools would enable physicians to better identify individuals at greater risk of acute events and begin preventive measures.
Understanding a different type of coronary disease: Microvascular disease
Some people who experience reduced flow of blood to the heart do not have narrowings of the larger coronary arteries caused by atherosclerotic plaque. Instead, they have coronary microvascular disease (MVD). MVD occurs much more often in women than men, particularly in premenopausal or younger women. In MVD, smaller blood vessels in the heart, which range from 100 micrometers (about the size of a human hair) to 200 micrometers constrict, preventing adequate oxygenated blood from reaching the heart muscle. As a result, people with MVD may have clear larger coronary arteries but still experience the symptoms of chest pain, although the discomfort is usually more diffuse and may last longer than with angina in CHD.
The causes of MVD are not yet clear, but chronic inflammation appears to play an important role. And the risks factors for CHD, such as high blood pressure (particularly before menopause), unhealthy cholesterol levels, smoking, and diabetes appear to contribute. Current research is also looking for possible risk factors unique to MVD as well as for more effective diagnostic techniques.
Knowing when chest pain is an emergency