Silent and not-so-silent heart attacks – HeartBeat
Cory SerVaas
Recently, a reader asked about “silent” heart attacks, a common but, unfortunately, little-understood health threat to Americans. She wrote, My husband’s doctor told him he ma have had a silent heart attack. Now, my husband is always reading about heart attacks, and I say, why should he worry if it didn’t hurt him.”
Just because her husband’s possible heart attack was painless doesn’t mean his heart muscle was undamaged by it. Signs of damage may be revealed by an EKG and other medical tests, and treatment can be started. Some silent heart attacks are so painless that patients may not recall even minor chest pain or other symptoms. This article makes a case for the benefits of knowledge for preventing disasters of the heart. Heart catastrophes occur when the heart muscle is deprived of oxygen, and often this happens when blood vessels have been blocked. Blood clots are the most common cause of such blockage, and they are most likely to occur in vessels already clogged with cholesterol plaque. This block may be total or only partial. Sometimes as a result of stressful situations, coronary vessels may be temporarily constricted, causing the inside diameter of the vessels to be diminished. As a result of limited blood flow through coronary vessels, part of the myocardial muscle may be damaged. When an afflicted area is large, the patient has classic symptoms of a severe heart attack. When the arterial block is not complete, the oxygen-starved heart area will not be large, and clinical symptoms may be almost imperceptible. This type of heart attack is called a silent heart attack. Even after heart attack damage is revealed by an EKG, patients may not recall experiencing any discomfort. Others diagnosed with heart damage remember various symptoms that may have signaled the attack, but at the time they chose not to consult their doctors because they wanted to believe these symptoms were not heart related. (Their reasoning: “Maybe it was only a touch of indigestion; maybe it had been just a little stuffy in the room.”) Some estimate that 20 to 30 percent of all heart attacks are silent; other experts feel that as many as 60 percent of all heart attack victims do not realize what has happened. As our reader suggests, such ignorance may be less worrisome to her and her husband. But if ignorance is bliss, knowledge will help one live longer.
The outlook for those who have suffered silent heart attacks can be as serious as for those who have had more painful attacks. However, after a silent heart attack a patient can vastly improve the odds of enjoying the golden years by seeking medical treatment.
The classic symptoms of a heart attack (the medical parlance is “myocardial infarction”) appear unexpectedly. Commonly, the first sign is a burning pain in the chest. Then, the pain often radiates out to the abdomen, upper arms and shoulders, or even up into the neck and jaw. The pain may be stabbing, constricting, or crushing. Pain is often accompanied by nausea or vomiting, shortness of breath, weakness, dizziness, or a cold sweat. Any or all of these symptoms may occur–or none of them.
A pain that lasts only a few seconds is generally not heart related and may be, as many people would hope, merely a mild stomach upset. If pain seems to come and go with shifts in posture or with especially deep breaths, it’s probably not cardiac in nature. If discomfort is eased by lying down or taking a few sips of water, again, it is probably not a heart attack.
But cardiologists will tell you: Don’t wait to find out. If you suspect you might be having a heart attack, go to the hospital immediately. Get someone to drive you, or call an ambulance. Minutes count in getting such drugs as TPA started at the hospital or in the ambulance. TPA is an enzyme which, when injected immediately after a thrombosis, can dissolve the clot and lessen the damage to the heart muscle. While waiting for an ambulance or an automobile, the patient should be placed in a horizontal position with collar opened and constricting clothing released.
By its very nature, the silent heart attack is much harder to detect and thus to treat early in the important post-heart-attack period. And in many instances, doctors struggle against the patient’s understandable but ultimately unhealthy desire to deny the problem.
Daily aspirin is advised for those who have had either a silent heart attack or a painful one. Landmark medical trials strongly confirm that aspirin does have a therapeutic value in the prevention of recurrent attacks in both groups. Aspirin is a “thrombolytic agent” (from thrombus,” meaning a blood clot, and “lysis,” meaning to dissolve), which means that it helps break down and dissolve any blood clots that may form in the coronary artery and eventually lead to a kind of heart attack called a coronary thrombosis.
Regular aspirin taken daily on a preventive basis could irritate the lining of the stomach and perhaps lead to stomach ulcers. But newly developed delayed-release tablet coatings delay digestion of the aspirin tablet until it has passed through the stomach and entered the small intestine.
Patients with unstable angina have also been shown to have better prognosis when aspirin was prescribed. Patients with stable angina have chest pains with exercise or during other conditions in which myocardial oxygen demand is increased. Individuals with unstable angina may also have pain at rest; the pain lasts for longer periods, and it becomes more difficult to relieve.
And Dr. T. J. Hartney of the Medical College of Georgia reported: “Unstable angina is associated with a high risk of progression to acute myocardial infarction…. Two completed randomized, double-blind, placebo-controlled trials have established aspirin’s effectiveness in patients with unstable angina. The Veterans Administration Cooperative Study administered 324 mg of buffered aspirin solution [per day] to 1,266 male patients for 12 weeks, starting within 48 hours of hospital admission. A significant 51% lower incidence of death or acute myocardial infarction was noted. The frequency of non-fatal myocardial infarction was also reduced 51%. These results compare favorably to the Canadian Multicenter Trial.”
At this time, the jury is still out as to whether aspirin should be used as a prophylaxis, perhaps as little as 80 mg twice per day, for some persons who aren’t heart patients. Only a patient’s physician should help make the determination whether daily aspirin should be used, and the quantity.
But everyone should be responsible for some basic prophylactic measures in an effort to remain as heart healthy as possible. This is particularly important for those with a family history of heart attack or stroke. Our list includes: (1) follow an exercise program as approved by your physician; (2) use no tobacco; (3) learn as much as you can about saturated and unsaturated fats in your diet, as well as soluble and insoluble fiber; (4) know your total cholesterol level and your HDL and LDL fractions; (5) monitor your blood sugar for signs of diabetes; (6) have your doctor check your blood pressure regularly; (7) discuss with your doctor the latest research in aspirin therapy and whether you should be taking it; (8) ask your doctor whether you’re a candidate for magnesium supplementation. Magnesium is a biologically essential element that has recently received much attention in cardiology circles. “Decreased magnesium stores [in the body’s cells] have been implicated in the development and complications of atherosclerosis, myocardial infarction, hypertension and dysrhythmias,” wrote Dr. Michael Ralston recently in Circulation, a journal read by cardiologists.
A new method for finding the correct amount of intracellular magnesium is an important recent research development because serum magnesium tests aren’t accurate enough. This is partially because less than one percent of the magnesium in the body is in the blood serum-the rest is in the cells of the bones, the muscles and other soft tissues, and other body fluids.
Dr. Barry Crevey, associate professor of internal medicine at Indiana University and clinical cardiologist at Indianapolis’ Methodist Hospital, is interested in research on magnesium supplementation for possible prevention of heart attacks caused by arrhythmias.
He told us, “Magnesium is essential for normal muscle functions, and muscle is rich in magnesium. Virtually every patient who has any significant amount of heart failure will be on diuretics, and they are set up for hypomagnesemia [low magnesium levels in the blood]. So we now see a new area of interest in cardiology where physicians are focusing on treating heart failure-not just arrhythmias, but heart failure itself-trying to improve the muscle function and pump function by administering magnesium.”
For the past decade, Dr. Mildred Seelig has been telling us about the need for magnesium by athletes and her belief that unexpected heart attacks in healthy athletes may be caused by arrhythmias brought on by magnesium depletion. In the early 1980s she told us, “East bloc countries have been giving their athletes magnesium for some time as it is felt it also improves muscle function and endurance.”
To the best of our knowledge, magnesium supplementation was not being used by U.S. athletes at that time.
But Dr. Crevey told us, “A lot of attention is now being directed toward athletes, and magnesium repletion has become a very important part of almost all training programs. Athletes as a group tend to run low in intracellular magnesium-probably for a variety of reasons, and it is not just perspiration. Athletes are using large muscle groups, and magnesium is an integral part of muscle function.”
Dr. Crevey is a runner. We asked him the crucial question: “Do you take supplemental magnesium?” He does. He told us he takes enteric-coated magnesium chloride daily.
Dr. Crevey was the first to tell us about a new test for measuring intercellular magnesium. He learned about it at a meeting of the American Heart Association in New Orleans last fall:
They scrape some cells from beneath your tongue and place them on a slide. The slide is sent off to a lab, where it is run through a machine that basically uses X-ray defraction to measure the amount of magnesium in the cells. It’s just amazingly accurate. I really think you’re going to see all sorts of new things happening now in terms of magnesium. In fact, when I was there, they ran this on me. They were doing it for all the cardiologists. My magnesium turned out to be terribly low, which is typical for runners. So I put myself back on Slow-Mag. I am having myself tested again here in another few weeks. I feel terrific.
“One wonders why we didn’t catch on to this sooner,” Dr. Crevey said. “As you know, people who take certain kinds of diuretics often have loss of potassium, and many, many Americans are on diuretics and are taking potassium supplements. This is extremely common. But at the same time, the diuretics cause a loss of magnesium, and this works in several ways. It turns out that almost anything that causes the loss of potassium will tend to promote magnesium loss. It also turns out that diuretics will cause the loss of magnesium independent of potassium, so the two of these work together to lead to a substantial magnesium loss. And for years we’ve had patients where we’ve had great difficulty maintaining their potassium, and then when we did maintain the potassium they would still have lots of trouble with arrhythmias, rapid irregular heartbeat. Now that the role of magnesium is becoming more clear, we find that when we supplement many of these patients who have advanced heart disease-patients who are on powerful diuretics, who have a tendency to lose potassium-their arrhythmias have become much easier to control. Some of the responses here have been positively dramatic.
“This [interest] began years ago when we would use magnesium intravenously, in the hospital setting for someone who was having recurrent, very, very serious arrhythmias that many times were intractable, and within half an hour of giving magnesium everything would just quiet down. Now we begin to see the same thing, although drawn out over a longer period of time, when magnesium is given orally, and in many of these cases the serum magnesium is normal, both before and after we give it, so we have to assume that what we’re doing is raising the magnesium levels in the cells themselves. in fact, in many cases we don’t even bother to check the magnesium anymore; it’s just become a standard supplemental addition to someone taking diuretics.”
We asked Dr. Crevey if he thought the new test would soon be available t doctors to check intracellular magnesium levels on all their patients taking diuretics. He told us: “The machine would very quickly become overwhelmed, given the number of specimens that are potentially out there. And that’s why it will be important to have more of these machines and for them to become less expensive and easier to use. But we don’t test the potassium levels of all the patients on diuretics, yet we routinely put them on supplemental potassium. I think we should put them on magnesium on the same assumption.
“I think the addition of magnesium chloride to the armamentarium has done a great deal to popularize the routine use of magnesium. It is well-absorbed by virtue of the fact that there is chloride traveling along with the magnesium. Virtually all of the magnesium that is absorbed is absorbed in the intestine; very little is absorbed in the stomach. It comes right across the intestinal tract and is absorbed better than just about any other magnesium preparation.”
We asked Dr. Crevey about the advisability of supplementing magnesium intake for patients who consume large amounts of alcohol, to which he replied: “If one traces the awareness of magnesium in medicine, one finds that very early on, physicians knew that alcoholics do have trouble with low magnesium, and most young physicians learned early on to check the blood level in people who have high alcohol consumption. Often the blood level is low, but as we’ve already learned, if one has an obviously low blood level, one can pretty well deduce that one has an even lower cellular level. So the upshot is that alcohol very definitely leads to magnesium loss, both in the short term and in the long run.”
Dr. David Lauler explained, “In patients with acute and chronic alcohol abuse, magnesium depletion occurs by osmotic diuresis induced by excreted alcohol molecules, that remove magnesium ions as part of the osmotic diuresis. The same phenomenon of osmotic diuresis is thought to play a role in the magnesium depletion that occurs in diabetic patients with overt glucosuria [glucose in the urine].”
We asked Dr. Crevey if he felt the magnesium loss from alcoholics’ diuresis was more important than the malnutirition in this group.
“You often read about that,” he said. “But even if alcoholics have good nutrition, they often have low magnesium. I daresay that most of us as cardiologists have a lot to learn about the average American diet. Magnesium is found in dark green leafy vegetables, and many individuals don’t eat enough of those. To make the situation even worse, the modem cultivation practices often lead to a loss of magnesium. And most people today who live in areas where water is hard will opt for some kind of water softener. Water softeners are notorious for causing a relative loss of magnesium.” Dr. Richard Reinhart concurred: “The softening of ‘hard’ water removes variable quantities of magnesium and may contribute to reduced intake of magnesium.” He added, “Dietary intake of magnesium in the United States may be less than the recommended amount, leading to a frank or borderline state of hypomagnesemia in much of our population.”
The suggestion of a magnesium deficit in ischemic (lack of oxygen due to clogged vessels) heart disease patients is supported by Danish studies, which show that muscle and blood lymphocyte (white blood cell) magnesium concentrations are low in ischemic (lack of oxygen due to clogged vessels) heart disease patients.
Diabetics suffer from more heart attacks than nondiabetics do. When we asked Dr. Crevey about that, he explained as follows: “We know that the magnesium ion has a strong effect on blood vessels. It tends to cause vasodilation; that is, the relaxation of blood vessels. So a magnesium deficit tends to cause the opposite, which would be a constriction of blood vessels.
“In fact, magnesium, given intravenously, is a time-honored treatment for eclampsia, which is a condition in pregnancy characterized by extremely high life-threatening blood pressure. I’m sure you gave plenty of magnesium in your training to women who were suffering from eclampsia to bring the blood pressure down and keep it down, and that’s still being used.”
A great deal of research is going on involving the efficacy of magnesium supplementation as a nonphamacologic means of controlling blood pres, sure in hypertensive patients. The jury is still out while we wait for the research results.
In the meantime, Dr. R. B. Singh, in Acta Cardiologica, has recently suggested that a &et rich in magnesium may be used for prevention of hypertension in predisposed communities because of the other advantages of such a diet.
Dr. Lauler reported in the American Journal of Cardiology, “Clinical and research evidence continues to accumulate that magnesium deficiency likewise contributes to triggering ventricular ectopic activity and sudden cardiac death. The magnesium ion is emerging as a premier cardiovascular cation.” According to Dr. Lauler, “The most frequent causes of magnesium depletion in cardiovascular medicine are diuretic drugs. Other causes of magnesium depletion include impaired intestinal absorption, chronic diarrhea, renal loss due to diabetes, alcohol abuse, and excessive sweating.” Dr. Sandvad Rasmussen of Denmark reported an interesting double-blind, placebo-controlled study in the May 1989 Archives of Internal Medicine. Forty-seven patients with ischemic heart disease and acute myocardial infarction were given three months of treatment with oral magnesium or a placebo. Before, during, and after the patients’ treatment, blood samples were taken to determine their serum concentrations of cholesterol; triglycerides; and high-density, low-density, and very low-density lipoprotein levels. Triglycerides, and thereby very low-density lipoprotein concentrations (the very bad cholesterols), decreased by 27 percent after the magnesium treatment as compared with much smaller decreases in the placebo group. Likewise, the researchers found tendencies toward an increase in high-density lipoprotein cholesterol (the good cholesterols that lessen one’s heart attack risk) after the magnesium treatment.
Dr. Edmund Flink of the University of West Virginia found that during hypomagnesemia (low magnesium blood level) the concentration of free fatty acids (FFA) in the blood is elevated. This is important because elevated FFA levels cause an increase in the oxygen need of the myocardium (heart muscle).
“All this information indicates that hypomagnesemia is accompanied by lipid metabolism disturbances, which lead to pathological changes of blood vessels,” Dr. Flink said.
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