There are many kinds of heart disease, and they can affect the heart in several ways. But the ultimate problem with all varieties of heart disease is that, in one way or another, they can disrupt the vital pumping action of the heart.
Coronary Heart Disease (CHD) is not a single disease, but a complex of diseases of varied etiology. Some of the recognized causes of heart disease include damage to the heart muscle or valves due to a congenital defect; or to inflammation and damage associated with various viral, bacterial, fungal, rickettsial or parasitic diseases. Rheumatic fever or syphilis can lead to heart disease, as can genetic or autoimmune disorders in which cellular proteins in the heart muscle are deranged or which disrupt enzymes affecting cardiac function.
These factors probably contributed to most cases of heart disease recorded in the early part of the century, when rates of infectious diseases were much higher and antibiotics were not in use. Nevertheless, heart disease was relatively rare in 1900, accounting for approximately 8 percent of all deaths in the US.
But by 1950, CHD was the leading cause of mortality in the US, causing more than 30 percent of all deaths, and the figure has been climbing ever since. Today CHD accounts for about 45 percent of all deaths. The incidence rose most precipitously between 1920 and 1960. Since that time, mortality rates from CHD have declined somewhat. This means that victims of heart disease are living longer, due most likely to improved surgical techniques, the advent of angioplasty and the use of anti-clotting drugs given to heart attack victims. But the morbidity rates—the incidence of heart disease—continue to rise, although at a lower rate than before. Of greatest concern is the high rate of heart disease in American men between the ages of 45 to 65—during the period of greatest family and career responsibilities.
The interesting thing is that most cases of heart disease in the twentieth century are of a form that is new, namely heart attack or myocardial infarction—a massive blood clot leading to obstruction of a coronary artery and consequent death to the heart muscle. Myocardial infarction (MI) was almost nonexistent in 1910 and caused no more than 3,000 deaths per year in 1930. Dr. Paul Dudley White, who introduced the electrocardiograph machine to America, stated the following during a 1956 American Heart Association televised fund-raiser: "I began my practice as a cardiologist in 1921 and I never saw an MI patient until 1928." By 1960, there were at least 500,000 MI deaths per year in the US. Rates of stroke have also increased and the cause is similar—blockage in the large arteries supplying the brain with blood.
The factors that initiate a heart attack (or a stroke) are twofold. One is the pathological buildup of abnormal plaque, or atheromas, in the arteries, plaque that gradually hardens through calcification. Blockage most often occurs in the large arteries feeding the heart or the brain. This abnormal plaque or atherosclerosis should not be confused with the fatty streaks and thickening that is found in the arteries of both primitive and industrialized peoples throughout the world. This thickening is a protective mechanism that occurs in areas where the arteries branch or make a turn and therefore incur the greatest levels of pressure from the blood. Without this natural thickening, our arteries would weaken in these areas as we age, leading to aneurysms and ruptures. With normal thickening, the blood vessel usually widens to accommodate the change. But with atherosclerosis the vessel ultimately becomes more narrow so that even small blood clots may cause an obstruction.
The other half of the MI equation is the blood clot or thrombus that blocks blood flow to the heart or brain. Thus, any search for the causes of heart disease must consider complex factors in the blood that promote clotting at inappropriate times, that is, other than in response to bleeding from a rupture or wound. In fact, while a great deal of attention has been focused on the cause and solution to atherosclerosis, the role played by clotting factors in the blood has been relatively neglected. Yet a heart attack due to a clot can occur even in the absence of arterial blockages.
Inflammation may also cause blockages. In fact, a new view of coronary artery disease is that it is an inflammatory process, characterized by cycles of irritation, injury, healing and reinjury inside the blood vessels.1 The inflammatory response is actually a defense mechanism that helps the body heal but when the inflammatory process goes awry, plaques may rupture, provoking clots that lead to heart attacks.
The health and integrity of the blood vessel walls is another factor that must be considered. Aneurysms, the dilation and rupture of blood vessels due to weakness in the vessel walls, will naturally provoke a clotting response, not to mention the more immediate danger of rapid blood loss. In addition, biochemical imbalances in the smooth muscle cells may result in spasms that can be just as effective as a blood clot in cutting off blood flow to the heart.
Finally, arrythmias—abnormalities in the rhythm of the heart's pumping mechanism—can lead to interrupted blood flow, oxygen starvation of the heart muscle or complete shut down of the heart—the so-called cardiac arrest. Regulation of the nervous impulses that govern the heart depends on a large number of factors—from mineral status to the integrity of the myelin sheath.
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