Diseases

Yes. Not uncommonly, people with coronary artery disease have more than one heart attack over the years. In fact, by looking at the heart tissue at autopsy, pathologists can tell when myocardial infarctions occurred. Thus, very recent (acute, hours old) infarctions may appear as a pale brown region, infarctions days old (subacute) appear yellow, and healed (weeks to years old) infarctions appear as white scars in the heart muscle. Figure 5 shows three myocardial infarctions of different ages in the muscle of a left ventricle. Figure 5: Three Myocardial Infarctions of Different Ages; Slice Across Heart Ventricles

The coronary arteries carry blood to the heart to supply oxygen and necessary nutrients. As seen in Figure 1, the wall of a coronary artery has 3 distinct layers: the inner (intima), middle (media), and outer (adventitia) layers. The wall of the artery surrounds the lumen of the artery, which is the channel through which blood flows. Figure 1: Normal Coronary Artery; Cross-sectional Microscopic View Picture of Normal Coronary Artery In Figure 1, smooth muscle is red, and connective (supporting) tissue is black (elastic) or blue (collagen). The intima is best seen in the close-up view in Figure 1. It is composed of a layer of so-called endothelial cells that covers the artery's inner (lumenal) surface, connective (supporting) tissue (collagen and elastin), and a layer of compact elastic tissue called the internal elastic lamina (IEL). In the past, the intima was thought to be simply a passive layer whose major purpose was to serve as a barrier. Now, however, we know that the endothelial cells actually keep track of the pressure, flow, and "health" of the artery. Moreover, endothelial cells secrete chemicals that can adjust the function of the artery (e.g., vasodilator chemicals to widen and vasoconstrictors to narrow it) and growth of the artery wall (e.g., growth factors). The media (M) is a layer made up primarily of smooth muscle cells (SMCs). The muscle can contract and relax to control the blood pressure and flow in the artery. Elastic tissue and collagen in the media, along with elastic tissue in the IEL, increase the elasticity and strength of the wall of the artery, as the artery contracts and relaxes. The adventitia is a layer of connective tissue and cells (e.g., SMCs) that produce this connective tissue. The adventitia contains potent factors, including one called tissue thromboplastin, that promote blood clotting. The clots are useful when the artery becomes injured because they can limit excessive bleeding from the injured artery.

In coronary artery disease (coronary atherosclerosis), injury to the intima of the artery leads to the formation of plaques, which are regions of thickening on the inner lining of the artery. How then do the plaques form? In response to the injury, the smooth muscle cells (SMCs) from the media and perhaps from the adventitia move (migrate) into the intima. In the intima, these SMCs reproduce themselves (divide) and make (synthesize) connective tissue. These processes of migration, division, and synthesis, which collectively are referred to as intimal proliferation (buildup), cause thickening of the intima. When cholesterol, other fats, and inflammatory cells, such as white blood cells, enter the proliferating, thickened intima, the result is an atherosclerotic plaque. Then, as these plaques grow, they accumulate scar (fibrous) tissue and abundant calcium. (Calcium is the hard material in our teeth and bones.) Hence, the plaques are often hard, which is why atherosclerosis is sometimes referred to as "hardening of the arteries."

According to medical studies, 50% to 75% of people survive their first heart attack Others die during the heart attack because the decreased coronary blood flow causes a severe abnormal heart rhythm or extensive death of heart muscle. Figure 4 shows the heart of a patient who died 5 days after a heart attack. The photos show his myocardial infarction as it appears on the surface of the left ventricle and when the heart is sliced to view the muscle wall. About 90% of myocardial infarctions involve only the left ventricle (LV), which pumps oxygen-rich blood that comes from the lungs to the entire body. The other 10% also involve the right ventricle (RV), which pumps the blood to the lungs. Figure 4: Myocardial Infarction Caused by Heart Attack; Views of Heart Surface and Slice Across Heart Picture of Myocardial Infarction Caused by Heart Attack If a person survives a heart attack, the heart muscle may return to normal or become a region of dead heart muscle (the myocardial infarction). The amount and health of the remaining heart muscle is the major determinant of the future quality of life and longevity for a patient after a heart attack. A heart attack can interrupt the normal electrical wiring of the heart, leading to abnormal heart rhythms. The heart attack can also weaken the pumping action of the heart causing shortness of breath due to heart failure. Each of these complications of a heart attack can occur at any time during the recovery period as a result of dead, dying, or scarring heart muscle.

A heart attack is a layperson's term for a sudden blockage of a coronary artery. This blockage, which doctors call a coronary artery occlusion, may be fatal, but most patients survive it. Death can occur when the occlusion leads to an abnormal heartbeat (severe arrhythmia) or death of heart muscle (extensive myocardial infarction). In both of these situations, the heart can no longer pump blood adequately to supply the brain and other organs of the body. Almost all heart attacks occur in people who have coronary artery disease (coronary atherosclerosis). So, this photo essay will review the structure (anatomy) of the normal coronary artery, the structural abnormalities (pathology) of the coronary artery in atherosclerosis, and the effect of these abnormalities on the heart.

Most adults in industrialized nations have some plaques (atherosclerosis) on the inner (lumenal) surface of their coronary arteries. Autopsy studies of young soldiers who died in World War II, the Korean War, and the Vietnam War showed that even young adults in their 20s usually have coronary arteries that exhibit localized (focal) thickening of the intima. This thickening is the beginning of intimal proliferation and plaque formation. The distribution, severity (amount of plaque), and rate of growth of the plaques in the coronary arteries vary greatly from person to person. Figure 2 shows a coronary artery with an uneven (asymmetric), stable atherosclerotic plaque. A stable plaque may grow slowly, but has an intact inner (lumenal) surface with no clot (thrombus) on this surface. Figure 2: Coronary Artery with Stable Atherosclerotic Plaque; Cross-sectional Microscopic View Picture of Stable Atherosclerotic Tissue Rupture of a stable plaque in a coronary artery is the initial pathological event leading to a heart attack. When the rupture occurs, a clot suddenly forms in the lumen (channel) of the artery at the site of the rupture. Bleeding into the plaque often accompanies the rupture. The clot then blocks (occludes) the artery and thereby decreases the blood flow to the heart. This sequence of events in the coronary arteries is the basic problem in over 75% of people who suffer a heart attack. In some patients, more often women, there is just an erosion or ulceration of the plaque surface, rather than a full rupture that leads to clot formation in the coronary artery. Figure 3 shows an atherosclerotic plaque rupture and a clot in a coronary artery. Figure 3: Rupture of Atherosclerotic Plaque in Coronary Artery; Cross-sectional Microscopic View