Iknow what you’re thinking. I’ve just extolled the virtues of that magnificent biological pumping machine (with built-in redundancy) that we call the human heart. So why are there so many heart attacks? According to the latest figures from the Centers for Disease Control (CDC), approximately 1.5 million heart attacks and related strokes occur every year in the United States, and more than eight hundred thousand people die each year from a “failed heart” caused by cardiovascular disease.
That’s a lot of heart problems.
So, why does it happen? The short answer is that there are many reasons why heart attacks happen. Practically speaking, however, the vast majority of heart attacks have one simple cause: not enough blood is flowing through one or more of the coronary arteries. In most instances, the flow is blocked by fatty deposits in the coronary arteries that build up at an extremely slow rate, thickening and hardening the arteries, causing atherosclerosis (or arteriosclerosis). The accumulation of this porridge-like material first narrows and then eventually may completely block the coronary arteries.
A heart attack occurs, as a rule, only when the artery becomes completely blocked. But it has become quite clear in recent years that major problems can arise even when the arteries are only minimally or moderately narrowed by the atherosclerosis. Oxygen starvation of the heart is the most important cause of angina (chest pain), the death of heart tissue (“heart attacks”), malfunctions of heart rhythms (palpitations or “skipping” of the heart), and sudden death.
Completely silent (painless) episodes of heart oxygen starvation may occur anytime, even at the beginning of the atherosclerotic process, when the fatty material is just beginning to be deposited in the coronary arteries and even though significant blockages have not yet developed.
Silent heart attacks are by definition painless or at least free of the classic symptom (a gripping pain in the chest). The undetected transient or momentary decrease of coronary artery blood supply that causes a silent heart attack may last for only a few seconds or, on the other hand, for many minutes or even hours.
For obvious reasons, cardiologists and pathologists in past years have focused only on atherosclerotic blockage of the coronary arteries as the principle cause of heart attacks, malfunctions of heart rhythms, and/or sudden death. In fact, obstruction of the blood flow in the coronary arteries by atherosclerotic fatty deposits was, and still is, considered to be the single most important cause of these events. But scientific evidence is forcing doctors to go beyond the concept of simple narrowing or blockage of a coronary artery to that of a more dynamic and complex process being responsible for most coronary heart problems.
Both silent and painful coronary heart problems are caused by narrowing or complete blockage of the coronary arteries resulting from various permutations and combinations of intermittently active narrowing of the muscular coronary artery wall in regions of fixed arteriosclerotic plaque. In other words, if the lumen (passageway) of a coronary artery has been narrowed to, say, 70 percent of its normal size by a cholesterol plaque, it may be yet further narrowed (or completely closed) by spasm of the arterial wall itself or by an unpredictable and intermittently increased tendency for rapidly flowing blood to clot in certain key locations in the heart chamber or in the coronary arteries.
Episodes of poor coronary artery blood flow, or ischemia, in silent heart disease, are totally symptom-free (no pain or other warning sensations) in at least three out of four instances. In virtually all cases the telltale signs of a painless heart strain or attack are detectable even in these very early stages with relatively simple tests.
I’m reminded of a patient of mine—a famous Hollywood actress—who was convinced that she was not a candidate for silent heart disease, even though she had several risk factors that indicated otherwise. I knew her socially, so finally after much cajoling, I convinced her to visit my office at the Southern California Cardiology Group in Beverly Hills. By the time her exam was over, it was clear she was suffering from silent heart disease and had already had several silent (painless) heart attacks. She was on the verge of a massive, and potentially fatal, heart attack. When I showed her the results of her diagnostic tests, she could hardly believe her eyes, but at last she was convinced of the danger. She immediately embraced a treatment regimen specific to her medical condition and risk factors. I’m happy to report that she continues today to pursue an active career in film and television.
The point here is that early discovery of ischemia, especially in the symptom-free individual, is terribly important since the person may never know that she or he is afflicted with heart disease until an acute heart attack or failure. In fact, sudden death may be the first sign of a heart problem in many unfortunate cases. Because physicians in the past have relied primarily upon angina (chest pain) to alert them to the onset of significant coronary heart disease, the true onset of meaningful heart disease has frequently not been detected during the smoldering days, weeks, or years prior to the onset of symptoms or the occurrence of sudden death.
When Jim Fixx first took up running, he was an overweight magazine editor who smoked two packs of cigarettes a day. In the first race he ever ran, when he was thirty-five years old, he came in last in a field of fifty runners with a sixty-year-old man handily beating him. Still, he famously did not give up and went on to write a book that helped to launch the fitness boom in the 1970s, The Complete Book of Running. The book remained on the New York Times best-seller list for two years and made him a millionaire.
The book became a bible for joggers everywhere because Fixx preached a gospel that was compelling: virtually anyone can run (you don’t need special training or equipment), and running will make you healthier. Those arguments were, well, hard to argue with. There’s no doubt that aerobic exercise like running does make you healthier for a variety of reasons.
The great irony of James Fixx’s life was his death: he died of a massive heart attack caused by silent heart disease while on a solitary jog in Vermont at the age of fifty-two. How a man who was the picture of perfect health died so suddenly and unexpectedly had to do with how the heart works.
The amount of blood ejected from the heart at any time depends on the body’s needs at that moment. More blood is required if one is exercising, experiencing anxiety or stress, or taking certain drugs. These activities cause the heart to beat faster. Thus, the heart itself requires more blood to be delivered through the coronary arteries to nourish the heart muscle.
The amount of blood being delivered through abnormally narrowed or diseased arteries may be more than adequate to supply the needs of a heart beating at a slow or resting rate if the body’s requirements are relatively minimal, such as when sleeping or resting. But if the body’s blood-flow requirements are increased—for example, with exercise—the heart rate speeds up, and there is a resulting need for more blood flow through the coronary arteries.
If this demand for increased blood flow is beyond the ability of the narrowed arteries to deliver, a significant heart reaction or event, notably chest pain or a heart attack, will occur. Surprisingly enough, most episodes of ischemia in patients with and without angina pectoris (chest pain) are not brought on by increases in the heart rate. Only rarely does the heart rate increase, usually at the very beginning of a period of ischemia.
In the case of James Fixx, his autopsy revealed that two of his coronary arteries were sufficiently blocked to have warranted a bypass operation. According to his friends and family, he had no physical warning signs of heart disease (no pain), although he had a family history of heart disease and was a former smoker.
Unfortunately, the premature and, yes, ironic death of Jim Fixx reinforced a popular misconception: too much exercise will kill you.
In fact, the heart rate associated with most episodes of silent heart disease is usually significantly lower than the rates observed in the same patient while on a treadmill (even when the heart rate is much higher because of the effects of exercise). Silent heart disease frequently occurs in patients with only minimally narrowed, fixed arteriosclerotic lesions (when the artery is narrowed only by 20 to 30 percent).
This symptom-free transient coronary artery narrowing or blockage is caused by a sudden artery spasm. Spasm in the coronary circulation is particularly ominous, since it usually occurs quite suddenly and without warning, in diseased or even in perfectly normal arteries, commonly when the heart rate is slow or normal. Thus, a silent heart disease episode may not be triggered by a stress test (treadmill test) and may therefore not be detected.
Episodes of silent heart disease are probably due to transient decreases in coronary artery blood flow rather than simply due to increases in oxygen need precipitated by the increased heart rates produced by exercise, emotions, drugs, and so forth. A combination of these factors is almost certainly present in every patient with silent heart disease. The concept of chest pain caused by a fast heart rate as the only warning sign of heart disease is no longer accepted by the medical profession. We now know most episodes of inadequate blood flow to the heart are not painful and are not caused or triggered by an increased heart rate.
As it turns out, Jim Fixx likely suffered at least some of his fatal coronary damage from his silent heart disease when he was watching television at night as opposed to when he was vigorously training for his next race.
The sequence of occurrence, magnitude, and duration of episodes of silent heart disease are totally unpredictable for the individual patient, but certain key patterns have emerged over the past three decades. Episodes can occur in the same patient with angina (chest pain) on one occasion and without angina on another. Such episodes may be prolonged at some times and quite brief at others.
It is interesting to note that chest pain may develop toward the end of episodes of myocardial ischemia (partial or complete blockage of a coronary artery), which in the beginning are virtually silent. It’s not an either-or proposition—either no pain or intense chest pain—as many patients experience both. Even in those patients who do not have chest pain, considerable overlap may exist between silent and painful episodes. Ischemia (inadequate blood supply) may be present for sixty minutes or longer or may be as brief as 10 to 15 seconds.
In 1983, Drs. John Deanfield, Andrew Selwyn, and their colleagues in London clearly demonstrated that the greatest frequency of both painful and pain-free episodes took place in the morning between 6:00 a.m. and 12 p.m. When this data was analyzed for “time of awakening,” the early-morning increase of silent heart disease episodes was striking. More episodes took place in the first and second hour after patients rose, at a time when they were least likely to be exerting themselves and their heart rates were usually quite slow. The episodes were found to generally follow a twenty-four-hour, biological time sequence known as the circadian rhythm pattern.
Subsequent research over the past thirty years has reconfirmed the finding that our circadian clocks are tightly related to cardiovascular functions. New research has shown a strong correlation between disruption of circadian rhythms and cardiovascular events like heart attacks. As we’ll learn in Part II, disruptive sleep patterns including sleep apnea are a significant risk factor for silent heart disease. Given the disruptions to normal circadian rhythms caused by life in the modern world—shift work, artificial light, transmeridian air flight, and smartphones—you see why cardiologists are concerned by silent heart disease risk factors that did not even exist a couple of generations ago.
Heart attacks have been found to be randomly distributed throughout the months of the year and the days of the week; their onsets tend to follow the same circadian pattern as do episodes of silent heart disease, occurring more frequently from 6 a.m. to 12 p.m., with the maximum number between 9 a.m. and 10 a.m.
It is interesting to note that these findings are consistent across all classifications of patients, old and young, men and women, smokers and nonsmokers, coffee drinkers and non–coffee drinkers. It doesn’t even matter if the patient has had a previous history of angina (chest pain) or heart attack; the pattern is the same in this case as for those who have no such history.
We know that approximately 90 percent of all heart attacks are caused by an arteriosclerotic nodule or plaque mostly made up of cholesterol and frequently found to be ruptured or spontaneously broken up, resulting in blockage of a coronary artery. It should be clear, however, that heart attacks occur not simply because of the plaque rupture itself but also because of the enlargement of the blood thrombus (or clot) that forms around the plaque (usually following rupture) and blocks the flow of blood through a coronary artery.
Clotting occurs because there is the tendency for blood elements known as platelets to clump together, quite possibly because of an increased production of the “stress hormones” adrenalin and noradrenaline (i.e., epinephrine and norepinephrine) by one of the body’s special nervous systems, the sympathetic nervous system. Other factors may also be important in facilitating blood clotting, but platelet clumping appears to be the main cause. Simple aspirin is still one of the best drugs we have to prevent platelet clumping, and it is widely used to prevent and treat heart attacks. For a while studies indicated that virtually all adults could benefit from taking a children’s dosage of aspirin every day; however, subsequent research showed that this isn’t the case. The only true beneficiaries of a daily aspirin regimen are those who have previously had a heart event or are at risk of heart disease (again, for a variety of factors that we will explore later in the book).
While plaque rupture and associated blood clotting are considered to be the most important trigger mechanisms of heart attacks, a host of other physiological mechanisms may also occur, usually in the early morning hours. First, there is frequently a blood pressure surge of twenty to thirty millimeters of mercury, which increases the likelihood of plaque rupture. Next, the muscular tension in the walls of the coronary arteries may increase, and if this transient increase in muscle tone is superimposed on a previously existing critical narrowing of the artery, further narrowing, decreased blood flow, and predisposition toward a complete blockage of the artery may occur.
A combination of these events and possibly others appears to be responsible for the clear-cut fact that heart attacks, with or without pain, and sudden death tend to occur more frequently during the morning hours. This information has proven to be of extraordinary value in designing a preventative program to avoid these events. Coronary artery spasm severe enough to cause an acute heart attack or sudden death is a complex and dynamic process that may occur even when the fixed arteriosclerotic narrowing in a coronary artery is relatively minor. These events may happen especially if, at the very moment of artery spasm, there is an increased demand for more coronary artery blood flow because of a rapid heart rate in response to exercise, stress, and/or drugs. A dynamic response such as constriction (and therefore narrowing) of a coronary artery occurs in seconds, thrombosis or clotting occurs in minutes, and development of atherosclerotic lesions requires many months or years.
The overall process starts when we are extremely young and ends with the heart damaged or even death of the heart. So, if narrowing of the arteries is the main culprit in ischemic heart disease, the question becomes, What causes clogged arteries? In other words, why do arteries become clogged with cholesterol plaques? That is precisely the question we’ll be tackling in Part II. But until then, it’s time for a closer look at the types of silent heart disease in Chapter 3 and ways the heart can become permanently damaged in Chapter 4.