Silent heart disease is usually the result of an inadequate supply of coronary artery blood—and here comes the important part—that is pain-free. It’s “silent” because it gives no clues, such as chest pain, that suggests strain or damage to the heart. Within that narrow definition of silent heart disease, there are variations.
In April 1986, a group of prominent cardiologists met at the request of the National Heart Institute in Bethesda, Maryland. They defined silent myocardial ischemia—what we’re referring to in this book as silent heart disease—and devised a classification system. Symptom-free patients without a history of heart disease but afflicted with intermittently inadequate coronary artery blood flow were henceforth to be called Type 1; those with symptom-free silent heart disease who had previously suffered a heart attack would be called Type 2; and patients afflicted with or without anginal chest pains and constricted arteries who had not previously suffered a heart attack would be Type 3.
This categorization was more than an academic exercise because with each silent heart disease classification came a singular set of challenges.
If silent heart disease is diagnosed in a symptom-free patient, the outlook is as grave as it is for a similar patient with angina pains; in other words, silent heart disease is bad whether it is associated with chest pain or not.
Contrary to popular belief, most people today do not die from a heart attack. In fact, 90 percent survive. That wasn’t the case just a few decades ago when nearly half of heart attack victims died within a few days.
The survivors of heart attacks living in the United States form an extremely large, growing, and readily identifiable subset of patients with known coronary heart disease. This group in aggregate now totals at least 5 million. It’s no small irony that while the death rate due to heart disease among the general population has decreased over the last twenty years, the rate of those who suffer from heart disease has increased because good medical therapy has increased the number of heart attack survivors.
Over the past decade, it has become common practice to perform a low-level stress test on heart attack subjects one to three weeks after the acute heart injury has occurred. The cardiologist uses this test to be assured that patients are able to resume the increasingly vigorous physical activities required of them when they return home from the hospital without developing signs or symptoms suggestive of heart ischemia or rhythm malfunctions. Routine and/or thallium stress testing is also extensively employed weeks, months, and years after a heart attack in order to determine (1) the functional capacity of the heart, including its ability to withstand an increased heart rate such as might occur in stressful or even relatively ordinary activities, and (2) whether or not silent heart disease is present.
It has been estimated that at least 40 percent of the 1 million heart attack survivors in the United States each year will subsequently have abnormal treadmill stress tests, with 50 percent of these having been symptom-free—the classic Type 2 patient. Similarly, wearable monitoring devices reveal that that as many as 33 percent of heart attack survivors will have silent heart disease.
Post–heart attack patients who demonstrate pain-free ischemia on either test have a much higher incidence of recurrent heart attacks, new onset of anginal chest pain, and sudden death than do patients who do not demonstrate changes on these tests.
To frame it another way, patients afflicted with silent heart disease after a heart attack are ten times more likely to die within one year than are patients without symptoms, and almost one-third of them do. Finding silent heart disease in these patients is important because it can be treated, and the incidence of serious health problems and death thus can be reduced or eliminated.
The millions of Americans who have silent heart disease and angina are more likely to have an early adverse outcome, including recurrent heart attacks, increasing angina, or even sudden death, than are the angina patients without silent heart disease. Wait a minute, you’re probably thinking. Didn’t we earlier define silent heart disease as symptom-free, painless ischemia (inadequate blood flow to the heart)? Can a patient have it both ways?
The answer is yes. Some patients do have it both ways—inadequate blood flow to the heart, sometimes with pain and at other times without pain; sometimes the condition is symptomatic and at other times asymptomatic. We know this because patients might experience chest pains for the first time and go to a cardiologist, who confirms their chest pains are symptomatic of an intermittently constricted blood flow to the heart. But guess what? Further diagnostic analysis shows the telltale damage to the heart was caused by past, painless episodes of silent heart disease or classic angina pectoris resulting in heart scars.
It is of utmost importance to properly and carefully study all angina patients with exercise testing and/or Holter recording (more on this later) to determine if silent ischemia is present. Research indicates that EKG abnormalities on treadmill or Holter tests may even occur more frequently in patients without chest pain than in patients with chest pain.
The outlook for developing cardiac complications or sudden death is related to the presence and degree of inadequate blood flow to the heart, painful or not.
Ironically, chest pain can be a life-saving warning if addressed in time. Symptom-free, high-risk heart patients with numerous risk factors (smoking, high cholesterol, high blood pressure, positive family history, all of which we’ll explore in Part 2) have a much higher mortality rate from heart attacks and incidence of sudden death than do patients without abnormal risk factors, angina, and/or known coronary heart disease. Patients with silent heart disease who have previously suffered an acute heart attack or who have unstable angina are at very high risk for death and recurrent heart attacks compared to similar patients without silent heart disease and/or a history of cardiac symptoms or events. Diabetics and high-blood-pressure patients are particularly prone to silent heart disease and silent (symptom-free) heart attacks.
The absence of pain does not mean that silent heart disease is benign. Although approximately 50 percent of all patients with significant heart disease go to their physicians because of chest pain or other symptoms, sudden death or an acute heart attack is the initial event for the other 50 percent. The vast majority of patients with symptom-free heart disease do not seek medical attention because they are totally unaware of their life-threatening heart condition.
It is imperative that doctors identify which patients have symptom-free heart disease, because we now have specific therapies available that can delay or possibly even prevent heart attacks or sudden death. Let’s remind ourselves one more time: physicians and patients should not rely on chest pains as the first warning of a significant heart condition.
While we refer to the classic heart attack as being characterized by chest pain, it’s more than that. Angina pectoris literally means “choking in the chest,” and the pain experienced by patients suffering from it is unique. Some describe it as a heaviness on the chest, others as an extreme tightness or squeezing, often accompanied by extreme fatigue.
The association between heart attack and angina is literally engrained in medical history, which why it was initially so difficult for my colleagues and me, over thirty years, to convince our fellow cardiologists that there was such a thing as silent heart disease.
No doubt, the ancients experienced heart disease and heart attacks. We know that because modern-day diagnostic technology has revealed the signs of it in Egyptian mummies. The Romans, who were fanatical about recording everyday life, mention symptoms associated with heart attack and heart disease but made no connection between the symptoms and the pathology of heart disease.
Likely the first written account of heart disease was by a seventh-century Arab poet who was lovesick, mourning for a partner forced to marry another and move away:
My heart is firmly seized
By a bird’s claws;
My heart is tightly squeezed,
When Lila’s name flows.
My body is tightly bound,
My body is tightly bound,
Is like a finger ring around.
That certainly sounds like angina to me, and indeed, as we’ll learn later, stress hormones caused by extreme emotional anxiety can facilitate a heart event that is colloquially called a “broken heart.”
Renaissance man Leonardo da Vinci (1452–1519) was the first to investigate and then record his finding of pathology in the coronary arteries. William Harvey (1578–1657), King Charles I of England’s personal royal physician, discovered that blood moves around the body in a circulatory manner from the heart, an important next step in understanding the connection between angina and heart attack. German professor of medicine Friedrich Hoffmann (1660–1742), in his classic medical text, observed that coronary heart disease started in the areas where there is a “reduced passage of the blood within the coronary arteries.” Credit Americans William Osler (1849–1919) and James B. Herrick (1861–1954) for the determination that the narrowing of the coronary arteries was the most likely cause of angina and heart attacks.
When angina is of new onset, when it suddenly increases in intensity, frequency, or duration, and happens repeatedly, occurring even at rest or with only minimal exertion, or when it is associated with profuse sweating, nausea, vomiting, shortness of breath, rapid palpitations, or profound malaise, it is called unstable angina. This is a sign of an impending or evolving acute heart attack. It is considered a medical emergency; the coronary circulation is deteriorating, suddenly becoming inadequate. It must not be ignored; immediate medical attention is necessary.
Time is of the essence. If unable to reach a doctor for advice or instruction, the sufferer should immediately call for emergency help by telephone or get to the nearest hospital emergency room by the fastest means. Don’t wait!
While not all heart attacks are associated with chest pains, it is also true that not all chest pain is due to a heart attack or heart failure.
Chest pain may be due to a variety of medical problems other than coronary artery disease. Some individuals experience chest discomfort in response to anxiety and tension, much as many people subject to unusual emotional stress and strain suffer headaches. Chest pain may originate in the muscles or bones (inflammation of the rib joints, arthritis of the spine), gastrointestinal tract (esophagitis, esophageal spasm, peptic ulcer, gall bladder disease, acute pancreatitis), and lungs (lung emboli or clots, pneumonia, cancer). Or it may be due to heart or blood vessel problems other than coronary artery disease—for example, inflammation of the heart or its enveloping sack may cause chest pain.
That said, it’s worth underscoring that people should not play Russian roulette with their health and attempt to guess the true cause of their chest pain. Take no chances. If you have chest pain—of any degree or variety—let a medical professional determine if it’s heartburn or angina (or something else).
Let’s end this chapter with the eight-hundred-pound gorilla in the room: Why don’t the many millions of people with silent heart disease experience any chest pains?
The short answer, after thirty years of research, is that we still don’t know. But we do have clues. Some people simply may not feel any pain possibly because of certain painkilling substances mysteriously produced within their bodies. Others may be suffering from long-standing damage to nerve endings that occurs more frequently in diabetics, those with chronic kidney disease, or hypertensives (sufferers of high blood pressure), three groups with a disproportionally high incidence of silent and/or symptomatic heart attacks.
Still others actually do suffer symptoms of a heart attack—just not the gripping chest pain of angina that has been depicted repeatedly in popular culture. (Hollywood loves a good heart attack with lots of angina!) A famous country musician who was my patient had brushed aside his occasional bouts of intense heartburn—sometimes lasting a day or more—as nothing more than too much barbeque. Another patient, a much-in-demand indoor cycling instructor, could not figure out why she could lead a class up a virtual hill one week with no problem and then the next week felt completely winded on the same ride. Both of their examinations revealed silent heart disease, which they had probably suffered with for years before coming to see me.
Bottom line: If something doesn’t make sense or feel right, even if you can’t quite put your finger on it, have it checked by your doctor. Detection is the first step in receiving treatment for silent heart disease and the prevention of heart attacks.