Now for some good news. Just a few short decades ago, surviving an acute heart attack was essentially a fifty-fifty proposition, with half of victims dying with a few days. Doctors had only the vaguest idea of the physiology underlying heart attacks, and the treatment was pretty much let the body try to heal itself and hope for the best.
Today, 90 percent of all heart attack victims survive. And except in the most extreme cases, they can go on to live long and prosper, because early detection and treatment of complications are the rule rather than the exception.
Indeed, as we learned earlier in Part I, until recently myocardial ischemia (inadequate coronary blood flow) had been considered an all-or-none process. Heart damage was known to occur if the ischemia was prolonged or severe (that is, a heart attack). But if the episode was only transient or brief (mild angina or silent myocardial ischemia), the effects on the heart were often found to be only minimal in degree and usually completely reversible. Also, it was found that after coronary flow had been restored, metabolism and function would rapidly return to normal, and heart structure would usually be preserved. Inadequate coronary artery blood flow was considered an event that simply began with a particular kind of severe chest pain (angina) and ended after the coronary blood flow had returned to normal and the chest pain had subsided.
We now know that, in most instances, angina and even a heart attack are the final—not the first—expression of heart disease. New understanding of the biochemical and physiologic effects of reduced coronary artery blood flow has led us to the conclusion that any reduction of the usual blood supply to the heart, whether intermittent or prolonged, whether painful or not, may be the beginning of a cascade of abnormal events.
In this chapter, we learn how silent heart disease can damage the heart.
The first response of the oxygen-deprived heart is to malfunction in its pumping action, which is not necessarily followed by electrocardiographic changes or chest pain.
Late in the process, and virtually always only after the pumping and electrocardiographic abnormalities have developed, chest discomfort (angina) will occur in a small percentage of instances; more commonly, chest pain does not occur, and the ischemia (poor coronary blood flow) is then called silent myocardial ischemia (SMI). Thus, the ischemic cascade always begins with poor coronary artery blood flow (for the heart’s needs at that moment), resulting in heart muscle malfunction, followed, on occasion, by electrocardiographic changes. Finally, in the minority of instances, this series of events is concluded with chest pain or discomfort; angina is usually the late or final expression of the ischemic cascade, not the beginning one.
The concept of the ischemic cascade helps us to understand why completely silent (or, less frequently, painful) episodes of diminished coronary artery blood flow can result in completely symptom-free, transient (or permanent), significant injuries to the heart muscle itself. These recurrent injuries may eventually diminish the pumping capacity of the heart, whether or not chest discomfort has ever occurred during any of these episodes.
Since silent episodes of heart ischemia are at least three times more frequent than painful ones, and since chest pain is usually a late feature of the ischemic cascade, significant damage to the heart’s pumping abilities may occur long before chest pains develop. In other words, by the time patients start to complain of chest pains, they almost always are already afflicted with disturbed heart function of a more intense degree than appears on the surface.
Vigorous and effective treatment is therefore absolutely necessary to prevent not just the obvious episodes characterized by chest pain but, more importantly, to stop the ischemic cascade from beginning, thus giving your doctor time to take medical action to prevent temporary or permanent malfunction of the heart muscle itself and to prevent sudden death.
It was previously thought that (1) when the heart’s oxygen balance was restored before permanent injury (heart attack) occurred, heart function returned rapidly to normal, and (2) when the blood flow to the heart was diminished and prolonged beyond a critical point, irreversible heart damage occurred, and, as a result, complete recovery of its pumping function could never be restored. It has now been clearly demonstrated that periods of ischemia (inadequate coronary artery blood flow), even if too brief to cause heart damage, may nevertheless be associated with profound structural and biochemical changes that will result in diminished function of the heart as a pump. This dysfunction has been found to persist for prolonged periods—hours, days, or even weeks after the blood flow has been restored.
In other words, if a heart is “stunned” by even a brief episode of ischemia, lasting hours or in some cases even just minutes, prolonged impairment of the pumping ability of the heart may result. Stunning will occur whether or not chest pain is associated with the episode of poor coronary blood flow, and therefore three to four episodes of pain-free stunning may occur for every ischemic episode associated with chest pain.
Temporary blockage of a coronary artery produces SMI or angina; complete blockage will cause a heart attack, usually with resulting permanent damage of heart muscle. But if the artery is opened quickly—with nitroglycerine, spontaneous relaxation of the coronary artery spasm, dissolution of the clot, bypass surgery, or angioplasty—before permanent damage occurs, the heart will only be temporarily stunned. It then “hibernates,” waiting to recover its full function. The duration of the stunning effect is always much longer than the duration of the episode of poor blood flow; if permanent damage has not occurred, return of normal heart function will take place, but usually many hours or days after the episode of previously inadequate coronary artery blood flow has been improved.
The heart’s functional ability will therefore be only temporarily affected, and total recovery will usually be permanent unless the process starts all over again. If heart stunning occurs repeatedly because of recurrent ischemia, whether painful or pain-free, the heart may never have a chance to recover completely, and permanent heart damage will result. Damage may therefore be occurring silently in persons afflicted with silent myocardial ischemia.
It may also be occurring silently and progressively in patients even with mild angina, which in the past has inappropriately been considered a minor symptom by both patients and their doctors. Eventually, repeat stunning may result in ischemic cardiomyopathy, a condition in which heart function is altered and severe heart failure may occur whether or not chest pain occurs. Patients with this condition are at greater risk of heart attack or even sudden death, so treatment must be immediate and vigorous.
Since chest pain is not a reliable guide, all episodes of ischemia, silent or not, should be treated. Only in this way can stunning be avoided. If stunning does occur, coronary artery flow should be restored as quickly as possible in order to avoid permanent damage. If the circulation is restored, the stunned heart will “hibernate” and then quite probably will be restored to normal function in time.
Inadequate coronary artery blood flow can have four distinct results:
1.Transient ischemia with or without chest discomfort, electrocardiographic changes, and disturbed heart function (a category that includes patients with typical angina)
2.Severe ischemia causing heart damage and permanent heart dysfunction (i.e., a classic heart attack)
3.Heart stunning consisting of abnormal function in the heart’s pumping activities as a result of prolonged ischemia
4.Severe persistent heart dysfunction secondary to chronic (days, months, or years) inadequate coronary artery blood flow with resultant extremely poor (albeit usually recoverable) heart function
If heart damage has not occurred, heart function can be improved with drugs or revascularization, including surgery and angioplasty. In a significant number of instances, chest pains do not occur even when the coronary artery blood flow has been critically reduced to the point where either electrocardiographic or profound mechanical pumping abnormalities result. Angina occurs on the average in only 16 to 25 percent of these episodes and even less frequently in patients who are diabetic or hypertensive.
A malfunction of the pumping activity of the heart occurs first in response to inadequate coronary artery blood flow, followed by electrocardiographic abnormalities, which may then be followed on occasion by chest pain. Repeated stunning of the heart by ischemic episodes, silent or painful, results in permanent damage to the heart. In many instances, however, the damage may not be permanent, the heart will only be “hibernating,” and function will improve if circulation can be restored.
All episodes of ischemia should be vigorously treated to prevent permanent damage. The untoward effects of repeated ischemia can be avoided or diminished in intensity if these episodes, whether painful or silent, can be reduced or eliminated.
As we’ve just discussed, an episode of restricted blood flow to the heart doesn’t necessarily have to result in permanent damage. Rather, the heart can merely be stunned and then hibernate until it heals itself. That’s not the case with sudden cardiac arrest, which usually results in permanent heart damage and death, or sudden cardiac death.
Sudden cardiac arrest is the largest cause of natural death in the United States, causing about 325,000 adult deaths each year and responsible for half of all heart disease deaths. Only approximately 10 percent survive a sudden cardiac arrest, and only 8 percent of those will survive with good neurologic function.
Sudden cardiac arrest is not a heart attack, but the two are closely related. Heart attacks are caused by restricted blood flow to the heart, causing impaired functioning, but the heart usually keeps beating and the person remains conscious. In sudden cardiac arrest the heart stops functioning completely. Most heart attacks do not lead to cardiac arrest, but when cardiac arrest occurs, heart attack is a common cause. And, by the way, there are other causes of sudden death besides cardiac. The cessation of heart function also can be caused by trauma, drowning, drug overdose, asphyxia, and severe blood loss, to name a few. However, by far the most common cause of sudden death is heart related, caused by cardiac rhythm malfunction.
These totally unexpected cardiac-related deaths occur usually within one hour of the onset of symptoms. The usual cause of sudden death is an abnormal heart rhythm called ventricular fibrillation, which, if not promptly treated, causes death within three to four minutes. This chaotic rhythm consists of a completely disorganized quivering pattern of pumping activity resulting from attempts by many parts of the heart to contract simultaneously; the heart looks and acts like a beached jellyfish.
Coordinated contraction is impossible, and as a result pumping of blood from the heart into the circulatory system ceases. When this abnormal rhythm is found to be present in a coronary care unit, an emergency room, or even by a trained paramedic in the field, it frequently can be restored to normal rhythm using a defibrillator, a device that sends a controlled electric shock to the heart and is now required on all U.S. airlines and frequently found in other public places, including concert halls, shopping malls, and even restaurants.
Sudden death increases in frequency with increasing age, even though symptoms suggestive of heart trouble may never have been present. The peak incidence occurs between ages seventy-five and eighty-four. It is four times more common in men than in women, possibly because men do not have the same protection from coronary artery disease enjoyed by premenopausal women. Approximately half of the people who die from cardiac arrest have previously suffered heart attacks (frequently silent), and only 20 to 27 percent of the episodes are caused by a new heart attack.
A U.S. Public Health Service study conducted among the residents of the town of Framingham, Massachusetts, since 1948 reports sudden death as the first symptom or event in about 20 percent of all coronary heart disease patients. Think of what that means: one in every five people who ever develop a heart problem will die suddenly as the first expression of their heart disease; they will never know what hit them, never even suspecting that they had a heart problem. During the first thirty years of the Framingham study, half the men and almost two-thirds of the women who died suddenly had no previous history of coronary heart disease.
While sudden cardiac arrest disproportionally affects the elderly, it does strike the middle-aged. And while the frequency of these episodes in youthful athletes in the United States is extremely rare, upward of six thousand Americans aged eighteen or under die each year from sudden cardiac arrest, including young athletes (about one in fifty thousand).
Although accidents, suicide, or drugs are the most frequent overall causes of death in persons under the age of thirty, abnormalities of the heart or blood vessels are the usual cause of youthful sudden death. Persons over the age of thirty who die suddenly, whether athletic or sedentary, usually have previously been totally symptom-free and, in the vast majority of instances, are found to have arteriosclerotic heart disease, premature aging of the coronary arteries due to atherosclerosis (with resultant narrowing and/or complete blockage of these important vessels).
Patients who die suddenly, whether or not risk factors have been identified or treated, may have significant symptoms that precede the event and should alert both the patient and his or her doctor to the increased risk of sudden death. Unfortunately, many of these early symptoms are vague and nonspecific.
Earlier, we learned that Jim Fixx, the famous marathon runner and author, died quite suddenly and unexpectedly at age fifty-two. His death was quite likely caused by ventricular fibrillation, a malfunction of the heart’s rhythm due to sudden inadequacy of coronary artery blood flow.
Now fast-forward to 2017, when rock star Tom Petty died suddenly and unexpectedly, just a few days after performing a sold-out concert at the Hollywood Bowl in Los Angeles. Like Fixx, who died at fifty-two, Petty’s death at sixty-six was premature as well. Neither had a history of heart disease.
The difference is that while Fixx’s sudden death probably was heart related (cardiac), Petty’s was most likely caused by an accidental overdose of painkillers, which then caused his heart to stop functioning. Fixx’s condition would be easily detected with today’s diagnostics and likely reversed with today’s treatment regimens. Petty’s death was largely unpredictable except for the fact that there is a long history of famous entertainers experiencing sudden death from accidental overdoses, including Judy Garland and Michael Jackson.
Even though as many as 33 percent of heart attack victims consult a physician because of new or increasing chest pains in the six months before the heart injury occurs, chest pain is a relatively infrequent symptom, occurring in no more than 10 percent of sudden death cases. Shortness of breath, weakness or fatigue, chest palpitations, and a variety of other relatively imprecise complaints—such as indigestion, back pain, pain in the shoulders, arms, or hands, and so forth—occur more frequently; even though vague, these symptoms frequently are of sufficient intensity to bring the patient to a physician days or weeks prior to the final event. As many as 46 percent of sudden death victims had preexisting complaints severe enough to have caused them to see a physician within four weeks prior to death. In fact, many of these patients visited their doctor only three to four hours prior to the event!
Because significant treatable abnormalities of heart rhythm were detected prior to the occurrence of sudden death in approximately 85 percent of the out-of-hospital survivors, patients should consult their physicians as soon as possible after the onset of any significant symptoms. There really just isn’t any excuse for not seeing your doctor once the red flag of symptoms is raised.
The greatest psychological danger to a patient with an acute heart attack or premonitory symptoms of sudden death is denial. Negation of personal danger by denial, one of the most common human reactions to situations of life stress, is similar to rationalization; that is, it is a patient’s unconscious attempt to minimize or eliminate the threat to his or her life or health. Denial leads to an average delay (the time interval from the onset of symptoms to the arrival at a medical facility) of between 2.9 and 5.1 hours.
The enormity of this problem becomes apparent when one realizes that at least 50 percent of all deaths from heart attacks occur within four hours of the onset of symptoms, usually before the patient reaches the hospital. The size of the heart attack (and therefore the severity of subsequent complications) appears to relate to delay in treatment; patients simply do not get to well-equipped medical facilities in time to prevent or treat major problems.
Those who recognize the true cause of their symptoms will get to the hospital sooner than those who explain away their symptoms as being due to a stomachache or muscle spasm. Ironically, husbands and wives are responsible for producing more delay than are friends, associates, or employers. Denial and delay must be avoided if the incidence of sudden death is to be reduced.
Specific drug and other treatments that can reduce or often completely eliminate the potential for sudden death are available to patients who present themselves quickly enough to a hospital emergency room. Chest pain of new onset, any change (in either frequency or intensity) in a long-standing pattern of chest discomfort, or even atypical chest symptoms known as “anginal equivalents” (pains occurring in the teeth, jaw, neck, shoulders, back, arms, elbows, or fingers) should cause one to seek immediate medical attention. Also, even vague symptoms such as shortness of breath, weakness, or fatigue, as well as recurrent palpitations, should not be ignored, especially if precipitated by minimal exertion.
Physicians should be consulted as frequently as is necessary to evaluate symptoms and answer questions, especially by persons who are at high risk. Prevention and treatment of abnormal risk factors, which we’ll explore in Part II of the book, will effectively reduce the incidence of sudden death.
One final note about sudden cardiac death. As with silent heart disease in general and nonfatal heart attacks, the vast majority of scientific studies have clearly demonstrated the peak onset of sudden death occurs between 6 a.m. and 12 p.m. The Massachusetts Department of Public Health and the Framingham Heart Study reported similar data. In addition, the latter group noted that the risk of sudden cardiac death was at least 70 percent greater between 7 a.m. and 9 a.m.