Dear Ann Landers,
Be sure your mother-in-law knows you are talking to her. Get her attention before you start. Face her. All deaf people lip- read to a certain extent and gather clues from your facial expression. Speak SLOWLY and more dis-tinctly. Enunciate clearly. Don't slur word endings. Use your lips and your hands when explaining something. Get to the point. Like a good news story, explain first the what, who, when and where. Then go on and elab-orate as much as you wish. She needs to know what you are talking about. When there are others present, help her by saying, "We are talking about 'Cousin Joe,' " This will prevent her from interrupting with inappro-priate remarks. Raise your voice only when necessary. Shouting in her ear will only make her nervous. If she asks you to repeat, use a different key word. Instead of, "We bought a new car," say, "We just bought a new Chevrolet." If you have to say it again, do so graciously. She feels bad enough having to ask you to repeat. Just smile sweetly and think of the stars you are getting in your crown, dear. Signed DEAF ALSO DEAR ALSO: Thank you for making a solid contribution to this space today. The millions of hard-of-hearing will bless you. Heart dear readers: Within this "Heart" section there are two articles-"Coro-nary Arterial Disease and the Bypass Operation" and "Valvular Heart Disease and Valve Replacement"-written especially for this encyclopedia by my good friend Dr. Michael E. DeBakey, one of the world's most dis-tinguished heart surgeons. Both articles are totally incomprehensible to me. Unless you have had at least two years of medical school you will not be able to understand them ei-ther. In an attempt to simplify these articles, I sat with a medical dictionary in my lap for nearly two hours. Finally I gave up. There are no simple, lay terms for "atherosclerotic plaques" or "myocardial infarction" or "electrocar-diography" or a couple of dozen other words which are sprinkled generously throughout Dr. DeBakey's articles. I'm sure his brilliant descriptions of these two surgical procedures will be greatly appreciated by countless professors in medical schools who teach heart surgery, but for the average person, like you and me-forget it. Ann Landers Coronary Arterial Disease and the Bypass Operation The blood supply that nourishes the heart is derived from the coronary arter-ies, which are so named because they encircle the surface of the heart like a crown. There are two major coronary arteries, a right and a left, originating from the ascending aorta, which is the large, hoselike structure about one inch in diameter that carries oxygenated blood from the heart to the rest of the body. The fine network of vessels that arises from these coronary arteries serves as tributaries to feed the heart. In the average adult the lumen or bore of these arteries is about one eighth of an inch in diameter, and each hour about fifteen gallons of blood are pumped through them. The development of atherosclerotic plaques, which consist essentially in a localized deposit of fatty material and cholesterol within the inner layer of the arterial wall, is the major cause of coronary arterial obstruction. These atherosclerotic plaques may occur in any segment of the artery, but they are usually localized to the proximal part, the distal segments being relatively healthy. This characteristic of the disease is important with regard to the by-pass operation, as will be indicated later. As these atherosclerotic plaques en-large, they project further into the lumen of the artery and thus produce a narrowing or constriction of the lumen which, in turn, diminishes the flow of blood through the artery. When the lumen becomes so obstructed that an in-adequate amount of blood is available to support the needs of the heart mus-cle, myocardial ischemia results, a condition characterized by an insufficient supply of oxygen to the cells of the heart muscle. The victim may then expe-rience a form of discomfort in the chest called angina pectoris, often brought on by physical and emotional exertion. The attack may begin with a choking or constricting sensation beneath the breastbone which may then extend up into the neck and down the arm. If the obstruction in the coronary artery is sufficient to produce sudden occlusion, the patient may suffer a heart attack or in medical terms, a myocardial infarction, which means death of a part of the heart muscle. The amount of muscle damaged in this way varies consid-erably. In some patients it may be extensive enough to cause death. From 15 to 25 percent of patients who have such an infarction die. Most patients will fortunately survive the first attack. The diagnosis of coronary arterial disease can be readily made by a physi-cian after examining the patient and performing some relatively simple tests, including electrocardiography, exercise electrocardiography and possibly echocardiography. Some patients, however, may also require coronary ar-teriography. This test is done by inserting a catheter through an artery in the arm or groin and threading it into the ascending aorta to the origin of the coronary arteries. A radiopaque material is then injected through the catheter to make the coronary arteries visible in X-ray movies. By this means the pre-cise location and extent of the obstructive atherosclerotic plaques in the coronary arteries can be determined. This test is absolutely essential in con-sidering the possibility of surgical treatment. Most patients with coronary arterial disease can be adequately treated by medical means. Some patients, however, may require surgical treatment, as for example, those with severe, disabling angina not adequately controlled by proper medical treatment, whose disease is localized to the proximal seg-ments, who have relatively normal coronary arteries beyond the obstruction and whose left ventricular function is not too severely impaired. Surgical treatment may also be indicated in certain patients who are threatened with myocardial infarction, those who have had a previous myocardial infarction and severe obstruction of the left main coronary artery and those who require surgical correction of valvular heart disease or an aneurysm of the left ventri-cle. Certain forms of the disease are not amenable to surgical treatment, such as diffuse involvement of the coronary arteries, particularly if there is exten-sive narrowing of the distal arterial segments, and extensive damage to the muscle of the left ventricle resulting in poor left ventricular function. Age it-self is not a surgical deterrent since experience has shown that properly selected patients in their seventies and eighties who are in reasonably good condition may be successfully operated on. The procedure of choice in most patients requiring surgical correction is the bypass operation. It was first performed by us in 1964, and since then, literally thousands of patients have had the operation with increasingly better results. The operation is performed with the patient under general anesthesia and supported by the heart-lung machine. A segment of the saphenous vein, which is a large superficial vein in the leg, is removed for use as a substitute artery or vein graft in the bypass procedure. Since there are sufficient other veins in the leg to replace its function, its absence causes no circulatory dis-turbances in the leg. The heart is exposed through a midline opening in the breastbone. Since the coronary arteries are on the surface of the heart, it is relatively easy to identify the proper segment for attachment of the vein graft as determined by the arteriogram. An incision, about one-fourth inch long, is made in a reasonably normal segment of the coronary artery beyond the ob-structive process. One end of the vein graft is beveled and trimmed to fit the opening in the artery and then is attached to the edges of the incision in the coronary artery by a fine plastic suture. After this anastomosis, or attachment of the vein graft to the opening in the coronary artery, has been completed, a special partial occluding clamp is applied to the anterior wall of the ascend-ing aorta to pinch off and isolate a part of the wall of the ascending aorta. A longitudinal incision about one-fourth inch long is then made in this isolated or pinched-off segment. The other end of the vein graft is tailored to fit this opening and is attached to the edges by a fine plastic suture. After completion of this procedure, the partial occluding clamp on the ascending aorta is re-moved to allow blood to flow through the vein graft into the distal coronary artery. In this manner blood is shunted around the obstructing lesion and into the relatively normal coronary artery beyond the blocked segment- hence the term "bypass operation." Additional bypasses may be performed to other coronary arteries depending on the extent of the occlusive lesions. The results of the operation are excellent, insofar as relief of chest pain and restoration of the patients to relatively normal activity are concerned. In a recent analysis of our own experience, follow-up studies of patients five or more years after operation show that 92 percent are still living with excellent results and 80 percent have returned to work. Other medical centers have re-ported similar results. The risk of operation in most experienced medical cen-ters is now only about 1 to 2 percent. credit: Michael E. DeBakey, M.D., President, Chairman of the Cora and Webb Mading Department of Surgery; Director of the National Heart and Blood Vessel Research and Demonstration Center, Baylor College of Medicine, Houston, Texas; co-author with Antonio M. Gotto, M.D., The Living Heart, New York: David McKay Company. Heart Attacks and Sex Statistics on death during sexual intercourse are difficult to obtain. The sur-viving partner usually will not tell the truth and physicians signing the death certificate usually describe it as occurring during slgep. Nevertheless, Dr. George C. Griffith, University of Southern California cardiologist, believes the incidence is larger than believed and that cardiacs should receive medical counsel rather than a simple "take it easy." They should know there is greater risk too soon after eating or drinking. It is wise to wait three hours, Dr. Griffith said. A fatigued condition can be hazardous. The optimal time is in the morn-ing, followed by another rest period. Tension and fear have an impact. Coitus should take place in an atmos-phere of relaxation instead of under furtive, anxious conditions. Sex with a partner toward whom there is resentment can be hazardous. "Congenial partners who are accustomed to each other and whose tech-nique is habituated can achieve sexual satisfaction without great strain on the heart," Dr. Griffith commented in the journal Heart and Lung. "Mutual tenderness and intelligent co-operation lead to expressions of affection and relaxation." Eighty percent of the patients surviving a heart attack can resume their normal life, including coitus, within four to eight weeks, said Dr. Griffith. If there are complications, such as recurring pain, or abnormal heart rhythms or pump failure, then work on the job as well as sex activity must be denied for a time or severely curtailed, he said, adding, "The patient should report the following occurrences to his physician: (a) anginal pain that oc-curs during or after intercourse; (b) palpitation that continues for fifteen minutes or more; (c) sleeplessness caused by sexual exertion; and (d) marked fatigue during the following day." credit: Arthur J. Snider, Science and Medicine, Chicago Sun-Times. How the Heart Works for You MOST FEARED DISEASES A Gallup poll, the results of which were reported in 1977, representing the views of 1,600 people across the United States, revealed that the ailments most feared are: 2% 1% 1% 3% 0) (2) (3) (4) (5) 58% 21% 10% 2% 2% (6) (7) (9) Cancer Blindness Heart Disease Arthritis Polio Loss of Limb Tuberculosis Deafness Undecided These statistics were especially interesting when one considers that heart disease is the number-one killer in the United States-and has been since 1900. Consider the work of the heart. It normally beats anywhere from 60 to 100 times a minute (the average rate in adults is about 75 per minute). When you're excited, when you run or exercise your heart beat may get up to 180 per minute. On the other hand, if you're a trained athlete with an efficient cir-culation, it may beat as slowly as 45 or 50. Your calculator will tell you that this amounts to approximately 100,000 beats a day or 3.5 million heartbeats every year-and each contraction depends on every other part of your body. So for sixty minutes every hour, twenty-four hours every day and night as long as you live, your heart beats steadily-for a lifetime-without an oil change or the need to replace worn- out parts. Whatever goes wrong with the heart is due to disease-and has nothing to do with wear and tear. In fact, patients with heart trouble are often en-couraged to exercise. Do you know any man-made machine that can com-pare to this? Now here's the paradox. Even though the heart is one of the toughest and most durable organs of the body, it is nevertheless responsible for the greatest number of deaths in the "civilized" world. Why then, despite its strength, does heart trouble cause about 650,000 Americans to die every year? What is it that goes wrong? Most people don't really understand what heart disease is all about. Ask them, and they're apt to answer, "I have a condition. I take this little white pill every morning." In order for you to appreciate the kinds of cardiac trouble that may affect you, you must understand how the heart is put together and what it does. The heart muscle itself functions like a pump-and normally, a very efficient one. Its job is to deliver blood to every part of the body. The oxygen in this blood keeps us alive. The brain, kidney, liver, legs, the digestive tract, muscles-all require a great deal of energy (oxygen) to perform their life- controlling functions. They cannot tolerate more than a few seconds of inter-ruption in that blood supply. So even when we sleep, and all our muscles are resting and relaxed, the heart keeps pumping. The normal heart, about the size of your fist, contains two kinds of blood. There is the "used" blood from which oxygen has been extracted and to which waste products have been returned. This "used" blood is returned to the heart in order to be recirculated in the lungs, where its oxygen supply is renewed. Then, "fresh" blood, full of oxygen, is returned from the lungs to the heart, which pumps it to the rest of the body. To keep these two types of blood separated there is a wall down the middle of the heart, dividing it into left and right sides. Sets of valves within the heart result in upper and lower chambers on each side. These valves are re-sponsible for controlling the flow of blood within the heart. Two of them are situated where the blood exits from the heart. It is their job to make sure that none of it leaks back. To keep itself supplied with energy, the heart has its own arteries-the coronary arteries. There are three major ones and they penetrate the heart muscle, delivering oxygen to all parts of it. So there you have the basic structure of the heart-muscle, valves and ar-teries. The muscle pumps the blood, the arteries carry the energy for it to do so and the valves control the flow of blood in and out of the heart. A heart "condition" means that something has gone wrong with either the mus-cle, the valves or the arteries. Let's discuss each of these potential sources of trouble. THE VALVES When a heart valve becomes diseased, two things may happen to it. Either it doesn't open all the way (stenosis) or it fails to shut tight (regurgitation). (Often, stenosis and regurgitation occur together in the same valve.) When that happens, the heart muscle has to work harder. If the valve opening is narrow, the heart has to squeeze more vigorously to get all the blood out. If the valve leaks, some of the blood ejected from die heart returns to it when it shouldn't. This increased load or volume of blood stretches the heart. What-ever the valve disorder may be, the net result is cardiac enlargement. As this situation continues for years without treatment, the heart gets bigger and bigger. When it can no longer enlarge, it starts to get weak, and loses its abil-ity to eject all the blood within it. When that happens the heart "fails" (heart failure). Such valve disorders are occasionally congenital, that is, you're born that way. Or, they may become deformed during life because of some infection, the most common of which is rheumatic fever. Usually rheumatic fever oc-curs in childhood due to a streptococcus germ. In the usual course of events, the child has a bad strep throat. A few weeks later the joints become swollen and tender. Nobody thinks much about the heart at that point because car-diac symptoms are not usually apparent. Years later, after the "rheumatism" or "growing pains" have been forgotten, a heart murmur appears. Murmurs are due to the swirling of blood across a deformed heart valve. When the doctor examines your heart he can tell from the quality of the murmur, its location on the chest wall and its timing in the heart cycle which valve is involved and whether it is narrowed or leaking. Regardless of how the valve becomes diseased, it can now be replaced surgically with a new artificial one. If we don't wait too long, heart valve replacement can restore normal function. This is an excellent example of how a formerly important cause of death and disability has been overcome by medical research and progress. THE CORONARY ARTERIES These are a network of small blood vessels within the heart which supply the oxygen to keep it pumping. The process of arteriosclerosis, popularly called "hardening of the arteries," causes fatty deposits (or plaques) to form in their walls. This makes them progressively narrower until finally they close -very much like rust depositing over the years in water pipes. When one or more of these coronary arteries are narrowed, they may still provide enough blood to take care of your ordinary needs. But when the heart has to pump a little harder or faster, for example, when you're running, making love, digest-ing a meal or when you get excited at a sports event, the narrowed arteries cannot deliver the extra blood required. When it lacks enough oxygen, the heart signals you to stop what you're doing. That signal is pain, 'pressure or constriction in the chest, and is called angina pectoris. If you stop running or whatever else you are doing, the pain goes away. Remember then that the characteristics of angina are that it is induced by stress or exertion and relieved by rest. When the narrowed artery finally closes, and the blockage is complete, you are said to have sustained a "coronary occlusion." When that happens, in-stead of just crying out for a little more blood with the symptom of angina pectoris, a portion of the heart muscle actually dies. The death of muscle fol-lowing a coronary occlusion is called a myocardial infarction or heart attack. If the diseased artery is a large one and the closure sudden, the myocardial infarction may be big enough to interfere so drastically with the function of the heart that it may cause death. Whether the heart attack is mild, severe or fatal depends on the size of the involved coronary artery, the speed with which it closed and how much damage was sustained by the heart muscle. One reason some patients die and others survive after a heart attack has to do with something called "collateral circulation." Nature has provided us with a wonderful protective mechanism called "collaterals." When the blood supply to the heart is diminished because the coronary arteries are narrowed and diseased, tiny new vessels open up. As the months and years go by, these new smaller branches gradually take over the job of feeding the heart muscle and delivering its precious oxygen. Collaterals can be so effective that in some cases, when the final closure of the coronary arteries occurs, the collat-eral circulation is so highly developed that there may not even be a heart at-tack at all. The muscle is not deprived of oxygen and does not die. Coronary artery disease accounts for the major portion of heart trouble and death. But that's not something you're born with. We enter this world with wide-open coronary arteries. But then, we start eating the wrong food, smoking, gaining weight, worrying, sitting around instead of exercising and raising our blood pressure. As the years go by, we gradually pay for all this by depositing sludge in our coronaries. Later fat deposits develop and go on to become hardened plaques that narrow the coronary arteries. These plaques are made up mostly of cholesterol and there is a definite relationship between how much cholesterol we have flowing in our arteries and the extent and severity of these plaques. Because of this, most doctors try to keep your cholesterol level as low as possible. When young American soldiers killed in the Korean war in the 1950s were studied after death, it was found that many of these apparently healthy eight-een- and nineteen-year-old boys already had significant narrowing of their coronary arteries! Korean soldiers of the same age did not show evidence of this disease. The reason? Who knows for sure? Probably lifestyle and diet. HEART MUSCLE The end result of any trouble in the heart is weakening of its muscle. As you have seen, diseased valves can make it get bigger and thicker until it finally weakens and "fails." Similarly, narrowed coronary arteries deprive it of blood, damaging and weakening it. Another most important and treatable cause of heart muscle weakness is high blood pressure. When the heart has to pump harder to push its blood into the body's arteries against an increased resistance, the heart enlarges. Certain viruses can also attack the heart, hurt-ing the muscle too. On rare occasions, cancers originate in or spread to the heart. Whatever the mechanism, a damaged heart muscle ultimately becomes so weak that it cannot perform its critical function of pumping blood to the rest of the body. The organs dependent on it for energy are not properly nourished and stop functioning as they should. When the pump fails, blood backs up into the body since the weakened heart can't accommodate its re-turn. The lungs fill up with this extra blood and shortness of breath results. The feet and later the abdomen swell. The physical ability of the patient in heart failure is drastically reduced because his muscles aren't getting enough blood and the air in his lungs has been replaced by fluid. That gives you the spectrum of "heart trouble"-congenital (what you're bom with) and acquired (what strikes you) during your lifetime. Since we control most of the processes that make the heart large, such as high blood pressure, bad valves and infections, the main problem facing us today is to understand why the coronary arteries close up and how to prevent them from doing so. Even though we don't fully understand the mechanism by which this occurs, we know that certain "risk factors" are important, in that they ap-pear to speed up the disease. The most important of these risk factors are high blood pressure, cigarette smoking, cholesterol and triglyceride levels (blood fats), overweight, a sedentary lifestyle (lots of sitting and no exer-cise) and nervous stress. High blood pressure can be easily controlled these days-if you co-operate with your doctor and faithfully take the few pills he prescribes, reduce your salt intake, take off weight if you are too heavy and keep it off. In 1975 and 1976 for the first time there was actually a drop in the number of deaths from heart disease in the United States. We believe this was largely due to a nationwide campaign urging people to get their blood pressure checked. (Half the people who have high blood pressure do not know it because there are often no symptoms.) The relationship between cigarette smoking and lung cancer has been so strongly emphasized that we sometimes forget that tobacco is also very bad for the heart. I see so many patients with heart attacks in their forties. They are thin, have normal blood pressure and reasonable cholesterol levels. Even their family history is good. What did them in, in my opinion, was their twenty or more cigarettes a day. Smoking is bad enough, but in addition if you have high blood pressure and an elevated cholesterol, you're really in trouble. And don't seek comfort in the fact that pipes and cigars are "okay." They may not be as dangerous as cigarettes, but you're better off without them. Doctors are beginning to prac-tice what they preach in this regard. Most medical meetings prohibit smoking and thousands of M.D.s have kicked the habit. As a matter of fact, improved survival statistics among doctors in England are attributed to the fact that they have stopped smoking cigarettes. CHOLESTEROL What about cholesterol? It's true that all the evidence is not yet in with re-spect to what causes narrowing of the arteries, but we are certain that a high cholesterol at best doesn't help. In fact, it's looking more and more like re-ducing cholesterol is good for you, especially if you don't wait for your first heart attack to do it. Even if you enjoy good health, follow a prudent diet. Try to avoid an excess of food rich in cholesterol such as eggs, dairy prod-ucts, fat meat and shellfish. We've talked about prevention so far. What about the millions of people who have already been stricken with some form of heart trouble? They can slow down further progress of their disease by paying attention to the risk factors. Then there is an operation called the coronary bypass, in which the sur-geon takes a piece of vein from your leg and sews it onto the surface of the heart. This "bypasses" the blocked coronary arteries. Almost 100,000 pa-tients are submitting to this procedure every year in the United States alone. It eliminates or reduces angina in most cases. Whether it actually will prevent a heart attack or prolong life is still not known, although we hope it will do so. The operation is safe, the risk is somewhere between 1 and 2 percent, depending on where you have it done and by whom. Stay away from hospi-tals that do one or two operations a week. Practice makes perfect, and the centers which have teams performing this procedure frequently provide your best chance for success. This is no time for loyalty to your community hospi-tal. In one recent series done at a large medical center 89.6 percent of pa-tients who had bypass operations for angina were alive and well after five years. So what does all this mean in terms of how to conduct your life so as to avoid heart trouble? If you had rheumatic fever as a child, you should be ex-amined at regular intervals to see whether you have developed a murmur. You should have your blood pressure checked at least once a year. A normal reading taken anytime during life is not binding forever. You can develop high blood pressure weeks or months after a normal reading just as you can develop cancer, diabetes or any other disease at any time during your life. If there is a strong family history of heart disease (parents, brothers or sisters before the age of sixty) you should be alert to your own vulnerability. Don't start smoking. If you smoke now-stop. Keep yourself physically fit. Don't take an elevator to the mezzanine. Walk. Try to avoid unnecessary emotional stress. Change your job if you have to-or your wife or husband! Maintain ideal weight. Follow a prudent, low-cholesterol diet. If you develop pain, pressure, heaviness or constriction in the chest, don't assume it's indigestion because you had a big meal with lots'of wine. Check it out with your doctor. Remember that angina and "gas" are both relieved by belching. Finally, keep your eye out on the fruits of research and do everything you can to support it-out of your own pocket, at the community level and by keeping your legislators interested and committed. Medical research is big business-your business. It will bring us new life-prolonging advances only if we pay for it. We need answers to some vital questions and we need them now. The questions are: What narrows the coronary arteries and how? How can we have new, safer and more tolerable drug control for high blood pres-sure and disturbances in heart rhythm? What new surgical techniques can be developed to improve operative results in congenital and valvular heart dis-ease? How much longer must we wait for the artificial heart? How can we get everyone to stop smoking? What are the secrets of obesity and how can we control it? Answers to these and a host of other critical questions will mean that you and I will reach old age feeling and staying young. That's the heart of the matter. credit: Isadore Rosenfeld, M.D., Clinical Associate Professor of Medicine, Cor-nell Medical Center, New York; author of The Complete Medical Checkup, New York; Simon & Schuster. A HEART-ATTACK SURVIVOR WITH A DEATH WISH DEAR ANN: Will you please do a great many wives of heart-attack vic-tims a favor and find some answers for us? My husband, Ted, and several of his friends were lucky enough to survive severe heart attacks. Ted and two of his pals are now off their diets and even worse, they've started to smoke again. The other wives are ignoring it, but I feel as if Ted had slapped me in the face. Isn't he saying to me, "I don't give a damn what I do to you?" Could it be that he has a death wish? This man needs every ounce of oxygen he can get, and here he is wasting it on smok-ing. What should I do? Every time I see Ted smoke a cigaret something in-side me dies. The love and respect I had for him for over 30 years is slip-ping away. What can I do about it? HEART-SICK WIFE DEAR HEARTSICK: Not a dam thing. So quit eating yourself up, or he'll bury YOU. People who defy doctors' orders do indeed have a death wish. A person must want to live in order to give up smoking or drinking or eating things he shouldn't. To wives who are in your shoes, I say quit nagging. You can't in-ject a person with the will to live if he doesn't have it. Just keep yourself in good shape and make sure his life in-surance is paid up. Heart Transplants • In December of 1967 the first human heart transplantation operation was performed in Capetown, South Africa, by Dr. Christiaan Barnard. In January of 1968 transplantation of the human heart was first done after a decade of significant animal research at Stanford. It was believed that the patient could survive following the removal of the heart if the healthy heart of an accident victim whose brain was dead could be put in its place. With the worldwide publicity, it appeared to some that human heart transplantation would be the miraculous "cure" for all difficult cardiac prob-lems. Unfortunately, this is not (and never was) correct. The initial transplants were applied as a result of a variety of heart diseases -coronary arteriosclerosis (hardening of the arteries), valvular heart dis-ease, congenital heart disease, acute myocarditis, and cardiomyopathy of the idiopathic variety. Of the initial group of patients during the first two years of heart trans-plantation, survival was so infrequent that many respected physicians ex-pressed the opinion that heart transplantation should no longer be permitted. Frequent pronouncements were and are still being made that coronary artery bypass graft surgery has eliminated any need for transplantation. It is nevertheless a fact that certain cardiac patients deteriorate to a point where no conventional surgery will relieve the patient's symptoms. When the problems become so severe that the chances for survival are bleak, the pa-tient and his family often beg the doctor for a transplant operation. Unfortu-nately, not every patient is a good candidate for this kind of surgery; what's more, it is not a simple matter to obtain a heart for transplantation. Patients are selected for heart transplantation who have heart muscle dam-age with severe heart failure and low cardiac output. In 105 of the first 109 patients who underwent heart transplantation at Stanford University in 1968-1975 coronary artery disease or primary disease of the heart muscle contributed to the need for a "new heart." Patients with heart valve disease are not candidates for heart transplantation, and neither are patients with acute inflammation of the heart or congenital heart disease. There are three factors which rule out selection of a patient for heart trans-plantation and an additional three factors that weigh heavily against a deci-sion for transplantation. The first is a high pulmonary vascular resistance which would make it very difficult for the transplanted heart to pump against the poor condition of the small pulmonary vessels. A second is the presence of infection. Thirdly, a poor tissue match between the donor and the recipi-ent. When the difference in genetic types is great, the transplant often fails within the first few days or weeks. Patients older than fifty years of age have a difficult time surviving the complication of infection which almost always occurs in the transplantation of any kind of tissue. Individuals of advanced age are not promising prospects for heart trans-plants. Persons who have had a long-time history of heart disease with definite changes in the liver and kidneys are poor candidates for trans-plantation. Finally, the presence of acute pulmonary disease means a serious breathing problem, and this would rule out the transplant. One of the interesting points in considering the Stanford University experi-ence in heart transplantation has been the discovery that patients who have undergone previous heart surgery show a greater rate of survival following heart transplantation rather than to the contrary. Conventional thought would suggest that exposure to multiple transfusions during heart surgery would sensitize the patient to a subsequent tissue graft. This has definitely not been the case. Since so many patients are being presented for heart trans-plantation who had poor results with conventional cardiac surgery, the fact of increased survival is all the more intriguing. All patients are treated with immune suppressing drugs. Prednisone and azathioprine or cyclophosphamide are the ones more frequently used. Rabbit antithymocyte globulin is given in the form of injection by needle during the first eight to twenty-one days after transplantation-after which the sub-stance can be discontinued. One half of all deaths after heart transplantation are caused by infection. Aggressive diagnostic and therapeutic measures for infection must be used, and an intensified form of medical management is necessary to assure the survival of patients following cardiac transplantation. It is gratifying to note that patients are much less restricted after heart transplantation than, for example, after pacemaker implantation, when the heart rate is totally dependent on the pacemaker. Even though the trans-planted heart is without central nervous system control, there is a compen-satory mechanism for heart rate changes when the patient exercises, becomes frightened, walks stairs, makes love-the same as his own heart would do. Retransplantation of the heart is not only feasible, but at Stanford Univer-sity it has been applied in seven instances. Three of these patients are pres-ently living, and it is probable that retransplantation will become a standard feature in the long-range plans for select patients after cardiac trans-plantation. The usual period of hospitalization after heart transplantation is three months at a cost of approximately $40,000. Patients are seen and fully evalu-ated annually. X-ray studies of the coronary arteries in the donor heart are routinely performed at that time to rule out vascular disease in the graft. Since the transplanted heart has no nerves, patients do not experience angina pectoris (severe chest pains) in the presence even of significant coronary dis-ease in the transplanted heart. Currently, 50 of 124 patients at Stanford University Hospital are alive from eight years to one month after heart transplantation. Ninety percent of the patients who live one year after transplantation are fully rehabilitated. At present the patient following cardiac transplantation can expect a 65 percent chance for one-year survival and a 50 percent chance for a five-year survival. These figures are on the conservative side, but they do reflect rather accurately the prospects that patients have today following heart replace-ment. credit: Norman Shumway, M.D., Stanford University Medical School, Stan-ford, California. Valvular Heart Disease and Valve Replacement The valves of the heart serve the important purpose of maintaining the flow of blood through the heart chambers. There are four heart chambers, two on the right, termed the right atrium and right ventricle, and two on the left side, termed the left atrium and left ventricle. Between each of the chambers is a valve. Thus, between the right atrium and right ventricle there is a valve known as the tricuspid valve, and between the right ventricle and pulmonary artery there is a valve known as the pulmonary valve. On the left side is a valve called the mitral valve between the left atrium and the left ventricle and an aortic valve between the left ventricle and the aorta. The function of these valves may be better understood by following the circulation cycle beginning in the right atrium, which is the collecting chamber for blood returning from the body. As the muscle fibers of the right atrium contract, the squeezing mo-tion exerts pressure on the blood in the atrium, forcing the tricuspid valve to open and allow the blood to enter the chamber of the right ventricle. After the right ventricle is filled, the muscles of this chamber contract, and in this way exert pressure on the blood in the chamber, which causes the tricuspid valve to close. Since the tricuspid valve opens only one way, there can be no return of blood from the right ventricle to the right atrium. As the pressure mounts in the right ventricle, the pulmonary valve is pushed open to allow blood to be pumped into the pulmonary artery and into the lungs to be ox-ygenated. The pulmonary valve also opens only one way, and after the blood is forced through it and the right ventricle relaxes, the pulmonary valve closes; this prevents blood from returning to the right ventricle. The blood, which is then oxygenated in the lung, is returned to the left side of the heart and is collected in the left atrium. Contraction of the left atrium then forces open the one-way mitral valve to allow blood to flow into the left ventricle. After the chamber of the left ventricle is filled, its muscular wall contracts and the mitral valve closes; the resultant pressure on the blood in the cham-ber forces open the aortic valve, and this allows blood to be pumped into the aorta. After the left ventricle is emptied, it relaxes, with the result of greater pressure in the aorta than in the left ventricle, and this differential in pressure slams shut the aortic valve so that the blood is prevented from re-turning into the left ventricle. Normally, these valves are delicate, thin-walled and highly flexible structures that are in the form of two or three leaflets. The tricuspid valve is so called because it consists of three leaflets. The aortic valve also consists of three leaflets, but the mitral valve consists of two leaflets. Disease affecting these valves may be congenital or acquired. In congenital valvular disease the infant is born with the defect because the malformation occurred during the development of the fetus. The aortic and mitral valves are most commonly involved and usually result in partial or severe obstruc-tion to the flow of blood across the valve. Acquired forms of valvular disease may be caused by infections, such as rheumatic fever or bacteria in the bloodstream. In other cases the cause may not be determined. Most commonly affected are the mitral and aortic valves and less frequently the tricuspid valve. They may be affected singly or in combination. Damage to the mitral valve produces thickening and loss of pliability of the valve leaflets with fusion of the edges, contraction and in some instances cal-cium deposits. These changes cause the opening of the valve to become nar-row. This condition, known as mitral stenosis, produces obstruction of blood flow between the left atrium and left ventricle. The damage may also result in the inability of the valve leaflets to close, a condition termed mitral insuffici-ency. Whereas one or the other of these dysfunctions may be predominant, there is often an element of both. Somewhat similar changes may occur in the aortic valve and produce nar-rowing or stenosis with obstruction of blood flow from the left ventricle into the aorta, or they may cause such severe destruction of the leaflets that in-competence is produced. Here too there is usually an element of both types of dysfunction. The effect on heart function varies with the degree of the changes in these valves. In mild forms of the disease the heart may compensate adequately so that there is little disability. Most patients, however, suffer gradual and pro-gressive changes over a period of years with increasing disability and ulti-mately heart failure and death unless proper treatment is given. The diagnosis can be readily made by a physician after proper examina-tion, which may include cardiac catheterization, particularly if surgical treat-ment becomes necessary. Treatment may be medical or surgical depending on the stage of the dis-ease, the effect on the heart and the degree of disability. Surgical treatment is indicated in patients who have symptoms of early heart failure and in certain patients in whom complications develop, such as the breaking off of a piece of blood clot in the left atrium, which then is swept into the bloodstream to lodge in a peripheral artery. This complication is called embolization. In ad-dition, surgical treatment may be indicated in some patients with aortic valvular disease without symptoms but with evidence of progressive disease and a strain developing on the left ventricle. Surgical treatment of mitral valvular disease consists in repair or replace-ment of the valve, depending on the extent of damage. In certain types of mi-tral stenosis, for example, in which the valve leaflets are not badly damaged and are still pliable, it may be possible to repair the valve by separating or di-viding the fused edges. This is preferably done by supporting the patient on the heart-lung machine to allow the surgeon to make an opening in the left atrium and thus permit direct vision of the mitral valve. This enables an ac-curate assessment of the damage and a more precise technique for dividing the fused edges. Most cases, however, require removal and replacement of the damaged valve. Most heart centers such as ours use an artificial valve, al-though a few surgeons prefer to use a heterograft valve (one taken from an animal, such as a pig). Great improvements have been made in artificial valves during the past decade, and a number of different types have been de-veloped, most of which use the ball-valve principle. The ball itself, however, may be in the form of a disc, especially when designed for mitral or tricuspid valvular replacement. In this type of valve the ball or disc is enclosed in a cage consisting of three or four wired struts with an opening at the bottom somewhat smaller than the ball or disc so that the opening is closed when the ball or disc is seated on it. With an increase in pressure on the inflow side of this opening, the ball or disc moves into the cage so that blood flows around it. With the drop in pressure that occurs in the next phase of the heart's cycle, the ball or disc drops back against the seat of the opening and prevents blood from flowing back. Thus, the artificial valve functions like the normal heart valve in having a one-way opening and thus maintaining unidirectional flow of blood through the heart. The operation is performed with the patient supported by the heart-lung machine to permit the surgeon to make an opening in the left atrium to ex-pose the damaged mitral valve, which is excised. Sutures are then placed cir- cumferentially in the edges of the excised valve and are then passed through the sewing ring (made of Dacron) at the base of the artificial valve. The valve is then seated into the annulus, and the sutures are tied to firmly attach the artificial valve to the annulus. The sutures are then cut, and the opening in the atrium is closed. The operation for aortic valvular replacement is per-formed in a similar manner except that the aortic valve is exposed through an opening in the ascending aorta just above the valve. Tricuspid valvular re-placement is also performed in a similar manner except that the valve is ex-posed through an opening in the right atrium. The surgical risk for these operations ranges from less than 5 percent to about 15 percent, depending on the degree of heart damage and the general condition of the patient. Most patients can resume normal activities, and long-term results extending for more than ten years are quite good. credit: Michael E. DeBakey, M.D., President, Chairman of the Cora and Webb Mading Department of Surgery; Director of the National Heart and Blood Vessel Research and Demonstration Center, Baylor College of Medicine, Houston, Texas; co-author with Antonio M. Gotto, M.D., The Living Heart, New York: David McKay Company. Help Where to Go to Get It Bamum was right when he said, "There's a sucker bom every minute." And I say there are two to take him. I know because the victims have been writ-ing to me every day for over twenty years. Ann Landers receives approximately seven thousand letters a week from readers who represent every conceivable socio-economic group. They live on suburban estates and in the city slums. My correspondents are from 6 to 110 years of age. They are double-dome intellectuals and borderline morons. Al-most half of the letters come from men. Every bag of mail contains at least 150 inquiries that drive me up the wall. "How can they be so stupid?" I ask myself. And then I answer the question. It's not merely stupidity. It's often a combination of desperation and wishful thinking that wipes out all reason and common sense. I become furious at the exploitation of these good people whose only crime is ignorance and vulnera-bility. Here are some examples that crossed my desk just this week: